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10.1371/journal.pone.0218003 http://scihub22266oqcxt.onion/10.1371/journal.pone.0218003 31170232!6553779!31170232     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=31170232&cmd=llinks): Failed to open stream: HTTP request failed! 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PINK1 attenuates mtDNA release in alveolar epithelial cells and TLR9 mediated profibrotic responses |pdf=|usr=}}{{31170232}} gab.com Text PINK1 attenuates mtDNA release in alveolar epithelial cells and TLR9 mediated profibrotic responses JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=31170232 #FOAvip We have previously shown that endoplasmic reticulum stress (ER stress) represses the PTEN inducible kinase 1 (PINK1) in lung type II alveolar epithelial cells (AECII) reducing mitophagy and increasing the susceptibility to lung fibrosis. Although increased circulating mitochondrial DNA (mtDNA) has been reported in chronic lung diseases, the contribution of mitophagy in the modulation of mitochondrial DAMP release and activation of profibrotic responses is unknown. In this study, we show that ER stress and PINK1 deficiency in AECII led to mitochondrial stress with significant oxidation and damage of mtDNA and subsequent extracellular release. Extracellular mtDNA was recognized by TLR9 in AECII by an endocytic-dependent pathway. PINK1 deficiency-dependent mtDNA release promoted activation of TLR9 and triggered secretion of the profibrotic factor TGF-beta which was rescued by PINK1 overexpression. Enhanced mtDNA oxidation and damage were found in aging and IPF human lungs and, in concordance, levels of circulating mtDNA were significantly elevated in plasma and bronchoalveolar lavage (BAL) from patients with IPF. Free mtDNA was found elevated in other ILDs with low expression of PINK1 including hypersensitivity pneumonitis and autoimmune interstitial lung diseases. These results support a role for PINK1 mediated mitophagy in the attenuation of mitochondrial damage associated molecular patterns (DAMP) release and control of TGF-beta mediated profibrotic responses. Twit Text FOAVip PINK1 attenuates mtDNA release in alveolar epithelial cells and TLR9 mediated profibrotic responses ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=31170232 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=31170232 #FOAvip English Wikipedia <ref>{{Cite pmid|31170232}}</ref> PINK1 attenuates mtDNA release in alveolar epithelial cells and TLR9 mediated profibrotic responses #MMPMID31170232 Bueno M; Zank D; Buendia-Roldan I; Fiedler K; Mays BG; Alvarez D; Sembrat J; Kimball B; Bullock JK; Martin JL; Nouraie M; Kaufman BA; Rojas M; Pardo A; Selman M; Mora AL PLoS One 2019[]; 14 (6): e0218003 PMID31170232show ga We have previously shown that endoplasmic reticulum stress (ER stress) represses the PTEN inducible kinase 1 (PINK1) in lung type II alveolar epithelial cells (AECII) reducing mitophagy and increasing the susceptibility to lung fibrosis. Although increased circulating mitochondrial DNA (mtDNA) has been reported in chronic lung diseases, the contribution of mitophagy in the modulation of mitochondrial DAMP release and activation of profibrotic responses is unknown. In this study, we show that ER stress and PINK1 deficiency in AECII led to mitochondrial stress with significant oxidation and damage of mtDNA and subsequent extracellular release. Extracellular mtDNA was recognized by TLR9 in AECII by an endocytic-dependent pathway. PINK1 deficiency-dependent mtDNA release promoted activation of TLR9 and triggered secretion of the profibrotic factor TGF-beta which was rescued by PINK1 overexpression. Enhanced mtDNA oxidation and damage were found in aging and IPF human lungs and, in concordance, levels of circulating mtDNA were significantly elevated in plasma and bronchoalveolar lavage (BAL) from patients with IPF. Free mtDNA was found elevated in other ILDs with low expression of PINK1 including hypersensitivity pneumonitis and autoimmune interstitial lung diseases. These results support a role for PINK1 mediated mitophagy in the attenuation of mitochondrial damage associated molecular patterns (DAMP) release and control of TGF-beta mediated profibrotic responses. |A549 Cells[MESH] |Adult[MESH] |Aged[MESH] |Aged, 80 and over[MESH] |Alveolar Epithelial Cells/*metabolism[MESH] |Animals[MESH] |Bronchoalveolar Lavage Fluid[MESH] |Cytokines/metabolism[MESH] |DNA, Mitochondrial/blood/*metabolism[MESH] |Disease Progression[MESH] |Female[MESH] |Fibroblasts/metabolism[MESH] |Humans[MESH] |Idiopathic Pulmonary Fibrosis/blood/*metabolism[MESH] |Inflammation/pathology[MESH] |Lung/pathology[MESH] |Male[MESH] |Mice, Inbred C57BL[MESH] |Mice, Knockout[MESH] |Middle Aged[MESH] |Models, Biological[MESH] |Oxidation-Reduction[MESH] |Protein Kinases/deficiency/*metabolism[MESH] |Toll-Like Receptor 9/*metabolism[MESH] |Transforming Growth Factor beta/metabolism[MESH]PINK1 attenuates mtDNA release in alveolar epithelial cells and TLR9 m(epmc).pdf DeepDyve Pubget Overpricing