1 40 2 Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.1111/jcmm.16224" target="_blank" rel="noreferrer noopener">http://doi.org/10.1111/jcmm.16224</a> Rights Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). ISSN 1582-1838 Search for Full-text Locate full-text within NEOMED Library's e-journal collections <a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.1111/jcmm.16224" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1111/jcmm.16224</a> <p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p> Update Year & Number March 2021 List NEOMED College NEOMED College of Medicine Student NEOMED Department NEOMED Student Publications Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource miR-467 regulates inflammation and blood insulin and glucose Publisher An entity responsible for making the resource available Journal Of Cellular And Molecular Medicine Subject The topic of the resource inflammation; insulin resistance; macrophages; microRNA/miR-467a-5p Creator An entity primarily responsible for making the resource Gajeton J; Krukovets I; Yendamuri R; Verbovetskiy D; Vasanji A; Sul L; Stenina-Adognravi O Description An account of the resource Obesity is associated with inflammation and insulin resistance (IR), but the regulation of insulin sensitivity (IS) and connections between IS and inflammation remain unclear. We investigated the role of miR-467a-5p, a miRNA induced by hyperglycaemia, in regulating inflammation and blood glucose handling. We previously demonstrated that miR-467a-5p is induced by hyperglycaemia and inhibits the production of thrombospondin-1 (TSP-1), a protein implicated in regulating inflammation. To investigate the role of miR-467 in blood glucose handling and tissue inflammation, WT C57BL/6 mice were fed chow or Western diet from 5 to 32 weeks of age and injected weekly with miR-467a-5p antagonist. Inhibiting miR-467a-5p resulted in 47% increase in macrophage infiltration and increased Il6 levels in adipose tissue, higher plasma insulin levels (98 ng/mL vs 63 ng/mL), and 17% decrease in glucose clearance without increase in weight or HDL/LDL. The antagonist effect was lost in mice on Western diet. Mice lacking TSP-1 lost some but not all of the miR-467 effects, suggesting Thbs1 (and other unknown transcripts) are targeted by miR-467 to regulate inflammation. miR-467a-5p provides a physiological feedback when blood glucose is elevated to avoid inflammation and increased blood glucose and insulin levels, which may prevent IR. Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.1111/jcmm.16224" target="_blank" rel="noreferrer noopener">10.1111/jcmm.16224</a> Format The file format, physical medium, or dimensions of the resource journalArticle Gajeton J Inflammation Insulin Resistance Journal of Cellular and Molecular Medicine journalArticle Krukovets I Macrophages March 2021 List microRNA/miR-467a-5p NEOMED College of Medicine Student NEOMED Student Publications Stenina-Adognravi O Sul L Vasanji A Verbovetskiy D Yendamuri R Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.1038/onc.2017.140" target="_blank" rel="noreferrer noopener">http://doi.org/10.1038/onc.2017.140</a> Pages 5189–5198 Issue 36 Volume 36 Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Thrombospondin-4 mediates TGF-beta-induced angiogenesis. Publisher An entity responsible for making the resource available Oncogene Date A point or period of time associated with an event in the lifecycle of the resource 2017 2017-09 Subject The topic of the resource Angiogenesis Inducing Agents/*metabolism; Animals; Cell Movement/drug effects; Cell Proliferation/drug effects; Cells; Chick Embryo; Cultured; Endothelium; Female; Gene Expression Regulation/drug effects; Humans; Inbred C57BL; Male; Mice; Muscle; Neovascularization; Pathologic/drug therapy/metabolism/*pathology; Signal Transduction/drug effects; Smooth; Thrombospondins/*physiology; Transforming Growth Factor beta/*pharmacology; Vascular/drug effects/metabolism/*pathology Creator An entity primarily responsible for making the resource Muppala S; Xiao R; Krukovets I; Verbovetsky D; Yendamuri R; Habib N; Raman P; Plow E; Stenina-Adognravi O Description An account of the resource TGF-beta is a multifunctional cytokine affecting many cell types and implicated in tissue remodeling processes. Due to its many functions and cell-specific effects, the consequences of TGF-beta signaling are process-and stage-dependent, and it is not uncommon that TGF-beta exerts distinct and sometimes opposing effects on a disease progression depending on the stage and on the pathological changes associated with the stage. The mechanisms underlying cell- and process-specific effects of TGF-beta are poorly understood. We are describing a novel pathway that mediates induction of angiogenesis in response to TGF-beta1. We found that in endothelial cells (EC) thrombospondin-4 (TSP-4), a secreted extracellular matrix (ECM) protein, is upregulated in response to TGF-beta1 and mediates the effects of TGF-beta1 on angiogenesis. Upregulation of TSP-4 does not require the synthesis of new protein, is not caused by decreased secretion of Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.1038/onc.2017.140" target="_blank" rel="noreferrer noopener">10.1038/onc.2017.140</a> Rights Information about rights held in and over the resource Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). 2017 Angiogenesis Inducing Agents/*metabolism Animals Cell Movement/drug effects Cell Proliferation/drug effects Cells Chick Embryo Cultured Department of Integrative Medical Sciences Endothelium Female Gene Expression Regulation/drug effects Habib N Humans Inbred C57BL Krukovets I Male Mice Muppala S Muscle NEOMED College of Medicine Neovascularization Oncogene Pathologic/drug therapy/metabolism/*pathology Plow E Raman P Signal Transduction/drug effects Smooth Stenina-Adognravi O Thrombospondins/*physiology Transforming Growth Factor beta/*pharmacology Vascular/drug effects/metabolism/*pathology Verbovetsky D Xiao R Yendamuri R