{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,23]],"date-time":"2026-08-23T16:44:57Z","timestamp":1787503497114,"version":"build-2736575974"},"reference-count":59,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2018,1,18]],"date-time":"2018-01-18T00:00:00Z","timestamp":1516233600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/100004411","name":"Heart and Stroke Foundation of Canada","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100004411","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Endocrino Diabet & Metabol"],"published-print":{"date-parts":[[2018,4]]},"abstract":"Summary<\/jats:title>\n \n Objectives and Design<\/jats:title>\n \n In this study, we examined the role of\n MALAT<\/jats:styled-content>\n 1, a highly conserved nuclear long non\u2010coding\n RNA<\/jats:styled-content>\n molecule, in chronic diabetic complications affecting the heart and kidneys using both in vitro and in vivo models: human endothelial cell culture and a Malat1 knockout mice model.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n Findings from our in vitro experiments demonstrated that\n MALAT<\/jats:styled-content>\n 1 was predominantly localized to nuclear speckles in endothelial cells and\n MALAT<\/jats:styled-content>\n 1 expression was significantly increased following incubation with high glucose in association with increased expression of inflammatory cytokines. As for our in vivo experiments, we used Malat1 knockout mice and wild\u2010type controls with or without streptozotocin\u2010induced diabetes over 2 months of follow\u2010up, where all of our diabetic animals showed hyperglycaemia and polyuria. Examination of cardiac and renal tissues demonstrated altered\n MALAT<\/jats:styled-content>\n 1\n RNA<\/jats:styled-content>\n expression in wild\u2010type diabetic animals. Such changes were associated with augmented production of downstream inflammatory molecules at the\n mRNA<\/jats:styled-content>\n and protein levels. Diabetes\u2010induced elevations of inflammatory markers were significantly decreased in Malat1 knockout diabetic animals. In addition to transcript and protein analyses, we examined functional changes in the heart and kidneys. Organ functions were affected in the wild\u2010type diabetic mice but were rescued in Malat1 knockout mice.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n Taken together, findings from this study will provide direct evidence and insight into the importance of\n MALAT<\/jats:styled-content>\n 1 in the pathogenesis of chronic diabetic complications involving the heart and kidneys.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1002\/edm2.10","type":"journal-article","created":{"date-parts":[[2018,1,18]],"date-time":"2018-01-18T00:09:31Z","timestamp":1516234171000},"source":"Crossref","is-referenced-by-count":42,"title":["MALAT1: A regulator of inflammatory cytokines in diabetic complications"],"prefix":"10.1002","volume":"1","author":[{"given":"Andrew Devon","family":"Gordon","sequence":"first","affiliation":[{"name":"Department of Pathology and Laboratory Medicine Western University London ON 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