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Culture of Murine Embryonic Metatarsals: A Physiological Model of Endochondral Ossification
Published on: December 3, 2016
From selenoprotein to endochondral ossification: a novel mechanism with microRNAs potential in bone related diseases?
Jian Sun1, Qingzhu Sun, Shemin Lu
1Department of Genetics and Molecular Biology, Xi'an Jiaotong University College of Medicine, Xi'an, Shaanxi 710061, PR China.
Abstract:
Selenium participates the formation of selenoprotein as the form of selenocysteine, the active-site residue essential for protein catalytic activity. It has been proved that selenium deficiency leads to the abnormality of selenoprotein biosynthesis, which may lead to disorders of brain, skeleton development and cartilage chondrocyte differentiation. The production of selenoproteins is regulated by selenocysteine insertion sequence (SECIS) and several trans-acting factors in eukaryotic cells. However, the mechanism of posttranscriptional modification of selenoproteins biosynthesis seldom needs to be elucidated. Recent evidence indicates that miRNAs are key points in the process of endochondral ossification. The hypothesis is that the expression of key selenoproteins may regulate directly or indirectly via trans-acting factors by miRNAs during skeleton development.
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