Mechanism of Abnormal Chondrocyte Proliferation Induced by Piezo1-siRNA Exposed to Mechanical Stretch. (5th November 2020)

• Record Type: Journal Article
• Authors: Sun, Yi; Leng, Ping; Li, Dawei; Gao, Huanshen; Li, Zhenghui; Li, Chenkai; Zhang, Haining
• Other Names: Liu Shen Academic Editor.
• Is Part Of: BioMed research international. Volume 2020(2020)
• Publication Date: 2020-11-05
• Subjects: Medicine -- Periodicals; Biology -- Periodicals; Biotechnology -- Periodicals; Life sciences -- Periodicals; 610.5
• DOI: 10.1155/2020/8538463
• Languages: English
• ISSNs: 2314-6133

Abstract

Abstract : Objective . To investigate the effect of small interfering RNA targeting mechanosensitive ion channel protein Piezo1 (Piezo1-siRNA) on abnormal chondrocyte proliferation exposed to mechanical stretch. Methods . Construct and screen effective Piezo1-siRNA sequences and explore an appropriate method to transfect lentiviral vector into chondrocytes exposed to mechanical stretch. Western blot and RT-PCR were used to detect the mRNA and protein expression of Piezo1, Kif18A, and β -tubulin, respectively. Flow cytometry was used to measure the changes in the chondrocyte cycle. The proliferation of chondrocyte was evaluated by cell counting kit-8. Results . According to the mRNA and protein expression of Piezo1, the effective siRNA sequence was successfully screened. Compared with the 0 h group, mechanical stretch upregulated the expression of Piezo1, Kif18A, and β -tubulin, resulting in chondrocyte cycle arrest and eventually inhibiting chondrocyte proliferation. Moreover, Piezo1-siRNA transfection effectively blocks this process and promotes the proliferation of chondrocyte. Conclusion . Piezo1-siRNA can reduce the inhibition of chondrocyte proliferation induced by mechanical stretch via downregulating the expression of Kif18A and inhibiting the depolymerization of microtubules. Piezo1-siRNA plays a protective role in chondrocytes, which provides a potential method for the treatment of OA under abnormal mechanical stimulation.