Low Selenium Diet Inhibited CaMKII Activation via miR-365-3p/SelT Signaling Axis, Resulting in Myoblast...

Selenium (Se) mainly functions in the form of selenoproteins. Low Se diet causes skeletal muscle injury and expression changes in miRNA and selenoprotein. Selenoprotein T (SelT) is reported to be a key molecule in Ca²⁺/CaMKII signaling. But the role of SelT/Ca²⁺/CaMKII signals in low Se diet induced skeletal muscle damage of broilers and their underlying mechanisms remain poorly investigated. Here, we randomly divided 40 1-day-old Ross 308 male broilers into two groups, feeding them either a low-selenium diet or a normal diet for 42 days, to establish control and selenium-deficient broiler models. In vitro, we established chicken embryo models, and cultured chicken primary myoblasts. We showed that Se deficiency resulted in skeletal muscle damage and atrophy in broilers, and the protein level of SelT was decreased significantly (p < 0.05). Mechanistically, myotube formation depended on SelT-mediated p-CaMKII upregulation. The absence of SelT suppressed CaMKII activation and impaired myotube development by decreasing the ER-Ca²⁺ content (p < 0.05). On the contrary, overexpressing SelT by pCDNA-SelT transfection induced robust myotube growth, manifested by a marked increase of MHC abundance, yet KN-93 treatment could block this process (p < 0.05). In addition, in this work, we first identified miR-365-3p, a microRNA which targets SelT mRNA to inhibit myoblast differentiation by disrupting Ca²⁺ homeostasis (p < 0.05). In summary, our findings revealed that SelT deletion-mediated Ca²⁺ level downregulation caused by low Se diet hindered myoblast differentiation and myotube formation through suppressing CaMKII activation. Our study provides an attractive target for the cultivated meat industry.