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

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.


a b s t r a c t
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.
&  Table   Subject area  Biology  More specific subject area Immunology and inflammation  Type of data  Figures and Tables  How data was acquired Renal function parameters were detected by a spectrophotometric method (Spectrophotometer Infinite M200, Tecan; Männedorf Suiza) and chemiluminescent Western blot were detected in an EC3 Imaging System (UVP BioImaging Systems, Cambridge, UK). Protein band densities were quantified by transmittance densitometry.

Data format
Processed data and raw data Experimental factors To analyze protective effects of ATRA, 4 experimental groups were evaluated; Control (CTL), Diabetic (DBT), Diabetic rats treated with ATRA (DBT þATRA) and control rats treated with ATRA (ATRA).

Experimental features
Western blot analyses were performed on isolated glomeruli, proximal and distal tubules of rat kidneys from the four experimental groups.

Data source location
Mexico City, México Data accessibility Data are available in this paper

Value of the data
The data show the nephroprotective effect of ATRA, leading to preservation of renal function by suppressing inflammation, in early stages of streptozotocin-induced diabetes in rats.
These data are useful as there are few reports on the anti-inflammatory protective effects of ATRA on early DN. The observed beneficial effects might represent a therapeutic alternative to reduce the progression of DN, which is one the pathologies leading to end stage renal disease worldwide.
In addition, these data may be relevant for (i) other researchers using ATRA in their studies since at low doses we used (1 mg/kg), it did not show untoward effects and (ii) we provide experimental protocols for isolation of different nephron segments: glomeruli, proximal and distal tubules by Percoll gradients and sieving, without microdissection. The data show the nephroprotective effect of ATRA leading to preservation of renal function by suppressing inflammation in early stages of streptozotocin-induced diabetes in rats.

Data
Inflammation play central role in the progression of DN that lead to renal failure. Our previous study demonstrated that early diabetic condition has a relationship with inflammatory response mediated by TLR4/NF-кB signaling in glomeruli and proximal tubules, respectively, in vivo [1]; and, these findings are consistent with previous study which reported that Inflammatory molecules in DNinduced renal injury [2]. The retinoid system plays a key role in maintaining the normal renal structure and attenuates the development of renal pathological changes [3]. The dataset presented in this paper provide information about nephroprotective role of ATRA (Figs. 1-3) and its effect on inflammatory molecules induced by diabetes in the kidney (Fig. 4). We analyzed the effects of its administration in isolated nephron segments: glomeruli, proximal and distal tubules to define their intrarenal selectivity in an early stage of experimental DN.

Experimental design
Wistar rats were obtained from the production and experimentation unit of laboratory animals (UPEAL) of CINVESTAV-IPN. All animal experiments were performed in accordance with the Mexican Official Norm NOM-062-ZOO-1999, and approved by the UPEAL guidelines (protocol # 0178-16). The  rats were divided into four groups of 10-12 animals in each group: a) Control group (CTL), normal rats received a single injection of citrate buffer; pH 4.5 (vehicle); b) Diabetic group (DBT), treated with a single tail-vein injection of streptozotocin (STZ) 60 mg/kg bw, in citrate buffer; pH 4.5); c) Diabetic group treated with ATRA (DBT þATRA), rats received ATRA (1 mg/kg) once a day intragastrically, until the end of the study (from days 3 to 21 after STZ injection), and d) ATRA group (ATRA), normal control rats received ATRA (1 mg/kg) given orally once a day from days 3 to 21 after single injection of citrate buffer. Rats were sacrificed 21 days after STZ or vehicle administration.

Biochemical and physical studies
Blood glucose and body weight were monitored at days 3, 7, 14 and 21 of the study. The blood glucose was determined by using a glucometer (One Touch s Ultra blood glucose meter). At day 21, blood was collected by cardiac puncture under anesthesia with sodium pentobarbital (30 mg/kg, i.p.) and serum was separated.

Renal function markers
At the end of the experimental period of 3 weeks, rats were housed in metabolic cages for 24 h to collect urine samples. Glomerular filtration rate (GFR) was evaluated through the creatinine clearance. It was calculated with the standard formula [4], and urinary and serum creatinine, were measured by modified Jaffé method. Proteinuria/creatininuria ratio was obtained by dividing urine protein concentration by urine creatinine concentration. Total urinary protein was determined by Lowry method (Bio-Rad Protein Assay Kit, CA, USA). Proximal tubular function was assessed through the urinary and serum sodium concentrations (measured by atomic absorption spectrophotometry) and fractional excretion of sodium (FeNa) was calculated with the following equations: FeNa% ¼ Sodium clearance/creatinine clearance x100.

Isolation of glomeruli, proximal and distal tubules
Glomeruli were isolated by gradual sieving techniques and suspensions of enriched populations of proximal and distal tubules were isolated from renal cortex slices by Percoll density-gradient centrifugation, as previously described [5].