Lyrm1 Gene Over-expression Of P19 Cell Differentiation, Proliferation And Apoptosis

Congenital heart disease (CHD) is always the leading cause of death in the first year of life. CHD is considered having something to do with environmental and genetic factors, and environmental factor plays the most important role. Although some genes were found in conection with CHD and the growth of myocytes, but the specific mechanism is unclear. Thus, identification and characterization of novel genes and proteins associated with CHD remain an important issue.LYRM1 gene is a new gene. A research has shown that it can promote proliferation and inhibit apoptosis of preadiprocytes. Many organizations expression profiles indicate that LYRM1 gene expressed in human heart tissue with medium abundance. And it was bound up with the mitochondrial function. During the development of vertebrate organs, both heart and adipose tissue result from mesoblast. And proliferation and inhibition of the cells are the two important processes of heart morphogenesis. Mitochondria are the important energy sources of heart tissue. And now the relation between LYRM1 and CHD is not clear. Therefore, this gene was selected for further analysis in this study.The LYRM1 is an mRNA of 1589 basepairs (bps) with a 369 bp open reading frame (ORF) which encodes a 122 amino acids (aas) protein with a molecular mass of 13.27 kDa. NCBI Map Viewer analysis revealed that the LYRM1 gene is located on chromosome 16 and is composed of 4 exons. Amino acid sequence analysis revealed that LYRM1 was not a membrane-spanning protein and was an unsecreted protein. LYRM1 localizes in the nucleus and has a LYR domain. A sequence comparison of mouse and rat LYRM1 orthologous genes suggests that LYRM1 represents a novel gene highly conserved across primates and rodents.P19 cell was derived from dysembryoma of C3H/He male mice. It is a kind of embryonic stem cell, which can be cultured in vitro. And it can be induced to be myocyte.We examined the effect of LYRM1 on cell differentiation, proliferation, and apoptosis in vitro by establishing a stable P19 cell line overexpressing LYRM1, and found that: (i) LYRM1 does not affect the differentiation of P19 cells; (ii) the result of the MTT assay indicated that LYRM1 can promote proliferation of P19 cell and cell cycle analysis showed that a non-significant increase in the percentage of cells in S-phase; and (iii) LYRM1 can prevent apoptosis induced by serum deprivation with the analysis of annexin V-FITC and caspase-3 activity. In summary, our data demonstrate that by increasing cell proliferation and lowering apoptotic rate, LYRM1 has the potential to affect the development of CHD.In conclusion, we characterized several original features and the relationship with P19 cells of LYRM1 gene. Which can provide new clue to the researchs of CHD.