Exosomal long non-coding RNA LIPCAR derived from oxLDL-treated THP-1 cells regulates the proliferation of human umbilical vein endothelial cells and human vascular smooth muscle cells

It has been reported that long non-coding RNA (lncRNA) LIPCAR is involved in the progression of atherosclerosis. However, the mechanism underlying the effects of LIPCAR on regulating the occurrence and development of atherosclerosis remains unclear. Reverse transcription-quantitative PCR was perform...

Celý popis

Uloženo v:

Podrobná bibliografie
Vydáno v:	Biochemical and biophysical research communications Ročník 575; s. 65 - 72
Hlavní autoři:	Hu, Nan, Zeng, Xixi, Tang, Feifei, Xiong, Sizheng
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	United States Elsevier Inc 20.10.2021
Témata:	apoptosis Apoptosis - physiology Atherosclerosis Atherosclerosis - blood Atherosclerosis - genetics Atherosclerosis - pathology biomarkers Cell Movement - physiology Cell Proliferation - physiology cyclin-dependent kinase Exosome Exosomes Foam cell foam cells Human Umbilical Vein Endothelial Cells Humans Knockdown Lipoproteins, LDL - pharmacology lncRNA LIPCAR low density lipoprotein Muscle, Smooth, Vascular - metabolism Muscle, Smooth, Vascular - pathology non-coding RNA oxidation proliferating cell nuclear antigen RNA, Long Noncoding - blood RNA, Long Noncoding - genetics smooth muscle THP-1 Cells Knockdown Foam cell Exosome lncRNA LIPCAR Atherosclerosis
ISSN:	0006-291X, 1090-2104, 1090-2104
On-line přístup:	Získat plný text
Tagy:	Přidat tag Žádné tagy, Buďte první, kdo vytvoří štítek k tomuto záznamu!

Abstract	It has been reported that long non-coding RNA (lncRNA) LIPCAR is involved in the progression of atherosclerosis. However, the mechanism underlying the effects of LIPCAR on regulating the occurrence and development of atherosclerosis remains unclear. Reverse transcription-quantitative PCR was performed to detect the levels of LIPCAR in the plasma of patients with atherosclerosis and in THP-1 macrophages. THP-1 cells were stimulated with oxidized low-density lipoprotein (ox-LDL) to induce foam cell formation. Furthermore, Transwell assay was carried out to evaluate the migration ability of vascular smooth muscle cells (VSMCs). The expression of LIPCAR in the plasma of patients with atherosclerosis was significantly higher compared with that in healthy subjects, while LIPCAR knockdown notably reversed ox-LDL-induced THP-1 cell apoptosis. In addition, LIPCAR was upregulated in exosomes derived from THP-1 cells treated with ox-LDL (THP-1/ox-LDL Exo). Furthermore, THP-1/ox-LDL Exo significantly increased the expression levels of CDK2 and proliferative cell nuclear antigen in human VSMCs, while these effects were reversed following LIPCAR silencing. The results of the present study suggested that exosomal lncRNA LIPCAR derived from ox-LDL modified THP-1 cells could promote the progression of atherosclerosis. Therefore, LIPCAR may be considered as a novel biomarker for the development of new strategies to treat atherosclerosis. •The level of Long non-coding RNAs (lncRNA) LIPCAR was upregulated in exosomes derived from THP-1 cells that were treated with oxidized low density lipoprotein (oxLDL).•THP-1/oxLDL Exo reduced the viability of human umbilical vein endothelial cells by inducing apoptosis; however, these phenomena were reversed by LIPCAR knockdown.•THP-1/oxLDL Exo obviously upregulated the levels of CDK2 and PCNA in human vascular smooth muscle cells (VSMCs).
AbstractList	It has been reported that long non-coding RNA (lncRNA) LIPCAR is involved in the progression of atherosclerosis. However, the mechanism underlying the effects of LIPCAR on regulating the occurrence and development of atherosclerosis remains unclear. Reverse transcription-quantitative PCR was performed to detect the levels of LIPCAR in the plasma of patients with atherosclerosis and in THP-1 macrophages. THP-1 cells were stimulated with oxidized low-density lipoprotein (ox-LDL) to induce foam cell formation. Furthermore, Transwell assay was carried out to evaluate the migration ability of vascular smooth muscle cells (VSMCs). The expression of LIPCAR in the plasma of patients with atherosclerosis was significantly higher compared with that in healthy subjects, while LIPCAR knockdown notably reversed ox-LDL-induced THP-1 cell apoptosis. In addition, LIPCAR was upregulated in exosomes derived from THP-1 cells treated with ox-LDL (THP-1/ox-LDL Exo). Furthermore, THP-1/ox-LDL Exo significantly increased the expression levels of CDK2 and proliferative cell nuclear antigen in human VSMCs, while these effects were reversed following LIPCAR silencing. The results of the present study suggested that exosomal lncRNA LIPCAR derived from ox-LDL modified THP-1 cells could promote the progression of atherosclerosis. Therefore, LIPCAR may be considered as a novel biomarker for the development of new strategies to treat atherosclerosis. It has been reported that long non-coding RNA (lncRNA) LIPCAR is involved in the progression of atherosclerosis. However, the mechanism underlying the effects of LIPCAR on regulating the occurrence and development of atherosclerosis remains unclear.Reverse transcription-quantitative PCR was performed to detect the levels of LIPCAR in the plasma of patients with atherosclerosis and in THP-1 macrophages. THP-1 cells were stimulated with oxidized low-density lipoprotein (ox-LDL) to induce foam cell formation. Furthermore, Transwell assay was carried out to evaluate the migration ability of vascular smooth muscle cells (VSMCs).The expression