American journal of kidney diseases : the official journal of the National Kidney Foundation · 2005
Expression of gremlin, a bone morphogenetic protein antagonist, in human diabetic nephropathy.
Сравнительное исследованиеСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Dolan Vincent, Murphy Madeline, Sadlier Denise, Lappin David, Doran Peter, Godson Catherine, Martin Finian, O'Meara Yvonne, Schmid Holger, Henger Anna, Kretzler Matthias, Droguett Alejandra, Mezzano Sergio, Brady Hugh R
Аннотация
BACKGROUND: We report the induction of gremlin, a bone morphogenetic protein antagonist, in cultured human mesangial cells exposed to high glucose and transforming growth factor beta (TGF-beta) levels in vitro and kidneys from diabetic rats in vivo.
METHODS: Gremlin expression was assessed in human diabetic nephropathy by means of in situ hybridization, immunohistochemistry, and real-time polymerase chain reaction and correlated with clinical and pathological indices of disease.
RESULTS: Gremlin was not expressed in normal human adult kidneys. Conversely, abundant gremlin expression was observed in human diabetic nephropathy. Although some gremlin expression was observed in occasional glomeruli, gremlin expression was most prominent in areas of tubulointerstitial fibrosis, where it colocalized with TGF-beta expression. Gremlin messenger RNA levels correlated directly with renal dysfunction, determined by means of serum creatinine level, but not with proteinuria level. There was a strong correlation between gremlin expression and tubulointerstitial fibrosis score.
CONCLUSION: In aggregate, these results indicate that the developmental gene gremlin reemerges in the context of tubulointerstitial fibrosis in diabetic nephropathy and suggests a role for TFG-beta as an inducer of gremlin expression in this context.
METHODS: Gremlin expression was assessed in human diabetic nephropathy by means of in situ hybridization, immunohistochemistry, and real-time polymerase chain reaction and correlated with clinical and pathological indices of disease.
RESULTS: Gremlin was not expressed in normal human adult kidneys. Conversely, abundant gremlin expression was observed in human diabetic nephropathy. Although some gremlin expression was observed in occasional glomeruli, gremlin expression was most prominent in areas of tubulointerstitial fibrosis, where it colocalized with TGF-beta expression. Gremlin messenger RNA levels correlated directly with renal dysfunction, determined by means of serum creatinine level, but not with proteinuria level. There was a strong correlation between gremlin expression and tubulointerstitial fibrosis score.
CONCLUSION: In aggregate, these results indicate that the developmental gene gremlin reemerges in the context of tubulointerstitial fibrosis in diabetic nephropathy and suggests a role for TFG-beta as an inducer of gremlin expression in this context.
Предметные рубрики MeSH
Bone Morphogenetic ProteinsCells, CulturedCytokinesDiabetic NephropathiesFibrosisGene Expression RegulationGlomerular MesangiumGlucoseHumansIn Situ HybridizationIntercellular Signaling Peptides and ProteinsKidney NeoplasmsNephritis, InterstitialProteinsRNA, MessengerReverse Transcriptase Polymerase Chain ReactionTransforming Growth Factor betaTransforming Growth Factor beta1