Molecular therapy for Pulmonary Fibrosis:Ursodeoxycholic acid increases Toll-like receptor 4 expression and extracellular matrix glycosaminoglycan Hyaluronan levels, promotes alveolar progenitor cell renewal and repair of lung injury and prevents severe pulmonary fibrosis via down-regulation of its target gene, 13/October/2016, 11.14 pm

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A study from the Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA; and Women’s Guild Lung Institute, Cedars-Sinai Medical Center, Los Angeles, California, USA shows that: “Hyaluronan and TLR4 promote surfactant-protein-C-positive alveolar progenitor cell renewal and prevent severe pulmonary fibrosis in mice.” This study was published in the 03 October 2016 issue of the journal “Nature Medicine” (One of the best journals in General Medicine with an IF of 30.357)by Prof. Noble PW, Liang J and others.

On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Molecular therapy for Pulmonary Fibrosis: Ursodeoxycholic acid increases Toll-like receptor 4 expression and extracellular matrix glycosaminoglycan Hyaluronan levels, promotes alveolar progenitor cell renewal and repair of lung injury and prevents severe pulmonary fibrosis via down-regulation of its target gene


Significance:

Given that: (1) Pulmonary disease (PD)/Pulmonary fibrosis (PF) is a progressive degenerative disease of the lung, with debilitating consequences; (2) drugs that are currently used to treat PF are ineffective; (3) molecular mechanisms involved in the development of pulmonary fibrosis is poorly understood; (4) 6.8-16.3 per 100,000 persons suffer from Idiopathic pulmonary disease; and (5) 5 million people worldwide are affected by PF, there is an urgent need to find: (i) a way to regenerate alveolar epithelial cells lost in pulmonary fibrosis patients; (ii) a side-effect-free natural product-based drug; and (iii) a way to effectively treat and cure PF.

Prof. Noble’s research team has recently shown that deletion of TLR4 or HA synthase 2 results in pulmonary fibrosis.

This study suggests, for the first time, that Ursodeoxycholic acid, by decreasing the expression of its target gene, it may increase the expression of TLR4 and HA synthase 2 (HAS2). 

Image result for :Ursodeoxycholic acid

Ursodeoxycholic acid impedes the progression of pulmonary fibrosis via up-regulation of TLR4 and Has2

Thereby, it may: (1) increase extracellular matrix glycosaminoglycan Hyaluronan on cell surface; (2) promote alveolar progenitor/stem cell renewal; (3) promote repair of lung injury; and (4) inhibit the development and progression of pulmonary fibrosis. Thus, pharmacological formulations encompassing Ursodeoxycholic acid or its analogs may be used to regenerate alveolar epithelial stem cells and treat pulmonary fibrosis.


Idea Proposed/Formulated by: Dr L Boominathan Ph.D.

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

To cite: Boominathan, Molecular therapy for Pulmonary Fibrosis:Ursodeoxycholic acid increases Toll-like receptor 4 expression and extracellular matrix glycosaminoglycan Hyaluronan levels, promotes alveolar progenitor cell renewal and repair of lung injury and prevents severe pulmonary fibrosis via down-regulation of its target gene, 13/October/2016, 11.14 pm, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org


Undisclosed information: How Ursodeoxycholic acid increases the expression of TLR4.

Amount: $300#

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