<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>7</volume><submitter>Chen TT</submitter><pubmed_abstract>Chronic obstructive pulmonary disease(COPD) is characterized by enhanced chronic inflammation in the airways, lung parenchyma, and circulation. We investigated whether SUV39H1, a histone methyltransferase, is causatively implicated in the abnormal inflammation observed in COPD. The SUV39H1 and H3K9me3 levels were reduced in peripheral blood mononuclear cells(PBMCs), primary human small airway epithelial cells(HSAEpCs) and lung tissues from COPD patients, which were correlated with poor lung function and the serum IL-8 and IL-6 levels. A specific SUV39H1 inhibitor, chaetocin, induced a distinct COPD panel of inflammatory cytokines in normal PBMCs. Mechanistically, chaetocin reduced the SUV39H1 and H3K9me3 levels in the native IL-8 promoter in normal HSAEpCs, which mimicked unstimulated COPD</pubmed_abstract><journal>Scientific reports</journal><pagination>46667</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5397975</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>SUV39H1 Reduction Is Implicated in Abnormal Inflammation in COPD.</pubmed_title><pmcid>PMC5397975</pmcid><pubmed_authors>Ho SC</pubmed_authors><pubmed_authors>Wu SM</pubmed_authors><pubmed_authors>Juang JN</pubmed_authors><pubmed_authors>Liu WT</pubmed_authors><pubmed_authors>Chen TT</pubmed_authors><pubmed_authors>Feng PH</pubmed_authors><pubmed_authors>Lee KY</pubmed_authors><pubmed_authors>Chuang HC</pubmed_authors><pubmed_authors>Liu CY</pubmed_authors><pubmed_authors>Hsiao TC</pubmed_authors><pubmed_authors>Chan YF</pubmed_authors><pubmed_authors>Kuo LW</pubmed_authors><pubmed_authors>Chen KY</pubmed_authors></additional><is_claimable>false</is_claimable><name>SUV39H1 Reduction Is Implicated in Abnormal Inflammation in COPD.</name><description>Chronic obstructive pulmonary disease(COPD) is characterized by enhanced chronic inflammation in the airways, lung parenchyma, and circulation. We investigated whether SUV39H1, a histone methyltransferase, is causatively implicated in the abnormal inflammation observed in COPD. The SUV39H1 and H3K9me3 levels were reduced in peripheral blood mononuclear cells(PBMCs), primary human small airway epithelial cells(HSAEpCs) and lung tissues from COPD patients, which were correlated with poor lung function and the serum IL-8 and IL-6 levels. A specific SUV39H1 inhibitor, chaetocin, induced a distinct COPD panel of inflammatory cytokines in normal PBMCs. Mechanistically, chaetocin reduced the SUV39H1 and H3K9me3 levels in the native IL-8 promoter in normal HSAEpCs, which mimicked unstimulated COPD</description><dates><release>2017-01-01T00:00:00Z</release><publication>2017 Apr</publication><modification>2025-04-19T03:51:23.005Z</modification><creation>2019-03-27T02:41:41Z</creation></dates><accession>S-EPMC5397975</accession><cross_references><pubmed>28425504</pubmed><doi>10.1038/srep46667</doi></cross_references></HashMap>