A recent study from the Department of Pediatrics and Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA, USA; The Vera Moulton Wall Center for Pulmonary Vascular Disease, Stanford University School of Medicine, Stanford, CA, USA showsthat “BMPR2 Preserves Mitochondrial Function and DNA during Reoxygenation to Promote Endothelial Cell Survivaland Reverse Pulmonary Hypertension.” This study was published in the 7 April 2015 issue of Cell Metabolism by Prof Rabinovitch M, Diebold I, 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 Pulmonary Hypertension: Treatment with antagomiR-100 reverses pulmonary hypertension via up regulation of BMPR2.
Significance: Prof Rabinovitch and his team members have shown recently that deletion of BMPR2 induces/develops: (1) mitochondrial dysfunction; (2) pro-inflammatory or pro-apoptotic state; and (3) hypoxia-induced pulmonary hypertension. This study suggests, for the first time, that miR-100, by suppressing the expression of its target gene BMPR2, it may cause pulmonary hypertension. Therefore, by suppressing the expression of miR-100, one may induce the expression of BMPR2, increase endothelial cell survival, and inhibit the progression of pulmonary hypertension. Together, pharmacological formulations encompassing “antagomiR-100 or miR-100 inhibitors” may be used to treat pulmonary hypertension.
Idea Proposed/Formulated by: Dr L Boominathan Ph.D.
Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/
To cite: Boominathan, MiRNA-based therapy for Pulmonary Hypertension: Treatment with antagomiR-100 reverses pulmonary hypertension via up regulation of BMPR2, 13/April/2015, 13.38 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
Courtesy: When you cite drop us a line at email@example.com
* Research cooperation