ArticleJournal of diabetes research2014
Altered expression profile of renal α(1D)-adrenergic receptor in diabetes and its modulation by PPAR agonists.
Article in Journal of diabetes research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 11 citations in OpenAlex.
- High-dose nitrate therapy recovers the expression of subtypes αBMC cardiovascular disorders · 2020Article
- Sympathetic regulation of NCC in norepinephrine-evoked salt-sensitive hypertension in Sprague-Dawley rats.American journal of physiology. Renal physiology · 2019Article
- Maternal separation diminishes α-adrenergic receptor density and function in renal vasculature from male Wistar-Kyoto rats.American journal of physiology. Renal physiology · 2017Article
- ISN Forefronts Symposium 2015: Nuclear Receptors and Diabetic Nephropathy.Kidney international reports · 2016Article
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Authors and funding
6 authors at 1 institution in 1 country.
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Abstract
Alpha(1D)-adrenergic receptor (α(1D)-AR) plays important roles in regulating physiological and pathological responses mediated by catecholamines, particularly in the cardiovascular and urinary systems. The present study was designed to investigate the expression profile of α(1D)-AR in the diabetic kidneys and its modulation by activation of peroxisome proliferator-activated receptors (PPARs). 12-week-old Zucker lean (ZL) and Zucker diabetic fatty (ZD) rats were treated with fenofibrate or rosiglitazone for 8-10 weeks. Gene microarray, real-time PCR, and confocal immunofluorescence microscopy were performed to assess mRNA and protein expression of α(1D)-AR in rat kidney tissue. Using microarray, we found that α(1D)-AR gene was dramatically upregulated in 22-week-old ZD rats compared to ZL controls. Quantitative PCR analysis verified a 16-fold increase in α(1D)-AR mRNA in renal cortex from ZD animals compared to normal controls. Chronic treatment with fenofibrate or rosiglitazone reduced renal cortical α(1D)-AR gene. Immunofluorescence staining confirmed that α(1D)-AR protein was induced in the glomeruli and tubules of diabetic rats. Moreover, dual immunostaining for α(1D)-AR and kidney injury molecule-1 indicated that α(1D)-AR was expressed in dedifferentiated proximal tubules of diabetic Zucker rats. Taken together, our results show that α(1D)-AR expression is upregulated in the diabetic kidneys. PPAR activation suppressed renal expression of α(1D)-AR in diabetic nephropathy.
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