of LIPCAR in the plasma of patients with atherosclerosis was significantly higher compared with that in healthy subjects, while LIPCAR knockdown notably reversed ox-LDL-induced THP-1 cell apoptosis. In addition, LIPCAR was upregulated in exosomes derived from THP-1 cells treated with ox-LDL (THP-1/ox-LDL Exo). Furthermore, THP-1/ox-LDL Exo significantly increased the expression levels of CDK2 and proliferative cell nuclear antigen in human VSMCs, while these effects were reversed following LIPCAR silencing.The results of the present study suggested that exosomal lncRNA LIPCAR derived from ox-LDL modified THP-1 cells could promote the progression of atherosclerosis. Therefore, LIPCAR may be considered as a novel biomarker for the development of new strategies to treat atherosclerosis. It has been reported that long non-coding RNA (lncRNA) LIPCAR is involved in the progression of atherosclerosis. However, the mechanism underlying the effects of LIPCAR on regulating the occurrence and development of atherosclerosis remains unclear. Reverse transcription-quantitative PCR was performed to detect the levels of LIPCAR in the plasma of patients with atherosclerosis and in THP-1 macrophages. THP-1 cells were stimulated with oxidized low-density lipoprotein (ox-LDL) to induce foam cell formation. Furthermore, Transwell assay was carried out to evaluate the migration ability of vascular smooth muscle cells (VSMCs). The expression of LIPCAR in the plasma of patients with atherosclerosis was significantly higher compared with that in healthy subjects, while LIPCAR knockdown notably reversed ox-LDL-induced THP-1 cell apoptosis. In addition, LIPCAR was upregulated in exosomes derived from THP-1 cells treated with ox-LDL (THP-1/ox-LDL Exo). Furthermore, THP-1/ox-LDL Exo significantly increased the expression levels of CDK2 and proliferative cell nuclear antigen in human VSMCs, while these effects were reversed following LIPCAR silencing. The results of the present study suggested that exosomal lncRNA LIPCAR derived from ox-LDL modified THP-1 cells could promote the progression of atherosclerosis. Therefore, LIPCAR may be considered as a novel biomarker for the development of new strategies to treat atherosclerosis. •The level of Long non-coding RNAs (lncRNA) LIPCAR was upregulated in exosomes derived from THP-1 cells that were treated with oxidized low density lipoprotein (oxLDL).•THP-1/oxLDL Exo reduced the viability of human umbilical vein endothelial cells by inducing apoptosis; however, these phenomena were reversed by LIPCAR knockdown.•THP-1/oxLDL Exo obviously upregulated the levels of CDK2 and PCNA in human vascular smooth muscle cells (VSMCs). It has been reported that long non-coding RNA (lncRNA) LIPCAR is involved in the progression of atherosclerosis. However, the mechanism underlying the effects of LIPCAR on regulating the occurrence and development of atherosclerosis remains unclear.BACKGROUNDIt has been reported that long non-coding RNA (lncRNA) LIPCAR is involved in the progression of atherosclerosis. However, the mechanism underlying the effects of LIPCAR on regulating the occurrence and development of atherosclerosis remains unclear.Reverse transcription-quantitative PCR was performed to detect the levels of LIPCAR in the plasma of patients with atherosclerosis and in THP-1 macrophages. THP-1 cells were stimulated with oxidized low-density lipoprotein (ox-LDL) to induce foam cell formation. Furthermore, Transwell assay was carried out to evaluate the migration ability of vascular smooth muscle cells (VSMCs).METHODSReverse transcription-quantitative PCR was performed to detect the levels of LIPCAR in the plasma of patients with atherosclerosis and in THP-1 macrophages. THP-1 cells were stimulated with oxidized low-density lipoprotein (ox-LDL) to induce foam cell formation. Furthermore, Transwell assay was carried out to evaluate the migration ability of vascular smooth muscle cells (VSMCs).The expression of LIPCAR in the plasma of patients with atherosclerosis was significantly higher compared with that in healthy subjects, while LIPCAR knockdown notably reversed ox-LDL-induced THP-1 cell apoptosis. In addition, LIPCAR was upregulated in exosomes derived from THP-1 cells treated with ox-LDL (THP-1/ox-LDL Exo). Furthermore, THP-1/ox-LDL Exo significantly increased the expression levels of CDK2 and proliferative cell nuclear antigen in human VSMCs, while these effects were reversed following LIPCAR silencing.RESULTSThe expression of LIPCAR in the plasma of patients with atherosclerosis was significantly higher compared with that in healthy subjects, while LIPCAR knockdown notably reversed ox-LDL-induced THP-1 cell apoptosis. In addition, LIPCAR was upregulated in exosomes derived from THP-1 cells treated with ox-LDL (THP-1/ox-LDL Exo). Furthermore, THP-1/ox-LDL Exo significantly increased the expression levels of CDK2 and proliferative cell nuclear antigen in human VSMCs, while these effects were reversed following LIPCAR silencing.The results of the present study suggested that exosomal lncRNA LIPCAR derived from ox-LDL modified THP-1 cells could promote the progression of atherosclerosis. Therefore, LIPCAR may be considered as a novel biomarker for the development of new strategies to treat atherosclerosis.CONCLUSIONThe results of the present study suggested that exosomal lncRNA LIPCAR derived from ox-LDL modified THP-1 cells could promote the progression of atherosclerosis. Therefore, LIPCAR may be considered as a novel biomarker for the development of new strategies to treat atherosclerosis.
