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Saturday, May.18, 2024
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miRNA: |
hsa-miR-208a |
Disease: |
cardiac hypertrophy |
Relationship type: |
Causal |
Detection method for miRNA expression: |
northern blot, qRT-PCR etc |
Expression pattern of miRNA: |
down-regulated |
Validated targets of miRNA from the reference: |
unknown |
Validated targets of miRNA from TarBase: |
unknown : More... |
Predicted targets: |
MIRANDA, TARGETSCAN, PICTAR-VERT |
Description: Here, we investigated the function and molecular mechanisms of the miR-208 family of miRNAs in adult mouse heart physiology. We found that miR-208a, which is encoded within an intron of alpha-cardiac muscle myosin heavy chain gene (Myh6), was actually a member of a miRNA family that also included miR-208b, which was determined to be encoded within an intron of beta-cardiac muscle myosin heavy chain gene (Myh7). These miRNAs were differentially expressed in the mouse heart, paralleling the expression of their host genes. Transgenic overexpression of miR-208a in the heart was sufficient to induce hypertrophic growth in mice, which resulted in pronounced repression of the miR-208 regulatory targets thyroid hormone-associated protein 1 and myostatin, 2 negative regulators of muscle growth and hypertrophy. Studies of the miR-208a Tg mice indicated that miR-208a expression was sufficient to induce arrhythmias. Furthermore, analysis of mice lacking miR-208a indicated that miR-208a was required for proper cardiac conduction and expression of the cardiac transcription factors homeodomain-only protein and GATA4 and the gap junction protein connexin 40. Together, our studies uncover what we believe are novel miRNA-dependent mechanisms that modulate cardiac hypertrophy and electrical conduction. |
Reference:
MicroRNA-208a is a regulator of cardiac hypertrophy and conduction in mice | PMID:19726871
Callis TE, Pandya K, Seok HY, Tang RH, Tatsuguchi M, Huang ZP, Chen JF, Deng Z, Gunn B, Shumate J, Willis MS, Selzman CH, Wang DZ.
J Clin Invest. 2009 Sep;119(9):2772-86. doi: 10.1172/JCI36154. Epub 2009 Aug 10. |
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