Influence of protein kinase RIPK4 expression on the apoptosis and proliferation of chondrocytes in osteoarthritis
- Lixue Zou
- Jun Liu
- Hougen Lu
Published online on: December 7, 2017
Copyright: © Zou et al.
This is an open access article distributed under the terms of Creative Commons Attribution License.
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The present study aimed to investigate the expression of receptor‑interacting protein kinase 4 (RIPK4) and its effect on the apoptosis and proliferation of chondrocytes in osteoarthritis (OA). A total of 28 OA cartilage tissues and 20 normal cartilage tissues were collected to detect the expression of RIPK4 by using reverse transcription‑quantitative polymerase chain reaction and western blot analysis. Chondrocytes were isolated from OA cartilage tissues and divided into OA, NC, si‑RIPK4, Wnt3a, and si‑RIPK4+Wnt3a groups, and those isolated from normal cartilage tissues were considered the Normal group. Chondrocytes proliferation was detected by MTT assay, cell apoptosis was indicated using flow cytometry and Wnt/β‑catenin signaling pathway related‑proteins were investigated using western blot analysis. RIPK4 mRNA and protein expression levels in OA cartilage tissues and OA chondrocytes were increased compared with normal controls (all P<0.05). Additionally, OA chondrocytes showed reduced cell proliferation, increased cell apoptosis and upregulated expression levels of Wnt/β‑catenin signaling pathway related‑proteins (all P<0.05). Once transfected with si‑RIPK4, the proliferation ability of chondrocytes was enhanced, but apoptosis was notably decreased. Furthermore, the expression levels of Wnt/β‑catenin signaling pathway related‑proteins were significantly downregulated (all P<0.05). Results indicated that Wnt3a reversed the effect of si‑RIPK4 on chondrocyte proliferation and apoptosis (all P<0.05). Thus, silencing RIPK4 promoted the proliferation and inhibited the apoptosis of chondrocytes. In addition, silencing RIPK4 blocked the Wnt/β‑catenin signaling pathway, thus contributing to alleviating the OA pathogenesis.