Author	Hu, Nan Tang, Feifei Xiong, Sizheng Zeng, Xixi
Author_xml	– sequence: 1 givenname: Nan surname: Hu fullname: Hu, Nan organization: Department of Cardiothoracic Surgery, Taihe Hospital, Hubei University of Medicine, Shiyan, Hubei, 442000, China – sequence: 2 givenname: Xixi surname: Zeng fullname: Zeng, Xixi organization: Department of Anatomy, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China – sequence: 3 givenname: Feifei surname: Tang fullname: Tang, Feifei organization: Department of Cardiothoracic Surgery, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China – sequence: 4 givenname: Sizheng surname: Xiong fullname: Xiong, Sizheng email: D201981805@hust.edu.cn organization: Department of Cardiothoracic and Vascular Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/34455222$$D View this record in MEDLINE/PubMed
BookMark	eNqFks9u1DAQxi1URP_AC3BAPnLJMnZiJ5G4rJZCK62gqorEzXLsSeuVExc7WZW34TE482R42e2FQznZGv2-bzzj75QcjWFEQl4zWDBg8t1m0XXRLDhwtoBmAaJ8Rk4YtFBwBtUROQEAWfCWfTsmpyltABirZPuCHJdVJQTn_IT8On8IKQzaUx_GW5o7FCZYl6_Xn5d0fXm1Wl5Ti9Ft0dI-hoGGh_WHdTFF1FMu3VxcFez3T4PeJxrxdva5nOh0h_Q-Bu96jHpyYaShp3fzoEc6D53zzuSOW3QjxdGGTHuXC3sXPdoDutXJZMNI0xAyRIc5GY977CV53muf8NXhPCNfP57frC6K9ZdPl6vlujBl005FncdEsKIs8y46UfcVSmFYB1XXlcxCxbVoWw6iRobcgBTMil4zLVhdg7HlGXm7983jfJ8xTWpwafcCPWKYk-KylHUredv8HxVSclE2jczomwM6dwNadR_doOMP9fgxGWj2gIkhpYi9Mm76u8kpaucVA7XLgNqoXQbULgMKGpUzkKX8H-mj-5Oi93sR5l1uHUaVjMPRoHURzaRscE_J_wDLV8xf
CitedBy_id	crossref_primary_10_1155_sci_9986368 crossref_primary_10_3389_fcvm_2023_1235953 crossref_primary_10_3389_fmed_2023_1193660 crossref_primary_10_3389_fphar_2022_857331 crossref_primary_10_1113_JP288459 crossref_primary_10_1007_s40120_023_00482_9 crossref_primary_10_1016_j_jad_2025_119653 crossref_primary_10_3389_fbioe_2022_913791 crossref_primary_10_3390_ijms23021002 crossref_primary_10_1016_j_bcp_2023_115572 crossref_primary_10_3389_fcvm_2023_1090909 crossref_primary_10_3390_ijms26031008 crossref_primary_10_3389_fphar_2025_1563800 crossref_primary_10_1016_j_molimm_2022_02_018 crossref_primary_10_3390_ijms23073534 crossref_primary_10_3390_ijms241512076 crossref_primary_10_3390_molecules27207025 crossref_primary_10_3390_cells12141832 crossref_primary_10_1038_s41598_022_11260_2 crossref_primary_10_1186_s12964_022_00949_6 crossref_primary_10_2174_0109298673302220240430173404
Cites_doi	10.1161/ATVBAHA.119.313749 10.1007/s00109-017-1575-8 10.1016/j.cub.2018.01.059 10.1038/s41418-018-0235-z 10.2147/DDDT.S194787 10.1002/stem.3061 10.1016/j.bbrc.2019.01.094 10.1159/000478872 10.1016/j.vph.2018.08.002 10.1038/s41419-019-1667-1 10.1016/j.pharmthera.2017.02.020 10.1016/j.lfs.2019.116733 10.3390/ijms21082992 10.1097/MD.0000000000010473 10.3389/fphar.2018.01105 10.2174/1574888X13666180403163456 10.1038/aps.2017.12 10.1093/cvr/cvz203 10.1016/j.apsb.2016.02.001 10.1161/CIRCRESAHA.115.307611 10.18632/aging.103034 10.1124/pr.118.017178 10.1039/C9FO02934F 10.1161/CIRCRESAHA.114.303915
ContentType	Journal Article
Copyright	2021 Elsevier Inc. Copyright © 2021 Elsevier Inc. All rights reserved.
Copyright_xml	– notice: 2021 Elsevier Inc. – notice: Copyright © 2021 Elsevier Inc. All rights reserved.
DBID	AAYXX CITATION CGR CUY CVF ECM EIF NPM 7X8 7S9 L.6
DOI	10.1016/j.bbrc.2021.08.053
DatabaseName	CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed MEDLINE - Academic AGRICOLA AGRICOLA - Academic
DatabaseTitle	CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) MEDLINE - Academic AGRICOLA AGRICOLA - Academic
DatabaseTitleList	MEDLINE AGRICOLA MEDLINE - Academic
Database_xml	– sequence: 1 dbid: NPM name: PubMed url: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: 7X8 name: MEDLINE - Academic url: https://search.proquest.com/medline sourceTypes: Aggregation Database
DeliveryMethod	fulltext_linktorsrc
Discipline	Anatomy & Physiology Chemistry Biology
EISSN	1090-2104
EndPage	72
ExternalDocumentID	34455222 10_1016_j_bbrc_2021_08_053 S0006291X21012304
Genre	Research Support, Non-U.S. Gov't Journal Article
GroupedDBID	--- --K --M -~X .~1 0R~ 1B1 1RT 1~. 1~5 23N 4.4 457 4G. 53G 5GY 5VS 6J9 7-5 71M 8P~ 9JM AABNK AACTN AAEDT AAEDW AAIAV AAIKJ AAKOC AALRI AAOAW AAQFI AAXUO ABFNM ABFRF ABGSF ABJNI ABMAC ABUDA ABYKQ ACDAQ ACGFO ACGFS ACNCT ACRLP ADBBV ADEZE ADUVX AEBSH AEFWE AEHWI AEKER AENEX AFFNX AFKWA AFTJW AFXIZ AGHFR AGUBO AGYEJ AIEXJ AIKHN AITUG AJOXV ALMA_UNASSIGNED_HOLDINGS AMFUW AMRAJ AXJTR BKOJK BLXMC CS3 D0L DM4 DOVZS EBS EFBJH EFLBG EO8 EO9 EP2 EP3 F5P FDB FIRID FNPLU FYGXN G-Q GBLVA IHE J1W K-O KOM L7B LG5 LX2 M41 MO0 N9A O-L O9- OAUVE OZT P-8 P-9 P2P PC. Q38 RNS ROL RPZ SCC SDF SDG SDP SES SPCBC SSU SSZ T5K TWZ WH7 XPP XSW ZA5 ZMT ~02 ~G- .55 .GJ .HR 1CY 3O- 9DU 9M8 AAHBH AAQXK AATTM AAXKI AAYJJ AAYWO AAYXX ABDPE ABEFU ABWVN ABXDB ACKIV ACLOT ACRPL ACVFH ADCNI ADFGL ADIYS ADMUD ADNMO AEIPS AEUPX AFJKZ AFPUW AGQPQ AGRDE AHHHB AIGII AIIUN AKBMS AKRWK AKYEP ANKPU APXCP ASPBG AVWKF AZFZN CAG CITATION COF EFKBS EJD FEDTE FGOYB G-2 HLW HVGLF HZ~ MVM OHT R2- SBG SEW UQL WUQ X7M Y6R ZGI ZKB ~HD ~KM AGCQF AGRNS BNPGV CGR CUY CVF ECM EIF NPM SSH 7X8 7S9 L.6
