DPP4 inhibition impairs senohemostasis to improve plaque stability in atherosclerotic mice

Senescent vascular smooth muscle cells (VSMCs) accumulate in the vasculature with age and tissue damage and secrete factors that promote atherosclerotic plaque vulnerability and disease. Here, we report increased levels and activity of dipeptidyl peptidase 4 (DPP4), a serine protease, in senescent V...

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Veröffentlicht in:The Journal of clinical investigation Jg. 133; H. 12; S. 1 - 18
Hauptverfasser: Herman, Allison B., Tsitsipatis, Dimitrios, Anerillas, Carlos, Mazan-Mamczarz, Krystyna, Carr, Angelica E., Gregg, Jordan M., Wang, Mingyi, Zhang, Jing, Michel, Marc, Henry-Smith, Charnae’ A., Harris, Sophia C., Munk, Rachel, Martindale, Jennifer L., Piao, Yulan, Fan, Jinshui, Mattison, Julie A., De, Supriyo, Abdelmohsen, Kotb, Maul, Robert W., Tanaka, Toshiko, Moore, Ann Zenobia, DeMouth, Megan E., Sidoli, Simone, Ferrucci, Luigi, Liu, Yie, de Cabo, Rafael, Lakatta, Edward G., Gorospe, Myriam
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States American Society for Clinical Investigation 15.06.2023
Schlagworte:
Aging
Arteriosclerosis
Atherosclerosis
Biomedical research
Blood circulation disorders
Cardiovascular diseases
Care and treatment
Cell cycle
Cell death
Cells
Coagulation factors
Development and progression
Diabetes
Disease
Disease susceptibility
Fibroblasts
Genotype & phenotype
Health aspects
Hemostasis
Hypoxia
Inflammation
Kinases
Muscle cells
Phenotypes
Protease inhibitors
Proteins
Scientific equipment and supplies industry
Senescence
Serine proteinase
Smooth muscle
Testing
Thrombin
Type 2 diabetes
Vascular biology
Vascular diseases
Vascular smooth muscle
United States
Maryland
Aging
Vascular Biology
Atherosclerosis
Cellular senescence
ISSN:1558-8238, 0021-9738, 1558-8238
Online-Zugang:Volltext
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Abstract Senescent vascular smooth muscle cells (VSMCs) accumulate in the vasculature with age and tissue damage and secrete factors that promote atherosclerotic plaque vulnerability and disease. Here, we report increased levels and activity of dipeptidyl peptidase 4 (DPP4), a serine protease, in senescent VSMCs. Analysis of the conditioned media from senescent VSMCs revealed a unique senescence-associated secretory phenotype (SASP) signature comprising many complement and coagulation factors; silencing or inhibiting DPP4 reduced these factors and increased cell death. Serum samples from persons with high risk for cardiovascular disease contained high levels of DPP4-regulated complement and coagulation factors. Importantly, DPP4 inhibition reduced senescent cell burden and coagulation and improved plaque stability, while single-cell resolution of senescent VSMCs reflected the senomorphic and senolytic effects of DPP4 inhibition in murine atherosclerosis. We propose that DPP4-regulated factors could be exploited therapeutically to reduce senescent cell function, reverse senohemostasis, and improve vascular disease.
AbstractList Senescent vascular smooth muscle cells (VSMCs) accumulate in the vasculature with age and tissue damage and secrete factors that promote atherosclerotic plaque vulnerability and disease. Here, we report increased levels and activity of dipeptidyl peptidase 4 (DPP4), a serine protease, in senescent VSMCs. Analysis of the conditioned media from senescent VSMCs revealed a unique senescence-associated secretory phenotype (SASP) signature comprising many complement and coagulation factors; silencing or inhibiting DPP4 reduced these factors and increased cell death. Serum samples from persons with high risk for cardiovascular disease contained high levels of DPP4-regulated complement and coagulation factors. Importantly, DPP4 inhibition reduced senescent cell burden and coagulation and improved plaque stability, while single-cell resolution of senescent VSMCs reflected the senomorphic and senolytic effects of DPP4 inhibition in murine atherosclerosis. We propose that DPP4-regulated factors could be exploited therapeutically to reduce senescent cell function, reverse senohemostasis, and improve vascular disease.Senescent vascular smooth muscle cells (VSMCs) accumulate in the vasculature with age and tissue damage and secrete factors that promote atherosclerotic plaque vulnerability and disease. Here, we report increased levels and activity of dipeptidyl peptidase 4 (DPP4), a serine protease, in senescent VSMCs. Analysis of the conditioned media from senescent VSMCs revealed a unique senescence-associated secretory phenotype (SASP) signature comprising many complement and coagulation factors; silencing or inhibiting DPP4 reduced these factors and increased cell death. Serum samples from persons with high risk for cardiovascular disease contained high levels of DPP4-regulated complement and coagulation factors. Importantly, DPP4 inhibition reduced senescent cell burden and coagulation and improved plaque stability, while single-cell resolution of senescent VSMCs reflected the senomorphic and senolytic effects of DPP4 inhibition in murine atherosclerosis. We propose that DPP4-regulated factors could be exploited therapeutically to reduce senescent cell function, reverse senohemostasis, and improve vascular disease.
