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HSF‐1 modulates autophagy via transcriptional regulation of autophagy‐related genes in A549 cells (738.3)
Author(s) -
Dokladny Karol,
Moseley Pope
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.738.3
Subject(s) - autophagy , microbiology and biotechnology , gene knockdown , biology , a549 cell , messenger rna , gene , cell , chemistry , genetics , apoptosis
Autophagy is an evolutionary conserved catabolic process employed by eukaryotic cells in response to nutrients starvation, hypoxia, high temperature, and acute exercise. Autophagy, along with other cellular processes, is required for a normal cell function and is responsible for degrading dysfunctional cellular constituents in double‐membrane structures called autophagosomes upon fusion with lysosomes. Recently, we have shown that HSF‐1 knockdown with siRNA increased the LC3 lipidation associated with formation of autophagosomal organelles and augmented both starvation and rapamycin‐induced autophagy. The aim of the present study was to evaluate whether HSF‐1 inhibition by siRNA changes mRNA levels of autophagy related genes in A549 cells (adenocarcinomic human alveolar basal epithelial cells). A549 cells were treated with HSF‐1 siRNA for 48h, total RNA was collected, cDNA was generated, and the quantitative RT‐PCR was performed. Exposure of A549 cells to HSF‐1 siRNA resulted in an increase in LC3, beclin, and Atg12, but not Atg7 mRNA expression. These changes in mRNA expressions were correlated with protein expressions. We conclude that HSF‐1 acts as a negative regulator of autophagy related genes and inhibits autophagy under control conditions. Grant Funding Source : UNM CTSA Grant UL1 TR000041 and UNM School of Medicine Research Allocation Committee Grant