ID	FETCH-LOGICAL-c389t-7522e0d533006b57f4e65c1b04bb31d042a5992057e1e2c0651d5fa1a51770cd3
ISICitedReferencesCount	26
ISICitedReferencesURI	http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000690878800005&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
ISSN	0006-291X 1090-2104
IngestDate	Wed Oct 01 14:36:21 EDT 2025 Sat Sep 27 20:16:46 EDT 2025 Mon Jul 21 05:58:10 EDT 2025 Tue Nov 18 20:51:52 EST 2025 Sat Nov 29 07:31:33 EST 2025 Fri Feb 23 02:43:07 EST 2024
IsPeerReviewed	true
IsScholarly	true
Keywords	Knockdown Foam cell Exosome lncRNA LIPCAR Atherosclerosis
Language	English
License	Copyright © 2021 Elsevier Inc. All rights reserved.
LinkModel	OpenURL
MergedId	FETCHMERGED-LOGICAL-c389t-7522e0d533006b57f4e65c1b04bb31d042a5992057e1e2c0651d5fa1a51770cd3
Notes	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
PMID	34455222
PQID	2566253886
PQPubID	23479
PageCount	8
ParticipantIDs	proquest_miscellaneous_2636796298 proquest_miscellaneous_2566253886 pubmed_primary_34455222 crossref_citationtrail_10_1016_j_bbrc_2021_08_053 crossref_primary_10_1016_j_bbrc_2021_08_053 elsevier_sciencedirect_doi_10_1016_j_bbrc_2021_08_053
PublicationCentury	2000
PublicationDate	2021-10-20
PublicationDateYYYYMMDD	2021-10-20
PublicationDate_xml	– month: 10 year: 2021 text: 2021-10-20 day: 20
PublicationDecade	2020
PublicationPlace	United States
PublicationPlace_xml	– name: United States
PublicationTitle	Biochemical and biophysical research communications
PublicationTitleAlternate	Biochem Biophys Res Commun
PublicationYear	2021
Publisher	Elsevier Inc
Publisher_xml	– name: Elsevier Inc
References	Elahi, Farwell, Nolta, Anderson (bib13) 2020; 38 Wang, Song, Li, Wu, Gu, Yuan (bib19) 2019; 13 Zárate, Manuel-Apolinar, Basurto, De la Chesnaye, Saldívar (bib1) 2016; 86 Kumarswamy, Bauters, Volkmann, Maury, Fetisch, Holzmann, Lemesle, de Groote, Pinet, Thum (bib16) 2014; 114 Yaghoubi, Movassaghpour, Zamani, Talebi, Mehdizadeh, Yousefi (bib12) 2019; 233 Wang, Yang, Lei, Tzvetkov, Liu, Yeung, Xu, Atanasov (bib5) 2019; 71 Herrington, Lacey, Sherliker, Armitage, Lewington (bib7) 2016; 118 Mushenkova, Summerhill, Zhang, Romanenko, Grechko, Orekhov (bib2) 2020; 21 Luan, Sansanaphongpricha, Myers, Chen, Yuan, Sun (bib28) 2017; 38 Meldolesi (bib22) 2018; 28 Guo, Wu, Li, Zheng, Ye, Dai, Kang, Lu, Xu, Xu, Xiao, Lu, Bai, Hu, Wang (bib8) 2019; 26 Chistiakov, Melnichenko, Myasoedova, Grechko, Orekhov (bib4) 2017; 95 Li, Jin, Xie, Wen, Chen, Xu, Ding, Ren, Xiao (bib14) 2018; 13 Chen, Yang, Guo, Chen, Zheng, Zeng, Tong (bib15) 2017; 12 Bian, Jing, Yang, Shi, Chen, Xu, Wang, Jiang, Yang, Zhang, Li, Wang, Wang, Sun, Zhang (bib9) 2020; 12 Wang, Li, Chen, Wei, Xu (bib17) 2019; 25 Fasolo, Di Gregoli, Maegdefessel, Johnson (bib6) 2019; 115 Barile, Vassalli (bib27) 2017; 174 Kalluri, LeBleu (bib23) 2020 Chen, Zhao, Ma, Zhang, Lu, Wang, Zong, Qin, Wang, Yingfeng Yang, Wang, Liu (bib18) 2017; 42 Baek, Kwak, Yoon, Kim, Lee (bib21) 2019; 510 Wang, Zhu, Shi, Zhao, Gao, Weng, Liu, Li, Zou, Hu, Sun, Ge (bib25) 2019; 10 Yao, Yan, Zhang, Li, Wan (bib10) 2018; 97 Liu, Li, Wu, Xie, Sun, Dai (bib24) 2018; 9 Ha, Yang, Nadithe (bib26) 2016; 6 Li, Li, Zhang, Shi, Yang, Zheng, Cao, Yue, Ma (bib20) 2020; 11 Maguire, Pearce, Xiao (bib3) 2019; 112 Sun, Fu, Gu, Xi, Peng, Wang, Sun, Wang, Qian, Qin, Qu, Piao, Zhong, Liu, Zhang, Fang, Tian, Li, Maegdefessel, Tian, Yu (bib11) 2020; 40 Ha (10.1016/j.bbrc.2021.08.053_bib26) 2016; 6 Wang (10.1016/j.bbrc.2021.08.053_bib5) 2019; 71 Li (10.1016/j.bbrc.2021.08.053_bib20) 2020; 11 Bian (10.1016/j.bbrc.2021.08.053_bib9) 2020; 12 Sun (10.1016/j.bbrc.2021.08.053_bib11) 2020; 40 Baek (10.1016/j.bbrc.2021.08.053_bib21) 2019; 510 Li (10.1016/j.bbrc.2021.08.053_bib14) 2018; 13 Wang (10.1016/j.bbrc.2021.08.053_bib19) 2019; 13 Luan (10.1016/j.bbrc.2021.08.053_bib28) 2017; 38 Kalluri (10.1016/j.bbrc.2021.08.053_bib23) 2020 Mushenkova (10.1016/j.bbrc.2021.08.053_bib2) 2020; 21 Herrington (10.1016/j.bbrc.2021.08.053_bib7) 2016; 118 Wang (10.1016/j.bbrc.2021.08.053_bib25) 2019; 10 Fasolo (10.1016/j.bbrc.2021.08.053_bib6) 2019; 115 Maguire (10.1016/j.bbrc.2021.08.053_bib3) 2019; 112 Elahi (10.1016/j.bbrc.2021.08.053_bib13) 2020; 38 Guo (10.1016/j.bbrc.2021.08.053_bib8) 2019; 26 Liu (10.1016/j.bbrc.2021.08.053_bib24) 2018; 9 Yao (10.1016/j.bbrc.2021.08.053_bib10) 2018; 97 Meldolesi (10.1016/j.bbrc.2021.08.053_bib22) 2018; 28 Yaghoubi (10.1016/j.bbrc.2021.08.053_bib12) 2019; 233 Barile (10.1016/j.bbrc.2021.08.053_bib27) 2017; 174 Chistiakov (10.1016/j.bbrc.2021.08.053_bib4) 2017; 95 Chen (10.1016/j.bbrc.2021.08.053_bib15) 2017; 12 Zárate (10.1016/j.bbrc.2021.08.053_bib1) 2016; 86 Kumarswamy (10.1016/j.bbrc.2021.08.053_bib16) 2014; 114 Wang (10.1016/j.bbrc.2021.08.053_bib17) 2019; 25 Chen (10.1016/j.bbrc.2021.08.053_bib18) 2017; 42
