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Silencing of TLR7 protects against lipopolysaccharide-induced chondrocyte apoptosis and injury by blocking the p21-mediated JAK2/STAT3 pathway.

ABSTRACT: Involvement of toll-like receptor 7 (TLR7) in the immune response has been reported in diverse inflammatory diseases. However, the role of TLR7 in the pathogenesis of osteoarthritis (OA) is poorly understood. In this study, we sought to investigate the contribution of TLR7 in regulating chondrocyte apoptosis, inflammation, and degradation of the extracellula matrix (ECM), and its underlying mechanisms. We found that TLR7 expression was increased in cartilage tissues of OA patients and in lipopolysaccharide (LPS)-induced chondrocytes. Silencing of TLR7 alleviated LPS-induced chondrocyte apoptosis, inflammation, and ECM degradation. Mechanistically, TLR7 silencing inhibited the JAK2/STAT3 signaling pathway by inducing p21 expression. Moreover, p21 knockdown and colivein (an activator of JAK2/STAT3 signaling) partially rescued the suppressive role of TLR7 silencing on chondrocyte apoptosis, the inflammatory response, and ECM underproduction. Taken together, our data revealed that knockdown of TLR7 attenuated chondrocyte apoptosis and injury by blocking the p21-mediated JAK2/STAT3 pathway, suggesting that TLR7 may be a therapeutic target in OA.

SUBMITTER: Liu D

PROVIDER: S-EPMC8748165 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature

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Silencing of TLR7 protects against lipopolysaccharide-induced chondrocyte apoptosis and injury by blocking the p21-mediated JAK2/STAT3 pathway.

Liu Dan D Liu Wei W Jiang Limin L Dong Shengjie S Ma Weihua W Wang Shijun S Wan Chao C

American journal of translational research 20211215 12

Involvement of toll-like receptor 7 (TLR7) in the immune response has been reported in diverse inflammatory diseases. However, the role of TLR7 in the pathogenesis of osteoarthritis (OA) is poorly understood. In this study, we sought to investigate the contribution of TLR7 in regulating chondrocyte apoptosis, inflammation, and degradation of the extracellula matrix (ECM), and its underlying mechanisms. We found that TLR7 expression was increased in cartilage tissues of OA patients and in lipopol ...[more]

PMID: 35035696

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Project description:ObjectiveAt present, studies have confirmed that NDRG4 is specifically expressed in the heart, while its effect on the heart is still unclear. This study is to explore the effect of NDRG4 on cardiomyocyte apoptosis caused by acute myocardial infarction (AMI).MethodsTwenty SD rats were randomly divided into Sham (left anterior descent of heart without ligation) and AMI groups. In this study, coronary artery ligation was used to establish an AMI model, and the AMI model was verified by auxiliary examination and pathological examination. Besides, quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting (WB) was used to detect the expression level of Bax and Bcl-2 in heart tissues, and NDRG mRNA levels in tissues were also detected. qRT-PCR technology was used to verify the transfection efficiency of NDRG4 in H9C2 cells, and the change of apoptosis level of H9C2 cells was detected by Cell Counting Kit-8 (CCK-8) assay and TUNEL staining; besides, the expression level of apoptosis-related factors was detected by WB and qRT-PCR technology. Simultaneously with the modeling of rats, we injected adenovirus (Ad) into the heart tissue and examined the structural and functional changes of the rat heart. Then, WB technology was used to detect the expression level of the JAK2/STAT3 signaling pathway.ResultsThe heart function and heart structure of rats in the MI group were dramatically worse, and the expression level of NDRG4 was also dramatically reduced. The overexpression of NDRG4 in H9C2 cells can effectively inhibit the ischemia/hypoxia- (I/H-) induced decrease in cell viability and increase in apoptosis rate and inhibit the increase in Bax/Bcl-2 ratio. Moreover, overexpression of NDRG4 in heart tissue can effectively improve the cardiac function and structural destruction caused by MI. In addition, NDRG4 can inhibit JAK2/STAT3 pathway activation.ConclusionThe expression of NDRG4 in the MI tissue of rats was suppressed, while overexpression of NDRG4 by injection of Ad can obviously protect the rat heart. Furthermore, overexpression of NDRG4 in H9C2 cells can effectively inhibit the I/H-induced decrease in cell viability and increase in apoptosis rate, and this may be related to the inhibition of the JAK2/STAT3 signaling pathway.

Dataset Information

Silencing of TLR7 protects against lipopolysaccharide-induced chondrocyte apoptosis and injury by blocking the p21-mediated JAK2/STAT3 pathway.

Publications

Silencing of TLR7 protects against lipopolysaccharide-induced chondrocyte apoptosis and injury by blocking the p21-mediated JAK2/STAT3 pathway.

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