<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Premadasa LS</submitter><funding>NIDA NIH HHS</funding><funding>NIAID NIH HHS</funding><funding>NIMH NIH HHS</funding><funding>National Institute on Drug Abuse</funding><funding>NIH HHS</funding><pagination>e167903</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10132162</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>8(7)</volume><pubmed_abstract>Intestinal epithelial barrier dysfunction, a hallmark of HIV/SIV infection, persists despite viral suppression by combination antiretroviral therapy (cART). Emerging evidence suggests a critical role for long noncoding RNAs (lncRNAs) in maintaining epithelial homeostasis. We simultaneously profiled lncRNA/mRNA expression exclusively in colonic epithelium (CE) of SIV-infected rhesus macaques (RMs) administered vehicle (VEH) or Δ-9-tetrahydrocannabinol (THC). Relative to controls, fewer lncRNAs were up- or downregulated in CE of THC/SIV compared with VEH/SIV RMs. Importantly, reciprocal expression of the natural antisense lncRNA MMP25-AS1 (up 2.3-fold) and its associated protein-coding gene MMP25 (attracts neutrophils by inactivating alpha-1 anti-trypsin/SERPINA1) (down 2.2-fold) was detecte</pubmed_abstract><journal>JCI insight</journal><pubmed_title>Cannabinoid enhancement of lncRNA MMP25-AS1/MMP25 interaction reduces neutrophil infiltration and intestinal epithelial injury in HIV/SIV infection.</pubmed_title><pmcid>PMC10132162</pmcid><funding_grant_id>P30 AI161943</funding_grant_id><funding_grant_id>P51 OD011104</funding_grant_id><funding_grant_id>R01 MH116844</funding_grant_id><funding_grant_id>R01 DA052845</funding_grant_id><funding_grant_id>R33 DA053643</funding_grant_id><funding_grant_id>P51 OD011133</funding_grant_id><funding_grant_id>R01DA042524,R01DA052845,R01DA050169,P30AI161943,P51OD011104,P51OD111033</funding_grant_id><funding_grant_id>R01 DA050169</funding_grant_id><funding_grant_id>R01 MH130193</funding_grant_id><funding_grant_id>U42 OD010442</funding_grant_id><funding_grant_id>R56 AI150371</funding_grant_id><funding_grant_id>R01 AI157850</funding_grant_id><funding_grant_id>R01 DA042524</funding_grant_id><pubmed_authors>Jayakumar S</pubmed_authors><pubmed_authors>Mohan M</pubmed_authors><pubmed_authors>Alvarez X</pubmed_authors><pubmed_authors>Ling B</pubmed_authors><pubmed_authors>McDew-White M</pubmed_authors><pubmed_authors>Premadasa LS</pubmed_authors><pubmed_authors>Okeoma CM</pubmed_authors><pubmed_authors>Byrareddy SN</pubmed_authors><pubmed_authors>Kulkarni S</pubmed_authors><pubmed_authors>Lee E</pubmed_authors></additional><is_claimable>false</is_claimable><name>Cannabinoid enhancement of lncRNA MMP25-AS1/MMP25 interaction reduces neutrophil infiltration and intestinal epithelial injury in HIV/SIV infection.</name><description>Intestinal epithelial barrier dysfunction, a hallmark of HIV/SIV infection, persists despite viral suppression by combination antiretroviral therapy (cART). Emerging evidence suggests a critical role for long noncoding RNAs (lncRNAs) in maintaining epithelial homeostasis. We simultaneously profiled lncRNA/mRNA expression exclusively in colonic epithelium (CE) of SIV-infected rhesus macaques (RMs) administered vehicle (VEH) or Δ-9-tetrahydrocannabinol (THC). Relative to controls, fewer lncRNAs were up- or downregulated in CE of THC/SIV compared with VEH/SIV RMs. Importantly, reciprocal expression of the natural antisense lncRNA MMP25-AS1 (up 2.3-fold) and its associated protein-coding gene MMP25 (attracts neutrophils by inactivating alpha-1 anti-trypsin/SERPINA1) (down 2.2-fold) was detecte</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Apr</publication><modification>2026-05-29T06:37:33.804Z</modification><creation>2025-02-19T02:04:05.813Z</creation></dates><accession>S-EPMC10132162</accession><cross_references><pubmed>37036007</pubmed><doi>10.1172/jci.insight.167903</doi></cross_references></HashMap>