References_xml	– volume: 11 start-page: 3053 year: 2020 end-page: 3065 ident: bib20 article-title: Donkey milk inhibits triple-negative breast tumor progression and is associated with increased cleaved-caspase-3 expression publication-title: Food & function – volume: 12 start-page: 6385 year: 2020 end-page: 6400 ident: bib9 article-title: Downregulation of LncRNA NORAD promotes Ox-LDL-induced vascular endothelial cell injury and atherosclerosis publication-title: Aging – start-page: 367 year: 2020 ident: bib23 article-title: The Biology, Function, and Biomedical Applications of Exosomes – volume: 42 start-page: 1165 year: 2017 end-page: 1176 ident: bib18 article-title: GLP-1/GLP-1R signaling in regulation of adipocyte differentiation and lipogenesis, cellular physiology and biochemistry publication-title: Inter. J. Exp. Cellular Physiol. Biochemist. Pharmacol. – volume: 510 start-page: 296 year: 2019 end-page: 302 ident: bib21 article-title: Role of ANTXR1 in the regulation of RANKL-induced osteoclast differentiation and function publication-title: BBRC (Biochem. Biophys. Res. Commun.) – volume: 12 year: 2017 ident: bib15 article-title: Exosomal lncRNA GAS5 regulates the apoptosis of macrophages and vascular endothelial cells in atherosclerosis publication-title: PloS One – volume: 233 start-page: 116733 year: 2019 ident: bib12 article-title: Human umbilical cord mesenchymal stem cells derived-exosomes in diseases treatment publication-title: Life Sci. – volume: 9 start-page: 1105 year: 2018 ident: bib24 article-title: Paeonol attenuated inflammatory response of endothelial cells via stimulating monocytes-derived exosomal MicroRNA-223 publication-title: Front. Pharmacol. – volume: 40 start-page: 1464 year: 2020 end-page: 1478 ident: bib11 article-title: Macrophage-enriched lncRNA RAPIA: a novel therapeutic target for atherosclerosis publication-title: Arterioscler. Thromb. Vasc. Biol. – volume: 71 start-page: 596 year: 2019 end-page: 670 ident: bib5 article-title: Targeting foam cell formation in atherosclerosis: therapeutic potential of natural products publication-title: Pharmacol. Rev. – volume: 174 start-page: 63 year: 2017 end-page: 78 ident: bib27 article-title: Exosomes: therapy delivery tools and biomarkers of diseases publication-title: Pharmacol. Therapeut. – volume: 118 start-page: 535 year: 2016 end-page: 546 ident: bib7 article-title: Epidemiology of atherosclerosis and the potential to reduce the global burden of atherothrombotic disease publication-title: Circ. Res. – volume: 13 start-page: 362 year: 2018 end-page: 368 ident: bib14 article-title: Mesenchymal stem cells-derived exosomes: a possible therapeutic strategy for osteoporosis publication-title: Curr. Stem Cell Res. Ther. – volume: 13 start-page: 1889 year: 2019 end-page: 1900 ident: bib19 article-title: Salvianolic acid A attenuates CCl(4)-induced liver fibrosis by regulating the PI3K/AKT/mTOR, Bcl-2/Bax and caspase-3/cleaved caspase-3 signaling pathways publication-title: Drug Des. Dev. Ther. – volume: 115 start-page: 1732 year: 2019 end-page: 1756 ident: bib6 article-title: Non-coding RNAs in cardiovascular cell biology and atherosclerosis publication-title: Cardiovasc. Res. – volume: 38 start-page: 754 year: 2017 end-page: 763 ident: bib28 article-title: Engineering exosomes as refined biological nanoplatforms for drug delivery publication-title: Acta Pharmacol. Sin. – volume: 26 start-page: 1670 year: 2019 end-page: 1687 ident: bib8 article-title: The role of the LncRNA-FA2H-2-MLKL pathway in atherosclerosis by regulation of autophagy flux and inflammation through mTOR-dependent signaling publication-title: Cell Death Differ. – volume: 21 year: 2020 ident: bib2 article-title: Current advances in the diagnostic imaging of atherosclerosis: insights into the pathophysiology of vulnerable plaque publication-title: Int. J. Mol. Sci. – volume: 38 start-page: 15 year: 2020 end-page: 21 ident: bib13 article-title: Preclinical translation of exosomes derived from mesenchymal stem/stromal cells publication-title: Stem Cells (Dayton) – volume: 114 start-page: 1569 year: 2014 end-page: 1575 ident: bib16 article-title: