Circulating Cell-Free mtDNA Contributes to AIM2 Inflammasome-Mediated Chronic Inflammation in Patients with Type 2 Diabetes

Mitochondrial dysfunction has been implicated in the pathogenesis of insulin resistance and type 2 diabetes. Damaged mitochondria DNA (mtDNA) may have a role in regulating hyperglycemia during type 2 diabetes. Circulating cell-free mitochondria DNA (ccf-mtDNA) was found in serum and plasma from pati...

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Vydáno v:Cells (Basel, Switzerland) Ročník 8; číslo 4; s. 328
Hlavní autoři: Bae, Jung Hwan, Jo, Seung, Kim, Seong Jin, Lee, Jong Min, Jeong, Ji Hun, Kang, Jeong Suk, Cho, Nam-Jun, Kim, Sang Soo, Lee, Eun Young, Moon, Jong-Seok
Médium: Journal Article
Jazyk:angličtina
Vydáno: Switzerland MDPI AG 08.04.2019
MDPI
Témata:
Aged
AIM2 inflammasome
Alzheimer's disease
Animals
Bone marrow
Cardiovascular disease
Case-Control Studies
Caspase-1
ccf-mtDNA
Cells, Cultured
Chronic illnesses
chronic inflammation
Cloning
Cytokines
Dehydrogenases
Diabetes
Diabetes mellitus (non-insulin dependent)
Diabetes Mellitus, Type 2 - metabolism
Diabetes Mellitus, Type 2 - pathology
DNA, Mitochondrial - blood
DNA-Binding Proteins - blood
Enrollments
Female
Health care
Human subjects
Humans
Hyperglycemia
IL-1β
Inflammasomes
Inflammasomes - metabolism
Inflammation
Inflammation - metabolism
Inflammation - pathology
Insulin
Insulin resistance
Interleukin 18
Interleukin-18 - blood
Interleukin-1beta - blood
Kidney diseases
Macrophages
Macrophages - metabolism
Macrophages - pathology
Male
Manufacturers
Melanoma
Middle Aged
Mitochondrial DNA
Plasma
Proteins
type 2 diabetes
Minneapolis Minnesota
United States > US
type 2 diabetes
AIM2 inflammasome
chronic inflammation
ccf-mtDNA
ISSN:2073-4409, 2073-4409
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Abstract Mitochondrial dysfunction has been implicated in the pathogenesis of insulin resistance and type 2 diabetes. Damaged mitochondria DNA (mtDNA) may have a role in regulating hyperglycemia during type 2 diabetes. Circulating cell-free mitochondria DNA (ccf-mtDNA) was found in serum and plasma from patients and has been linked to the prognosis factors in various human diseases. However, the role of ccf-mtDNA in chronic inflammation in type 2 diabetes is unclear. In this study, we hypothesized that the ccf-mtDNA levels are associated with chronic inflammation in patients with type 2 diabetes. The mtDNA levels were elevated in the plasma from patients with type 2 diabetes compared to healthy subjects. The elevated mtDNA levels were associated with interleukin-1β (IL-1β) levels in patients with type 2 diabetes. The mtDNA, from patients with type 2 diabetes, induced absent in melanoma 2 (AIM2) inflammasome-dependent caspase-1 activation and IL-1β and IL-18 secretion in macrophages. Our results suggest that the ccf-mtDNA might contribute to AIM2 inflammasome-mediated chronic inflammation in type 2 diabetes.
AbstractList Mitochondrial dysfunction has been implicated in the pathogenesis of insulin resistance and type 2 diabetes. Damaged mitochondria DNA (mtDNA) may have a role in regulating hyperglycemia during type 2 diabetes. Circulating cell-free mitochondria DNA (ccf-mtDNA) was found in serum and plasma from patients and has been linked to the prognosis factors in various human diseases. However, the role of ccf-mtDNA in chronic inflammation in type 2 diabetes is unclear. In this study, we hypothesized that the ccf-mtDNA levels are associated with chronic inflammation in patients with type 2 diabetes. The mtDNA levels were elevated in the plasma from patients with type 2 diabetes compared to healthy subjects. The elevated mtDNA levels were associated with interleukin-1β (IL-1β) levels in patients with type 2 diabetes. The mtDNA, from patients with type 2 diabetes, induced absent in melanoma 2 (AIM2) inflammasome-dependent caspase-1 activation and IL-1β and IL-18 secretion in macrophages. Our results suggest that the ccf-mtDNA might contribute to AIM2 inflammasome-mediated chronic inflammation in type 2 diabetes.
