ArticleDiabetologia2014
Maternal diabetes modulates kidney formation in murine progeny: the role of hedgehog interacting protein (HHIP).
Article in Diabetologia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 16 citations in OpenAlex.
- Epigenetic regulation of nephrogenesis: from Waddington's landscape to adult disease.American journal of physiology. Renal physiology · 2026Review
- Effects of Environmental Conditions on Nephron Number: Modeling Maternal Disease and Epigenetic Regulation in Renal Development.International journal of molecular sciences · 2021Article
- In utero exposure to maternal diabetes impairs nephron progenitor differentiation.American journal of physiology. Renal physiology · 2019Article
- Hedgehog Interacting Protein Promotes Fibrosis and Apoptosis in Glomerular Endothelial Cells in Murine Diabetes.Scientific reports · 2018Article
- Sonic hedgehog signaling in kidney fibrosis: a master communicator.Science China. Life sciences · 2016Review
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
aims/hypothesisWe hypothesised that maternal diabetes impairs kidney formation in offspring via augmented expression of hedgehog interacting protein (HHIP). Our gene-array results were performed in neonatal kidneys from our murine model of maternal diabetes and indicated that Hhip expression was significantly modulated by maternal diabetes.
methodsWe systematically examined the functional role of HHIP in kidney formation in our murine maternal diabetes model and elucidated the potential mechanisms related to dysnephrogenesis in vitro.
resultsThe kidneys of the offspring of diabetic dams, compared with those of the offspring of control non-diabetic dams, showed retardation of development--small kidneys and less ureteric bud (UB) branching morphogenesis. Augmented HHIP expression was observed in the offspring of diabetic dams, initially localised to differentiated metanephric mesenchyme and UB epithelium and subsequently in maturing glomerular endothelial and tubulointerstitial cells. The heightened HHIP targeting TGF-β1 signalling was associated with dysmorphogenesis. In vitro, HHIP overexpression decreased sonic hedgehog and paired box gene 2 proteins (SHH and PAX2, respectively) and increased transcriptional nuclear factor-kappa B (NFκB, p50/p65), phosphorylation of p53, and TGF-β1 expression. In contrast, overexpression of PAX2 inhibited HHIP and NFκB and activated SHH, N-myc and p27(Kip1) expression. Moreover, high glucose stimulated HHIP expression, and then targeted TGF-β1 signalling. Thus, PAX2, via a negative autocrine feedback mechanism, attenuated the stimulatory effect of high glucose on HHIP expression. CONCLUSIONS/
interpretationMaternal diabetes modulates kidney formation in young progeny mediated, at least in part, via augmented HHIP expression.
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