Circulating long noncoding RNA, LIPCAR, predicts survival in patients with heart failure publication-title: Circ. Res. – volume: 6 start-page: 287 year: 2016 end-page: 296 ident: bib26 article-title: Exosomes as therapeutic drug carriers and delivery vehicles across biological membranes: current perspectives and future challenges publication-title: Acta Pharm. Sin. B – volume: 25 start-page: 7645 year: 2019 end-page: 7651 ident: bib17 article-title: Expression of long noncoding RNA LIPCAR promotes cell proliferation, cell migration, and change in phenotype of vascular smooth muscle cells publication-title: Med. Sci. Mon. Int. Med. J. Exp. Clin. Res. : international medical journal of experimental and clinical research – volume: 28 start-page: R435 year: 2018 end-page: r444 ident: bib22 article-title: Exosomes and ectosomes in intercellular communication publication-title: Curr. Biol. : CB – volume: 97 year: 2018 ident: bib10 article-title: LncRNA ENST00113 promotes proliferation, survival, and migration by activating PI3K/Akt/mTOR signaling pathway in atherosclerosis publication-title: Medicine – volume: 95 start-page: 1153 year: 2017 end-page: 1165 ident: bib4 article-title: Mechanisms of foam cell formation in atherosclerosis publication-title: J. Mol. Med. (Berl.) – volume: 112 start-page: 54 year: 2019 end-page: 71 ident: bib3 article-title: Foam cell formation: a new target for fighting atherosclerosis and cardiovascular disease publication-title: Vasc. Pharmacol. – volume: 10 start-page: 422 year: 2019 ident: bib25 article-title: Exosomes derived from M1 macrophages aggravate neointimal hyperplasia following carotid artery injuries in mice through miR-222/CDKN1B/CDKN1C pathway publication-title: Cell Death Dis. – volume: 86 start-page: 163 year: 2016 end-page: 169 ident: bib1 article-title: [Cholesterol and atherosclerosis. Historical considerations and treatment] publication-title: Arch. Cardiol. Mex. – volume: 40 start-page: 1464 year: 2020 ident: 10.1016/j.bbrc.2021.08.053_bib11 article-title: Macrophage-enriched lncRNA RAPIA: a novel therapeutic target for atherosclerosis publication-title: Arterioscler. Thromb. Vasc. Biol. doi: 10.1161/ATVBAHA.119.313749 – start-page: 367 year: 2020 ident: 10.1016/j.bbrc.2021.08.053_bib23 – volume: 95 start-page: 1153 year: 2017 ident: 10.1016/j.bbrc.2021.08.053_bib4 article-title: Mechanisms of foam cell formation in atherosclerosis publication-title: J. Mol. Med. (Berl.) doi: 10.1007/s00109-017-1575-8 – volume: 28 start-page: R435 year: 2018 ident: 10.1016/j.bbrc.2021.08.053_bib22 article-title: Exosomes and ectosomes in intercellular communication publication-title: Curr. Biol. : CB doi: 10.1016/j.cub.2018.01.059 – volume: 26 start-page: 1670 year: 2019 ident: 10.1016/j.bbrc.2021.08.053_bib8 article-title: The role of the LncRNA-FA2H-2-MLKL pathway in atherosclerosis by regulation of autophagy flux and inflammation through mTOR-dependent signaling publication-title: Cell Death Differ. doi: 10.1038/s41418-018-0235-z – volume: 13 start-page: 1889 year: 2019 ident: 10.1016/j.bbrc.2021.08.053_bib19 article-title: Salvianolic acid A attenuates CCl(4)-induced liver fibrosis by regulating the PI3K/AKT/mTOR, Bcl-2/Bax and caspase-3/cleaved caspase-3 signaling pathways publication-title: Drug Des. Dev. Ther. doi: 10.2147/DDDT.S194787 – volume: 38 start-page: 15 year: 2020 ident: 10.1016/j.bbrc.2021.08.053_bib13 article-title: Preclinical translation of exosomes derived from mesenchymal stem/stromal cells publication-title: Stem Cells (Dayton) doi: 10.1002/stem.3061 – volume: 510 start-page: 296 year: 2019 ident: 10.1016/j.bbrc.2021.08.053_bib21 article-title: Role of ANTXR1 in the regulation of RANKL-induced osteoclast differentiation and function publication-title: BBRC (Biochem. Biophys. Res. Commun.) doi: 10.1016/j.bbrc.2019.01.094 – volume: 42 start-page: 1165 year: 2017 ident: 10.1016/j.bbrc.2021.08.053_bib18 article-title: GLP-1/GLP-1R signaling in regulation of adipocyte differentiation and lipogenesis, cellular physiology and biochemistry publication-title: Inter. J. Exp. Cellular Physiol. Biochemist. Pharmacol. doi: 10.1159/000478872 – volume: 112 start-page: 54 year: 2019 ident: 10.1016/j.bbrc.2021.08.053_bib3 article-title: Foam cell formation: a new target for fighting atherosclerosis and cardiovascular disease publication-title: Vasc. Pharmacol. doi: 10.1016/j.vph.2018.08.002 – volume: 10 start-page: 422 year: 2019 ident: 10.1016/j.bbrc.2021.08.053_bib25 article-title: Exosomes derived from M1 macrophages aggravate neointimal hyperplasia following carotid artery injuries in mice through miR-222/CDKN1B/CDKN1C pathway