Time Course Expression of Mechanosensitive Ion Channels in Rat Postural Muscle under Hindlimb Unloading

Atony and atrophy of mammalian postural muscles can result from mechanical unloading (weightlessness, hypokinesia). There is reason to believe that calcium-permeable mechanosensitive channels may contribute to the development of muscle atrophy caused by mechanical unloading. The aim of the study was to assess time course changes in the expression of key mechanosensitive channels in rat soleus muscle under conditions of mechanical unloading. Male Wistar rats were exposed to hindlimb suspension (HS) for 1, 3, 7 and 14 days. The expression of Piezo1, TRPC1, TRPC3, TRPC6, TRPM3, TRPM7 and TMEM63B mRNA was determined using PCR. Piezo1 protein content was assessed by Western blotting. Piezo1 mRNA expression transiently increased after 24 h of HS, but did not differ from the control after 3, 7 and 14 days of unloading. A decrease in Piezo1 protein content was observed after 3, 7 and 14 days of HS relative to the control. At the early stages of HS, there was a significant increase in the mRNA expression of TRPC3, TRPM3, TRPM7 and TMEM63B, while TRPC6 expression was reduced. The level of TRPC1 mRNA expression was increased only after 3 days of HS. Seven-day unloading did not cause changes in mRNA expression of TRPC1, TRPC3, TRPM3 and TMEM63B, but led to increased TRPM7 expression. After two weeks of HS, the soleus muscle exhibited a decrease in mRNA expression of TRPC1, TRPC6, TRPM3 and TMEM63B. Thus, at an early stage of mechanical unloading (1 and 3 days), there occurs a transient increase in mRNA expression of Piezo1, TRPC1, TRPC3 and TMEM63B, but at a later stage of unloading (14 days), the expression of TRPC1, TRPC6, TRPM3, TMEM63B at the mRNA level and Piezo1 at the protein level decreases.