Mitochondrial dysfunction has been implicated in the pathogenesis of insulin resistance and type 2 diabetes. Damaged mitochondria DNA (mtDNA) may have a role in regulating hyperglycemia during type 2 diabetes. Circulating cell-free mitochondria DNA (ccf-mtDNA) was found in serum and plasma from patients and has been linked to the prognosis factors in various human diseases. However, the role of ccf-mtDNA in chronic inflammation in type 2 diabetes is unclear. In this study, we hypothesized that the ccf-mtDNA levels are associated with chronic inflammation in patients with type 2 diabetes. The mtDNA levels were elevated in the plasma from patients with type 2 diabetes compared to healthy subjects. The elevated mtDNA levels were associated with interleukin-1 (IL-1)β levels in patients with type 2 diabetes. The mtDNA, from patients with type 2 diabetes, induced absent in melanoma 2 (AIM2) inflammasome-dependent caspase-1 activation and IL-1β and IL-18 secretion in macrophages. Our results suggest that the ccf-mtDNA might contribute to AIM2 inflammasome-mediated chronic inflammation in type 2 diabetes.Mitochondrial dysfunction has been implicated in the pathogenesis of insulin resistance and type 2 diabetes. Damaged mitochondria DNA (mtDNA) may have a role in regulating hyperglycemia during type 2 diabetes. Circulating cell-free mitochondria DNA (ccf-mtDNA) was found in serum and plasma from patients and has been linked to the prognosis factors in various human diseases. However, the role of ccf-mtDNA in chronic inflammation in type 2 diabetes is unclear. In this study, we hypothesized that the ccf-mtDNA levels are associated with chronic inflammation in patients with type 2 diabetes. The mtDNA levels were elevated in the plasma from patients with type 2 diabetes compared to healthy subjects. The elevated mtDNA levels were associated with interleukin-1 (IL-1)β levels in patients with type 2 diabetes. The mtDNA, from patients with type 2 diabetes, induced absent in melanoma 2 (AIM2) inflammasome-dependent caspase-1 activation and IL-1β and IL-18 secretion in macrophages. Our results suggest that the ccf-mtDNA might contribute to AIM2 inflammasome-mediated chronic inflammation in type 2 diabetes.
Mitochondrial dysfunction has been implicated in the pathogenesis of insulin resistance and type 2 diabetes. Damaged mitochondria DNA (mtDNA) may have a role in regulating hyperglycemia during type 2 diabetes. Circulating cell-free mitochondria DNA (ccf-mtDNA) was found in serum and plasma from patients and has been linked to the prognosis factors in various human diseases. However, the role of ccf-mtDNA in chronic inflammation in type 2 diabetes is unclear. In this study, we hypothesized that the ccf-mtDNA levels are associated with chronic inflammation in patients with type 2 diabetes. The mtDNA levels were elevated in the plasma from patients with type 2 diabetes compared to healthy subjects. The elevated mtDNA levels were associated with interleukin-1 (IL-1)β levels in patients with type 2 diabetes. The mtDNA, from patients with type 2 diabetes, induced absent in melanoma 2 (AIM2) inflammasome-dependent caspase-1 activation and IL-1β and IL-18 secretion in macrophages. Our results suggest that the ccf-mtDNA might contribute to AIM2 inflammasome-mediated chronic inflammation in type 2 diabetes.
Author Bae, Jung Hwan
Kim, Seong Jin
Kang, Jeong Suk
Kim, Sang Soo
Jo, Seung
Cho, Nam-Jun
Lee, Eun Young
Lee, Jong Min
Jeong, Ji Hun
Moon, Jong-Seok
AuthorAffiliation 3 Institute of Tissue Regeneration, College of Medicine, Soonchunhyang University, Cheonan 31151, Korea
4 Department of Internal Medicine, Pusan National University Hospital, Pusan 50612, Korea; drsskim7@gmail.com
1 Department of Integrated Biomedical Science, Soonchunhyang Institute of Medi-bio Science (SIMS), Soonchunhyang University, Cheonan-si, Chungcheongnam-do 31151, Korea; junier24@naver.com (J.H.B.); 309cho@naver.com (S.J.II); tjdwls515@naver.com (S.J.K.); whdals7034@naver.com (J.M.L.); jihun@sch.ac.kr (J.H.J.)
