Role of microRNA-26a in cartilage injury and chondrocyte proliferation and apoptosis in rheumatoid arthritis rats by regulating expression of CTGF
| Autor: | Liangde Jiang, Shuai Cao |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Physiology Clinical Biochemistry Type II collagen Arthritis Inflammation Apoptosis Chondrocyte Arthritis Rheumatoid Rats Sprague-Dawley 03 medical and health sciences 0302 clinical medicine Chondrocytes Downregulation and upregulation medicine Animals Collagen Type II Cell Proliferation Chemistry Connective Tissue Growth Factor Cell Biology medicine.disease Rats CTGF MicroRNAs 030104 developmental biology medicine.anatomical_structure Cartilage Gene Expression Regulation 030220 oncology & carcinogenesis Cancer research Tumor necrosis factor alpha medicine.symptom |
| Zdroj: | Journal of cellular physiology. 235(2) |
| ISSN: | 1097-4652 |
| Popis: | This study is carried out to investigate the role of microRNA-26a (miR-26a) in cartilage injury and chondrocyte proliferation and apoptosis in rats with rheumatoid arthritis (RA) by regulating expression of CTGF. A rat model of RA induced by type II collagen was established. The rats were assigned into normal, RA, RA + mimics negative control (NC), and RA + miR-26a mimics groups, and the cells were classified into blank, mimics NC, and miR-26a mimics groups. The degree of secondary joint swelling and arthritis index, expression of miR-26a, pathological changes, proliferation and apoptosis of chondrocytes, and expression of CTGF, interleukin-1β (IL-1β), IL-6, tumor necrosis factor-α, Bax, and Bcl-2 were also determined through a series of experiments. The targeting relationship between miR-26a and CTGF was verified. Initially, downregulated miR-26a was found in cartilage tissues and inflammatory articular chondrocytes of RA rats. In addition, CTGF was determined as a direct target gene of miR-26a, and upregulation of miR-26a inhibited CTGF expression in cartilage tissues of RA rats. Furthermore, upregulation of miR-26a reduced swelling and inflammation of joints, inhibited cartilage damage, apoptosis of chondrocytes, inflammatory injury, promotes proliferation, and inhibited apoptosis of inflammatory articular chondrocytes, which may be correlated with the targeting inhibition of CTGF expression. Collectively, the results demonstrate that upregulating the expression of miR-26a could attenuate cartilage injury, stimulate the proliferation, and inhibit apoptosis of chondrocytes in RA rats. |
| Databáze: | OpenAIRE |
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