SIRT4 suppresses the inflammatory response and oxidative stress in osteoarthritis.

SIRT4 inflammation osteoarthritis oxidative stress

Journal

American journal of translational research
ISSN: 1943-8141
Titre abrégé: Am J Transl Res
Pays: United States
ID NLM: 101493030

Informations de publication

Date de publication:
2020
Historique:
received: 07 10 2019
accepted: 08 04 2020
entrez: 9 6 2020
pubmed: 9 6 2020
medline: 9 6 2020
Statut: epublish

Résumé

Sirtuins have been involved in the osteoarthritis (OA) process. However, the functions of SIRT4 in the degeneration of human chondrocytes and OA are not fully understood. This study aimed to explore the role of SIRT4 during OA and mechanisms implicated. We extracted total protein and mRNA of the cartilage from OA patients and isolated the chondrocytes from the cartilage in different degenerated degrees for cell culture. Collagen II and SIRT4 levels of the tissues were analyzed by quantitative reverse-transcription polymerase chain reaction (RT-PCR) and Western blot. Chondrocytes were transferred with SIRT4-siRNA, treated with recombinant human SIRT4 protein for 24 h, respectively. Aggrecan, collagen I, collagen II, MMP-13, IL-6, TNF-α, SOD1, SOD2, and CAT expression, and ROS levels were investigated by Western blot, RT-PCR, immunofluorescence, enzyme-linked immunosorbent assay (ELISA), or flow cytometry. Collagen II decreased significantly in severely degenerated cartilage compared to the mild one, paralleling with SIRT4 expression both in protein and mRNA levels. Chondrocytes in severe OA grade were observed with a decrease in aggrecan, collagen II, SOD1, SOD2, CAT expression, nonetheless, an increase in collagen I, reactive oxygen species (ROS), MMP-13, IL-6, and TNF-α levels. However, SRIT4 protein treatment significantly upregulated aggrecan, collagen II, an antioxidant enzyme, and suppressed ROS and inflammatory response. Further analysis revealed that silencing of SIRT4 expression induced healthy chondrocytes, a decrease in aggrecan, collagen II and antioxidant enzyme expression, and an increase in ROS and inflammatory response, importantly, which can be reversed by SIRT4 protein stimuli. Our results elucidated that SIRT4 was tangled with the development of OA, and SIRT4 overexpression contributes to suppresses the inflammatory response and oxidative stress.

Identifiants

pubmed: 32509191
pmc: PMC7270038

Types de publication

Journal Article

Langues

eng

Pagination

1965-1975

Informations de copyright

AJTR Copyright © 2020.

Déclaration de conflit d'intérêts

None.

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Auteurs

Yuee Dai (Y)

Department of Anesthesiology, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China Chengdu 610072, China.

Shaoxing Liu (S)

Department of Anesthesiology, Chengdu second People's Hospital Chengdu 614000, China.

Jia Li (J)

Department of Anesthesiology, West China Hospital, Sichuan University Chengdu 610041, China.

Jiajia Li (J)

Department of ICU, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China Chengdu 610072, China.

Yunping Lan (Y)

Department of ICU, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China Chengdu 610072, China.

Hongfei Nie (H)

Department of Pain Management, West China Hospital, Sichuan University Chengdu 610041, China.

Yunxia Zuo (Y)

Department of Anesthesiology, West China Hospital, Sichuan University Chengdu 610041, China.

Classifications MeSH