MiRNA-based therapy for Idiopathic pulmonary fibrosis: Apoptosis-stimulating protein of p53 (ASPP-1) increases TRF1 expression and ameliorates pulmonary fibrosis via up regulation of its target gene, 31/August/2015, 10.33 pm

MiRNA-based therapy for Idiopathic pulmonary fibrosis: Apoptosis-stimulating protein of p53 (ASPP-1) increases TRF1 expression and ameliorates pulmonary fibrosis via up regulation of its target gene, 31/August/2015, 10.33 pm

MiRNA-based therapy for Idiopathic pulmonary fibrosis: Apoptosis-stimulating protein of p53 (ASPP-1) increases TRF1 expression and ameliorates pulmonary fibrosis via up regulation of its target gene, 31/August/2015, 10.33 pm 150 150

A study from the Spanish National Cancer Centre, Melchor Fernández Almagro 3, Madrid, Spain shows that: Mice with Pulmonary Fibrosis Driven by Telomere Dysfunction.” This study was published in the 14 July 2015 issue of the journal “Cell Reportsby Prof. Maria, Povedano JM and others.

On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Molecular therapy for Idiopathic pulmonary fibrosis: Apoptosis-stimulating protein of p53 (ASPP-1) increases TRF1 expression and ameliorates pulmonary fibrosis via up regulation of its target gene

Significance:

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 Idiopathic pulmonary fibrosis patients; (ii) side-effect-free natural product-based drug; and (iii) a way to effectively treat and cure IPF

A number of studies suggest that genes that promote telomere protection are mutated in Idiopathic pulmonary fibrosis. Prof. Maria’s research team has recently shown that deletion of telomeric repeat binding factor (TRF1) promotes pulmonary fibrosis.

This study suggests, for the first time, that Apoptosis-stimulating protein of p53 (ASPP-1), by increasing the expression of its target gene, it may increase the expression of TRF1. Thereby, it may: (1) alleviate DNA damage; (2) ameliorate telomere dysfunction and promote telomere function and integrity; (3) inhibit the development and progression of pulmonary fibrosis. Thus, pharmacological formulations encompassing Apoptosis-stimulating protein of p53 (ASPP-1) activators may be used to treat Idiopathic pulmonary fibrosis.

Undisclosed information: How Apoptosis-stimulating protein of p53 (ASPP-1) increases the expression of TRF1.

Idea Proposed/Formulated byDr L Boominathan Ph.D.

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To citeBoominathan, MiRNA-based therapy for Idiopathic pulmonary fibrosis: Apoptosis-stimulating protein of p53 (ASPP-1) increases TRF1 expression and ameliorates pulmonary fibrosis via up regulation of its target gene, 31/August/2015, 10.34 pm,  Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org