publication-title: Cell Death Dis. doi: 10.1038/s41419-019-1667-1 – volume: 174 start-page: 63 year: 2017 ident: 10.1016/j.bbrc.2021.08.053_bib27 article-title: Exosomes: therapy delivery tools and biomarkers of diseases publication-title: Pharmacol. Therapeut. doi: 10.1016/j.pharmthera.2017.02.020 – volume: 233 start-page: 116733 year: 2019 ident: 10.1016/j.bbrc.2021.08.053_bib12 article-title: Human umbilical cord mesenchymal stem cells derived-exosomes in diseases treatment publication-title: Life Sci. doi: 10.1016/j.lfs.2019.116733 – volume: 21 year: 2020 ident: 10.1016/j.bbrc.2021.08.053_bib2 article-title: Current advances in the diagnostic imaging of atherosclerosis: insights into the pathophysiology of vulnerable plaque publication-title: Int. J. Mol. Sci. doi: 10.3390/ijms21082992 – volume: 12 year: 2017 ident: 10.1016/j.bbrc.2021.08.053_bib15 article-title: Exosomal lncRNA GAS5 regulates the apoptosis of macrophages and vascular endothelial cells in atherosclerosis publication-title: PloS One – volume: 97 year: 2018 ident: 10.1016/j.bbrc.2021.08.053_bib10 article-title: LncRNA ENST00113 promotes proliferation, survival, and migration by activating PI3K/Akt/mTOR signaling pathway in atherosclerosis publication-title: Medicine doi: 10.1097/MD.0000000000010473 – volume: 9 start-page: 1105 year: 2018 ident: 10.1016/j.bbrc.2021.08.053_bib24 article-title: Paeonol attenuated inflammatory response of endothelial cells via stimulating monocytes-derived exosomal MicroRNA-223 publication-title: Front. Pharmacol. doi: 10.3389/fphar.2018.01105 – volume: 13 start-page: 362 year: 2018 ident: 10.1016/j.bbrc.2021.08.053_bib14 article-title: Mesenchymal stem cells-derived exosomes: a possible therapeutic strategy for osteoporosis publication-title: Curr. Stem Cell Res. Ther. doi: 10.2174/1574888X13666180403163456 – volume: 38 start-page: 754 year: 2017 ident: 10.1016/j.bbrc.2021.08.053_bib28 article-title: Engineering exosomes as refined biological nanoplatforms for drug delivery publication-title: Acta Pharmacol. Sin. doi: 10.1038/aps.2017.12 – volume: 115 start-page: 1732 year: 2019 ident: 10.1016/j.bbrc.2021.08.053_bib6 article-title: Non-coding RNAs in cardiovascular cell biology and atherosclerosis publication-title: Cardiovasc. Res. doi: 10.1093/cvr/cvz203 – volume: 6 start-page: 287 year: 2016 ident: 10.1016/j.bbrc.2021.08.053_bib26 article-title: Exosomes as therapeutic drug carriers and delivery vehicles across biological membranes: current perspectives and future challenges publication-title: Acta Pharm. Sin. B doi: 10.1016/j.apsb.2016.02.001 – volume: 118 start-page: 535 year: 2016 ident: 10.1016/j.bbrc.2021.08.053_bib7 article-title: Epidemiology of atherosclerosis and the potential to reduce the global burden of atherothrombotic disease publication-title: Circ. Res. doi: 10.1161/CIRCRESAHA.115.307611 – volume: 12 start-page: 6385 year: 2020 ident: 10.1016/j.bbrc.2021.08.053_bib9 article-title: Downregulation of LncRNA NORAD promotes Ox-LDL-induced vascular endothelial cell injury and atherosclerosis publication-title: Aging doi: 10.18632/aging.103034 – volume: 25 start-page: 7645 year: 2019 ident: 10.1016/j.bbrc.2021.08.053_bib17 article-title: Expression of long noncoding RNA LIPCAR promotes cell proliferation, cell migration, and change in phenotype of vascular smooth muscle cells publication-title: Med. Sci. Mon. Int. Med. J. Exp. Clin. Res. : international medical journal of experimental and clinical research – volume: 86 start-page: 163 year: 2016 ident: 10.1016/j.bbrc.2021.08.053_bib1 article-title: [Cholesterol and atherosclerosis. Historical considerations and treatment] publication-title: Arch. Cardiol. Mex. – volume: 71 start-page: 596 year: 2019 ident: 10.1016/j.bbrc.2021.08.053_bib5 article-title: Targeting foam cell formation in atherosclerosis: therapeutic potential of natural products publication-title: Pharmacol. Rev. doi: 10.1124/pr.118.017178 – volume: 11 start-page: 3053 year: 2020 ident: 10.1016/j.bbrc.2021.08.053_bib20 article-title: Donkey milk inhibits triple-negative breast tumor progression and is associated with increased cleaved-caspase-3 expression publication-title: Food & function doi: 10.1039/C9FO02934F – volume: 114 start-page: 1569 year: 2014 ident: 10.1016/j.bbrc.2021.08.053_bib16 article-title: Circulating long noncoding RNA, LIPCAR, predicts survival in patients with heart failure publication-title: Circ. Res. doi: 10.1161/CIRCRESAHA.114.303915
SSID	ssj0011469
Score	2.4945412
Snippet	It has been reported that long non-coding RNA (lncRNA) LIPCAR is involved in the progression of atherosclerosis. However, the mechanism underlying the effects...
