Selenium Deficiency Affects Uterine Smooth Muscle Contraction Through Regulation of the RhoA/ROCK Signalling Pathway in Mice.

Selenium (Se) is considered one of the essential micronutrients for humans and animals, and its effects on physiological functions are multifaceted. In the present study, we investigated the effects of Se deficiency on uterine smooth muscle contraction in mice by studying G protein Rho (RhoA)/Rho kinase (ROCK) signalling pathway-related molecules. The α-sma in smooth muscle tissue of mice was determined. The extracorporeal contraction curve for uterine smooth muscle in mice was determined. Both of these results indicate that Se deficiency impairs the contractile ability of uterine smooth muscle in mice. The expression of mRNA was measured by real-time quantitative PCR. The results showed that there was no significant change in mRNA expression of RhoA, ROCK, myosin light chain phosphatase (MLCP), or myosin light chain (MLC) in tissues. The protein levels were detected by Western blot. The results showed that there were no significant differences in RhoA, ROCK, MLCP, or MLC expression. However, compared with the CG, the concentration of phosphorylated MLC (P-MLC) increased in the SG and the concentration of P-MLC decreased in the DG. The activity of ROCK and MLCP was tested by liquid scintillation. The results suggest that the lack of Se may affect the regulation of MLCP by ROCK. Cellular experiments were performed to compare with results from tissues. There was no significant difference between the two models. The results indicated that Se deficiency affects uterine smooth muscle contraction by regulating the RhoA/ROCK signalling pathway. As the concentration of Se decreases, the activity of MLCP increases, which promotes the dephosphorylation of P-MLC, causing a decrease in contraction.