细胞质
河马信号通路
细胞生物学
肌动蛋白
免疫印迹
免疫荧光
核心
生物
污渍
信号转导
免疫学
抗体
遗传学
基因
作者
Cong Zhang,Feng Wang,Zhi‐Yang Xie,Lu Chen,Arjun Sinkemani,Hui Yu,Xiaotao Wu
摘要
Abstract Objectives Dysregulation of YAP by the Hippo signalling is associated with intervertebral disc degeneration ( IDD ). However, the relationship between the F‐actin and Hippo pathway in IDD , and their effects on YAP remain poorly understood. Methods The characteristics of Hippo pathway and F‐actin the in the NP (nucleus pulposus) and annulus fibrosus of immature, mature, ageing and disc degeneration model rats were observed by immunofluorescence, western blot and qPCR . Nucleus pulposus cells ( NPC s) were transfected with lentivirus Sh‐ LATS A, Sh‐ LATS B and harvested for SA ‐β‐gal staining, qPCR , western blotting and immunofluorescence staining to investigate the mechanism of Hippo pathway and F‐actin interact in NPC s. Results We observed moderate decreases in F‐actin and YAP expression with age in healthy intervertebral discs ( IVD s). F‐actin stress fibres distributed throughout the cytoplasm disappeared following treatment with latrunculin B (Lat B), resulting in a punctate distribution. Depletion of large tumour suppressor homologues 1/2 ( LATS 1/2) did not decrease the rate of cellular senescence, and YAP remained in the cytoplasm following Lat B treatment. Furthermore, angiomotin 130 ( AMOT 130) was associated with F‐actin through a conserved actin‐binding domain to retain YAP in the cytoplasm. Conclusions This study showed that a mechanism by which Hippo pathway and F‐actin synergize to modulate YAP activation and localization in the context of IDD and help to control NPC s proliferation.
科研通智能强力驱动
Strongly Powered by AbleSci AI