Aquaporin 1 contributes to chondrocyte apoptosis in a rat model of osteoarthritis

Abstract

Aquaporins (AQPs) have been found to be associated with a number of diseases. However, the role of AQP-1 in the pathogenesis of osteoarthritis remains unclear. We previously found that AQP-1 expression was upregulated in osteoarthritic cartilage and strongly correlated with caspase-3 expression and activity. The aim of this study was to further investigate the association of AQP-1 expression with chondrocyte apoptosis in a rat model of osteoarthritis, using RNA interference to knock down AQP-1. For this purspose, 72 male Sprague-Dawley rats were randomly assigned to 3 groups as follows: the control group not treated surgically (n=24), the sham-operated group (n=24), and the osteoarthritis group (n=24). Osteoarthritis was induced by amputating the anterior cruciate ligament and medial collateral ligament and partially excising the medial meniscus. Chondrocytes from the rats with osteoarthritis were isolated and cultured. shRNAs were used to knock down AQP-1 expression in the cultured chondrocytes. The expression of AQP-1 and caspase-3 was determined by reverse transcription-quantitative polymerase chain reaction. Caspase-3 activity was measured using a caspase-3 colorimetric assay. The rats in our model of osteoarthritis exhibited severe cartilage damage. The knockdown of AQP-1 decreased caspase-3 expression and activity in the cultured chondrocytes. In addition, the expression of AQP-1 positively correlated with caspase-3 expression and activity. Thus, the findings of our study, suggest that AQP-1 promotes caspase-3 activation and thereby contributes to chondrocyte apoptosis and to the development of osteoarthritis.

Depletion of aquaporin 1 decreased ADAMTS‑4 expression in human chondrocytes

“…However, AQP1 functions in the synovial tissue were not assessed in the present study and should be addressed in a future study. Second, a previous report showed that AQP1 expression positively correlated with caspase-3 expression and activity, suggesting that AQP1 promoted caspase-3 activation and thereby contributed to chondrocyte apoptosis and the development of OA ( 28 ). Thus, AQP1 roles in chondrocyte apoptosis should also be evaluated in future studies.…”

“…Recent reports have also described various AQP1 functions other than its role in water-dependent homeostasis ( 28 – 30 ). Meng et al ( 30 ) demonstrated that AQP1 enhances the migration of bone marrow mesenchymal stem cells by regulating the focal adhesion kinase and β-catenin.…”

Inhibitory effect of AQP1 silencing on adhesion and angiogenesis in ectopic endometrial cells of mice with endometriosis through activating the Wnt signaling pathway

“…In another study, the author confirmed that the AQP1 inhibitor-bacopaside II inhibited the viability, migration and tube formation of endothelial cells, and enhanced apoptosis [35]. Furthermore, it was found that the knockdown of AQP1 expression in chondrocytes from osteoarthritic rats using siRNA reduced the activity and expression of caspase-3, which indicated that AQP1 conduced to chondrocyte apoptosis and osteoarthritis development [36]. Thereby, AQP1 could regulate angiogenesis and apoptosis of cell in multiple diseases.…”

miRNA‑27a regulates arthritis via PPARγ in�vivo and in�vitro

“…There is a small amount of apoptosis in the normal cartilage tissue, which is usually confined to the surface of cartilage tissue (22). It is an essential physiological process to ensure the normal growth and development of cartilage, regulate function and maintain homeostasis (22). The excessive apoptosis in cartilage cells indicates pathological changes of cartilage tissue, which is considered to be the key factor leading to the onset of OA (20).…”