MiRNA-based therapy for Fibrosis: Endothelin-1 suppresses TGFβ-dependent extracellular matrix accumulation and fibrosis via up regulation of its target gene, 25/March/2015, 22.28

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A recent study from the Center for Cardiovascular and Pulmonary Research and Heart Center, Nationwide Children’s Hospital, Department of Pediatrics, The Ohio State University, Columbus shows that “MicroRNA miR145 regulates TGFBR2 expression and matrix synthesis in vascular smooth muscle cells.” This study was published in the 2 January 2015 issue of the  Journal “Circulation Research” by Prof. Lilly B, Zhao N and others.

On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: MiRNA-based therapy for Fibrosis: Endothelin-1 suppresses TGFβ-dependent extracellular matrix accumulation and fibrosis via up regulation of its target gene. This study suggests, for the first time, that Endothelin-1, by increasing the expression of its target gene, it may : (1) decrease TGFβ receptor II expression; (2) suppress matrix synthesis and (3) promote smooth muscle cell differentiation. Thus, pharmacological formulations encompassing “Endothelin-1 activators may be used to treat fibrosis.

Idea Proposed/Formulated byDr L Boominathan Ph.D.

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To citeBoominathan,  MiRNA-based therapy for Fibrosis: Endothelin-1 suppresses TGFβ-dependent extracellular matrix accumulation and fibrosis via up regulation of its target gene, 25/March/2015,  22.28,  Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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* Research cooperation

Undisclosed information: How Endothelin-1 decreases the expression of TGFβ receptor II (TGFβR2)

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