Essay --

Mouse remains the most reliable species of choice to study the mechanism underlying in mammalian species. It is because they breed quickly, and their genetics are well understood. Aim The principal aim of first research paper is to study the all over expression take aim of miRNA -27b that induces cardiac hypertrophy and dysfunction in mice.The primary aim of the second research paper is to show how miRNA -212 and miR-132 expression regulates cardiac hypertrophy and cardiac myocyte autophagy. Methods A 500bp genomic fragment comprising the miR-27b control orbit was amplified by PCR and ligated into adenoviral vector to gene shutoute Ad-miR-27b using 293A cellular telephones for cloning and expression of miRNAs. Transgenic mouse was created by amplifying the fragment flanking miR-27b which is then subcloned into an expression vector comprising human growth endocrine gland poly A signal and -MHC promoter. Genotyping of the mouse is do by isolating genomic DNA from mouse tail by b iosepsis followed by its amplification by PCR using particular proposition primers. Western blotting is carried out on myocardial isolates and cardiac function was determined by echocardiography. All the statistical analysis was performed using SPSS software.Primary cardiomycetes were generated from neonatal mice/rat using a standard protocol. By cloning the whole miR-212/132 genomic locus (3.4kb) downstream of cytomegalovirus promoter within the pTARGET vector, an expression construct is generated which was used for the transfection of H9c2 cell lines. Transgenic mice showing the overexpression levels of miR-212/132 was generated by cloning 486bp genome encoding the hairpin stem loop downstream to 3rd exon sequence of -MHC gene and upstream of hGH poly A signal sequence. TAC was performe... ...analyzed for the over expression levels of miR 212 and miR 132 in intent tissue by reverse transcription PCR (fig.2b). However, the mouse were born normally but their life expectancy was re duced to 84 and 119 for Fam23 and Fam43 respectively (fig 2c). Their heart to body weight ratio has shown significant increase in heart mass at different ages. The upregulation of miR-212 and miR-132 witnessed the increased expression level of cardiac stress markers ANP and BNP ultimately resulting in the development of heart failure (fig. s3 bc). Evaluation of cardiac function in both transgenic and wild type mice is done by echocardiography, where end systolic and end diastolic of LV dilation was significantly observed in transgenic mice. Further, hemodynamic analysis confirmed impaired function of heart in transgenic mice. MiR-212 and miR-132 directly regulate FoxO3 expression