2 Department of Internal Medicine, Soonchunhyang University Cheonan Hospital, Cheonan 31151, Korea; abalonea@naver.com (J.S.K.); c100086@schmc.ac.kr (N.-J.C.)
AuthorAffiliation_xml – name: 2 Department of Internal Medicine, Soonchunhyang University Cheonan Hospital, Cheonan 31151, Korea; abalonea@naver.com (J.S.K.); c100086@schmc.ac.kr (N.-J.C.)
– name: 4 Department of Internal Medicine, Pusan National University Hospital, Pusan 50612, Korea; drsskim7@gmail.com
– name: 3 Institute of Tissue Regeneration, College of Medicine, Soonchunhyang University, Cheonan 31151, Korea
– name: 1 Department of Integrated Biomedical Science, Soonchunhyang Institute of Medi-bio Science (SIMS), Soonchunhyang University, Cheonan-si, Chungcheongnam-do 31151, Korea; junier24@naver.com (J.H.B.); 309cho@naver.com (S.J.II); tjdwls515@naver.com (S.J.K.); whdals7034@naver.com (J.M.L.); jihun@sch.ac.kr (J.H.J.)
Author_xml – sequence: 1
  givenname: Jung Hwan
  surname: Bae
  fullname: Bae, Jung Hwan
– sequence: 2
  givenname: Seung
  surname: Jo
  fullname: Jo, Seung
– sequence: 3
  givenname: Seong Jin
  surname: Kim
  fullname: Kim, Seong Jin
– sequence: 4
  givenname: Jong Min
  surname: Lee
  fullname: Lee, Jong Min
– sequence: 5
  givenname: Ji Hun
  surname: Jeong
  fullname: Jeong, Ji Hun
– sequence: 6
  givenname: Jeong Suk
  surname: Kang
  fullname: Kang, Jeong Suk
– sequence: 7
  givenname: Nam-Jun
  surname: Cho
  fullname: Cho, Nam-Jun
– sequence: 8
  givenname: Sang Soo
  orcidid: 0000-0002-9687-8357
  surname: Kim
  fullname: Kim, Sang Soo
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– sequence: 10
  givenname: Jong-Seok
  orcidid: 0000-0002-2537-7854
  surname: Moon
  fullname: Moon, Jong-Seok
BackLink https://www.ncbi.nlm.nih.gov/pubmed/30965677$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Copyright 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
2019 by the authors. 2019
Copyright_xml – notice: 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
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Issue 4
Keywords type 2 diabetes
AIM2 inflammasome
chronic inflammation
ccf-mtDNA
Language English
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Snippet Mitochondrial dysfunction has been implicated in the pathogenesis of insulin resistance and type 2 diabetes. Damaged mitochondria DNA (mtDNA) may have a role...
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StartPage 328
SubjectTerms Aged
AIM2 inflammasome
Alzheimer's disease
Animals
Bone marrow
Cardiovascular disease
Case-Control Studies
Caspase-1
ccf-mtDNA
Cells, Cultured
Chronic illnesses
chronic inflammation
Cloning
Cytokines
Dehydrogenases
Diabetes
Diabetes mellitus (non-insulin dependent)
Diabetes Mellitus, Type 2 - metabolism
Diabetes Mellitus, Type 2 - pathology
DNA, Mitochondrial - blood
DNA-Binding Proteins - blood
Enrollments
Female
Health care
Human subjects
Humans
Hyperglycemia
IL-1β
Inflammasomes
Inflammasomes - metabolism
Inflammation
Inflammation - metabolism
Inflammation - pathology
Insulin
Insulin resistance
Interleukin 18
Interleukin-18 - blood
Interleukin-1beta - blood
Kidney diseases
Macrophages
Macrophages - metabolism
Macrophages - pathology
Male
Manufacturers
Melanoma
Middle Aged
Mitochondrial DNA
Plasma
Proteins
type 2 diabetes
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Title Circulating Cell-Free mtDNA Contributes to AIM2 Inflammasome-Mediated Chronic Inflammation in Patients with Type 2 Diabetes
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