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dc.contributor.authorKhamaneh, AM
dc.contributor.authorAlipour, MR
dc.contributor.authorHesari, FS
dc.contributor.authorSoufi, FG
dc.date.accessioned2018-08-26T07:43:10Z
dc.date.available2018-08-26T07:43:10Z
dc.date.issued2015
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/47952
dc.description.abstractThe current study was designed to explore the potential involvement of miR-155 in the pathogenesis of diabetes complications. Male rats were divided into control and diabetic groups (n = 6). Type 2 diabetes was induced by a single-dose injection of nicotinamide (110 mg/kg; intraperitoneal (i.p.)), 15 min before injection of streptozotocin (STZ; 50 mg/kg; i.p.) in 12-h fasted rats. Two months after induction of diabetes, the rats were sacrificed for subsequent measurements. The nuclear factor kappa B (NF-kappa B) activity was higher in diabetic peripheral blood mononuclear cells (PBMCs), aorta, heart, kidney, liver, and sciatic nerve, than the control counterparts. Also, apoptosis rate was increased in these tissues, except the aorta. NF-kappa B messenger RNA (mRNA) expression level was higher in the kidney, heart, PBMCs, and sciatic nerve of diabetic rats than their control counterparts. Except the liver, the miR-155 expression level was significantly decreased in diabetic kidney, heart, aorta, PBMCs, and sciatic nerve versus the controls. Moreover, the expression of miR-155 was negatively correlated with NF-kappa B activity and apoptosis rate. These results suggest that changes in the expression of miR-155 may participate in the pathogenesis of diabetes-related complications, but causal relationship between miR-155 dysregulation and diabetic complications is unknown.
dc.language.isoEnglish
dc.relation.ispartofJOURNAL OF PHYSIOLOGY AND BIOCHEMISTRY
dc.subjectDiabetes
dc.subjectMicroRNAs
dc.subjectNF-kappa B
dc.subjectInflammation
dc.subjectProinflammatory cytokines
dc.titleA signature of microRNA-155 in the pathogenesis of diabetic complications
dc.typeArticle
dc.citation.volume71
dc.citation.issue2
dc.citation.spage301
dc.citation.epage309
dc.citation.indexWeb of science
dc.identifier.DOIhttps://doi.org/10.1007/s13105-015-0413-0


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