Molecular and Cell Biology Program

Bethesda, MD, United States

Molecular and Cell Biology Program

Bethesda, MD, United States
SEARCH FILTERS
Time filter
Source Type

Bhattacharyya S.,Uniformed Services University of the Health Sciences | Kumar P.,Uniformed Services University of the Health Sciences | Tsuchiya M.,Molecular and Cell Biology Program | Bhattacharyya A.,Uniformed Services University of the Health Sciences | Biswas R.,Uniformed Services University of the Health Sciences
Biochemical and Biophysical Research Communications | Year: 2013

Cystic fibrosis (CF) is characterized by a massive pro-inflammatory phenotype in the lung arising from profound expression of inflammatory genes, including interleukin-8 (IL-8). We have previously reported that IL-8 mRNA is stabilized in CF lung epithelial cells, resulting in concomitant hyper-expression of IL-8 protein through elevated expression of miR-155. We therefore investigated what factors promote the enhanced aberrant expression of miR-155 in CF. Here we report for the first time, the role of mRNA-destabilizing inflammatory RNA-binding proteins, KSRP and TTP, in the regulation of miR-155 biogenesis in CF lung epithelial cells. We find that KSRP and TTP have an antagonistic role in miR-155 biogenesis. While KSRP promotes enhanced processing of miR-155 precursors to mature miR-155, over-expression of TTP in the CF lung epithelial cells suppresses expression of miR-155. We find that TTP induces the expression of miR-1, which appears to be a regulator of miR-155 biogenesis in CF lung epithelial cells. These data provide novel insights into the mechanisms that induce hyper-inflammatory phenotype of CF, and are potential candidates for anti-inflammatory therapeutics for CF. © 2013.

Loading Molecular and Cell Biology Program collaborators
Loading Molecular and Cell Biology Program collaborators