Specific knockdown of WNT8b expression protects against phosphate ‐induced calcification in vascular smooth muscle cells by inhibiting the Wnt–β‐catenin signaling pathway

WNT8b knockdown terminates phosphate ‐induced vascular calcification in vascular smooth muscle cells by inhibiting the Wnt–β‐catenin signaling pathway. In the last 10 years, the prevalence, significance, and regulatory mechanisms of vascular calcification (VC) have gained increasing recognition. The aim of this study is to explore the action ofWNT8b in the development of phosphate ‐induced VC through its effect on vascular smooth muscle cells (VSMCs) in vitro by inactivating the Wnt–β‐catenin signaling pathway. To explore the effect ofWNT8b on the Wnt –β‐catenin signaling pathway and VC in vitro, β‐glycerophosphate (GP)‐induced T/G HA‐VSMCs were treated with small interfering RNA against WNT8b (Si‐WNT8b), Wnt ‐β‐catenin signaling pathway activator (LiCl) and both, respectively. Reverse transcription quantitative polymerase chain reaction and western blot analysis were used to determine the messenger RNA and protein levels of WNT8b, α‐smooth muscle actin (α‐SMA), calcification‐associated mole cules, and molecules related to the Wnt signaling pathway. The TOP/FOP‐Flash reporter assay was performed to detect the transcription activity mediated by β‐catenin. Si‐WNT8b reduced calcium deposition and the activity of alkaline phosphatase (ALP), increased the α‐SMA level, and decreased bone morphogenetic protein 2, Pit1, MSX2, and Runt‐related transcription factor 2 levels, whereas stimulation of LiCl worsened β‐GP‐induced calc...
Source: Journal of Cellular Physiology - Category: Cytology Authors: Tags: ORIGINAL RESEARCH ARTICLE Source Type: research
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