Molecular therapy for pulmonary fibrosis: Ethinylestradiol decreases miR-34 expression, increases Sirtuin-1 expression, suppresses tumor suppressor p53 acetylation, prevents apoptosis in Alveolar epithelial cell (AEC), and improves pulmonary fibrosis via down regulation of its target gene, 22/March/2017, 11.22 pm

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What we say: 

Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Molecular therapy for pulmonary fibrosis: Ethinylestradiol decreases miR-34 expression, increases Sirtuin-1 expression, suppresses tumor suppressor p53 acetylation, prevents apoptosis in Alveolar epithelial cell (AEC), and improves pulmonary fibrosis via down regulation of its target gene


From significance of the study to public health relevance:

Given that: (1) Idiopathic pulmonary disease (IPD)/Idiopathic pulmonary fibrosis (IPF)  is a progressive degenerative disease of the lung, with debilitating consequences; (2) drugs that are currently used to treat IPF are ineffective; and (3) 6.8-16.3 per 100,000 persons suffer from  Idiopathic pulmonary disease, there is an urgent need to find: (i) a way to induce regeneration of lung cells in pulmonary fibrosis patients; (ii) side-effect-free natural product-based drug; and (iii) a way to effectively treat and cure PF


From research findings to therapeutic opportunity

This study suggests, for the first time, that Ethinylestradiol, by increasing the expression of its target gene, it may: (1) decrease the expression of p53 and its target gene miR-34a; (2) increase the expression of longevity-protein Sirtuin-1; (3) suppress p53 acetylation; (4) inhibit urokinase-type plasminogen activator (uPA) and the uPA receptor expression in AECs (Alveolar epithelial cells); (5) prevent apoptosis in AECs; and (6) inhibit the development and progression of pulmonary fibrosis. Thus, pharmacological formulations encompassing Ethinylestradiol or its analogues either alone or in combination with other drugs may be used to treat pulmonary fibrosis.


Details of the research findings: 

Idea Proposed/Formulated byDr L Boominathan Ph.D.

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/

Undisclosed mechanistic information: How Ethinylestradiol decreases miR-34 expression to improve pulmonary fibrosis

Amount: $100#

# Research cooperation


References

CitationBoominathan, L., Molecular therapy for pulmonary fibrosis: Ethinylestradiol  decreases miR-34 expression, increases Sirtuin-1 expression, suppresses tumor suppressor p53 acetylation, prevents apoptosis in Alveolar epithelial cell (AEC), and improves pulmonary fibrosis via down regulation of its target gene, 22/March/2017, 11.22 pm,  Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

Web: http://genomediscovery.org or newbioideas.com

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# Research cooperation

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