Data on nephroprotective effect of all-trans retinoic acid in early diabetic nephropathy

Abstract

Data showed in this report are related to the research article entitled “All-trans retinoic acid ameliorates inflammatory response mediated by TLR4/NF-кB during the initiation of diabetic nephropathy” by Sierra-Mondragon et al. (2018) [1]. Diabetic nephropathy (DN) has become the main cause of renal failure. Inflammatory molecules such as cytokines, chemokines and growth factors play a key role in DN-induced renal injury Pichler et al. (2016) [2]. Results illustrate the effect of all-trans retinoic acid (ATRA), an active metabolite of vitamin A, on the renal alterations related to diabetes, among them glomerular and tubular dysfunction, and its effect on renal inflammation in different nephron segments: glomeruli, proximal and distal tubules in an initial stage of DN. Data were obtained by physical-biochemical measurements and Western blot assays performed on isolated glomeruli, proximal and distal tubules from rat kidneys.

All-Trans Retinoic Acid Attenuates Fibrotic Processes by Downregulating TGF-β1/Smad3 in Early Diabetic Nephropathy

“…The cellular action of ATRA is mediated through RAR-α, β and γ, these receptors directly activate gene transcription [12]. We previously demonstrated that ATRA is a potent nephroprotective agent; its administration exerts antioxidant effects [17] and anti-inflammatory effects during initiation of DN [18,19]. These studies suggested that changes in ATRA signaling via the extracellular/intracellular ATRA level or the expression/activation of RAR-α, closely correlate with the development of diabetes.…”

“…Inflammation plays a critical role in the initiation and progression of renal fibrosis [1,2,3]. We have recently demonstrated that an inflammatory process is induced in initial stages of DN with increased cytokines, chemokines, cell adhesion molecules, and growth factors in glomeruli and proximal tubules [18,19]. However, further understanding of the mechanisms behind renal fibrogenesis is essential to develop therapies to prevent or reverse this process and slow its progression in DN to end-stage renal disease.…”

“…We previously reported that ATRA is a nephroprotective agent in a model of acute renal failure [16], and its administration exerts antioxidant effects that prevented the loss of renal tight junction proteins, claudins 5 and 2 in DN [17]. We also demonstrated the anti-inflammatory effect ATRA by suppressing the toll-like receptor 4 (TLR4) and the nuclear factor-кB (NF-кB) signaling in glomeruli and proximal tubules in a model of diabetes [18,19]. It has been reported that some ATRA signaling components are involved in the evolution of diabetic pathology.…”