Senescent vascular smooth muscle cells (VSMCs) accumulate in the vasculature with age and tissue damage and secrete factors that promote atherosclerotic plaque vulnerability and disease. Here, we report increased levels and activity of dipeptidyl peptidase 4 (DPP4), a serine protease, in senescent VSMCs. Analysis of the conditioned media from senescent VSMCs revealed a unique senescence-associated secretory phenotype (SASP) signature comprising many complement and coagulation factors; silencing or inhibiting DPP4 reduced these factors and increased cell death. Serum samples from persons with high risk for cardiovascular disease contained high levels of DPP4-regulated complement and coagulation factors. Importantly, DPP4 inhibition reduced senescent cell burden and coagulation and improved plaque stability, while single-cell resolution of senescent VSMCs reflected the senomorphic and senolytic effects of DPP4 inhibition in murine atherosclerosis. We propose that DPP4-regulated factors could be exploited therapeutically to reduce senescent cell function, reverse senohemostasis, and improve vascular disease.
Audience Academic
Author Michel, Marc
Maul, Robert W.
De, Supriyo
Moore, Ann Zenobia
Anerillas, Carlos
Harris, Sophia C.
DeMouth, Megan E.
Zhang, Jing
Sidoli, Simone
de Cabo, Rafael
Martindale, Jennifer L.
Lakatta, Edward G.
Tsitsipatis, Dimitrios
Ferrucci, Luigi
Munk, Rachel
Fan, Jinshui
Mattison, Julie A.
Tanaka, Toshiko
Liu, Yie
Herman, Allison B.
Mazan-Mamczarz, Krystyna
Wang, Mingyi
Gorospe, Myriam
Carr, Angelica E.
Piao, Yulan
Abdelmohsen, Kotb
Henry-Smith, Charnae’ A.
Gregg, Jordan M.
AuthorAffiliation 4 Laboratory of Molecular Biology and Immunology, National Institute on Aging (NIA) Intramural Research Program (IRP), NIH, Baltimore, Maryland, USA
5 Department of Microbiology and Immunology and
3 Translational Gerontology Branch, and
1 Laboratory of Genetics and Genomics
2 Laboratory of Cardiovascular Sciences
6 Department of Biochemistry, Albert Einstein College of Medicine, Bronx, New York, USA
AuthorAffiliation_xml – name: 2 Laboratory of Cardiovascular Sciences
– name: 4 Laboratory of Molecular Biology and Immunology, National Institute on Aging (NIA) Intramural Research Program (IRP), NIH, Baltimore, Maryland, USA
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/37097759$$D View this record in MEDLINE/PubMed
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Copyright American Society for Clinical Investigation Jun 2023
2023 Herman et al. 2023 Herman et al.
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Issue 12
Keywords Aging
Vascular Biology
Atherosclerosis
Cellular senescence
Language English
License http://creativecommons.org/licenses/by/4.0
This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
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Snippet Senescent vascular smooth muscle cells (VSMCs) accumulate in the vasculature with age and tissue damage and secrete factors that promote atherosclerotic plaque...
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StartPage 1
SubjectTerms Aging
Arteriosclerosis
Atherosclerosis
Biomedical research
Blood circulation disorders
Cardiovascular diseases
Care and treatment
Cell cycle
Cell death
Cells
Coagulation factors
Development and progression
Diabetes
Disease
Disease susceptibility
Fibroblasts
Genotype & phenotype
Health aspects
Hemostasis
Hypoxia
Inflammation
Kinases
Muscle cells
Phenotypes
Protease inhibitors
Proteins
Scientific equipment and supplies industry
Senescence
Serine proteinase
Smooth muscle
Testing
Thrombin
Type 2 diabetes
Vascular biology
Vascular diseases
Vascular smooth muscle
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Title DPP4 inhibition impairs senohemostasis to improve plaque stability in atherosclerotic mice
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