SourceID	proquest pubmed crossref elsevier
SourceType	Aggregation Database Index Database Enrichment Source Publisher
StartPage	65
SubjectTerms	apoptosis Apoptosis - physiology Atherosclerosis Atherosclerosis - blood Atherosclerosis - genetics Atherosclerosis - pathology biomarkers Cell Movement - physiology Cell Proliferation - physiology cyclin-dependent kinase Exosome Exosomes Foam cell foam cells Human Umbilical Vein Endothelial Cells Humans Knockdown Lipoproteins, LDL - pharmacology lncRNA LIPCAR low density lipoprotein Muscle, Smooth, Vascular - metabolism Muscle, Smooth, Vascular - pathology non-coding RNA oxidation proliferating cell nuclear antigen RNA, Long Noncoding - blood RNA, Long Noncoding - genetics smooth muscle THP-1 Cells
Title	Exosomal long non-coding RNA LIPCAR derived from oxLDL-treated THP-1 cells regulates the proliferation of human umbilical vein endothelial cells and human vascular smooth muscle cells
URI	https://dx.doi.org/10.1016/j.bbrc.2021.08.053 https://www.ncbi.nlm.nih.gov/pubmed/34455222 https://www.proquest.com/docview/2566253886 https://www.proquest.com/docview/2636796298
Volume	575
WOSCitedRecordID	wos000690878800005&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
hasFullText	1
inHoldings	1
isFullTextHit
isPrint
journalDatabaseRights	– providerCode: PRVESC databaseName: Elsevier SD Freedom Collection Journals 2021 customDbUrl: eissn: 1090-2104 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0011469 issn: 0006-291X databaseCode: AIEXJ dateStart: 19950105 isFulltext: true titleUrlDefault: https://www.sciencedirect.com providerName: Elsevier
link	http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtZ1bb9MwFICtbgPBC4KNy7hMRkJ7qTIlTpykj6W0Gqgq1ehQ3qJcHJGpTUpvKvwx_g-_hHNsJ22BTeOBlyiynNT1-WIf2-dCyBvAxE1YHBlOlqaGI0xuRHA1Ep9FzI8zU0jj8c99bzDwg6A1bDR-Vr4wq7FXFP563Zr-V1FDGQgbXWf_Qdz1S6EA7kHocAWxw_VWgu-uy3k5gZ4fYxohWN0bSSk9Vy4GbRirhp32RTOFhqxA1ZTOJeW6_65vSItzKBqdDw2rifv5eKAgE9VjFAjpUFWO0RBmo2TKA4DlBO1rUdQrgfFHihSdusa4E6_eglvzqmpt9jqflFCpOVnOofGq2s7pco55vDaBDOK8nFY86ehEaC-_5doy3-Cp54x6R1yo0SzI1_lmm0KV9QT8n7o0yLV58qf8-xehZ3S9IcKkRR4zt8ZwswUFOqvxmfhLmR74uce3hm6VsuKPGUVtblydxfEMI14yFfFVBTjeDd89-Bj2Lvv9cNQNRqfTrwZmNkMLAJ3mZY8cMI-3YOQ9aL_vBh_qsy6Yq1ryTF43Ubt2KSvE33_2OvXpuuWRVJNGD8kDvb6hbcXlI9IQxSE5ahfRopx8o6dUWhzLo5xDcvdtdXevU-UdPCI_KoApAkw3AFMAmCqAqQaYIsB0B2AqAaaSKVoDTAFJugMwLTMqqaQ1wBQBplsA67cAgrpqBTBVAFMFsKr2mFz2uqPOuaHTixgJaOkLw4OlhzBTNK823Zh7mSNcnlix6cSxbaUwm0UgLgYLGmEJloCubqU8i6yIW55nJqn9hOxDH4hnhHIeZTaP3chPEicTbuRlXspSZtuC2Y5pHxOrklqY6Nj7mAJmHFZGllchSjpESYeYF5bDM836mamKPHNjbV7BEGrdWenEIYB843OvK3JCkDP2V1SIcjkPYS3kMlCHfPeGOq6N-9Cs5R-Tpwq7uq2243DoYfb8Fr_wgtzffMkvyf5ithSvyJ1ktcjnsxOy5wX-if5sfgGdPQuT
linkProvider	Elsevier
openUrl	ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Exosomal+long+non-coding+RNA+LIPCAR+derived+from+oxLDL-treated+THP-1+cells+regulates+the+proliferation+of+human+umbilical+vein+endothelial+cells+and+human+vascular+smooth+muscle+cells&rft.jtitle=Biochemical+and+biophysical+research+communications&rft.au=Hu%2C+Nan&rft.au=Zeng%2C+Xixi&rft.au=Tang%2C+Feifei&rft.au=Xiong%2C+Sizheng&rft.date=2021-10-20&rft.issn=1090-2104&rft.eissn=1090-2104&rft.volume=575&rft.spage=65&rft_id=info:doi/10.1016%2Fj.bbrc.2021.08.053&rft.externalDBID=NO_FULL_TEXT
thumbnail_l	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0006-291X&client=summon
thumbnail_m	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0006-291X&client=summon
thumbnail_s	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0006-291X&client=summon