Author(s): Zhang Yan, Ma Rui-xia, Li Ming-hui, Xue Ting, Chi Cheng-mei
Download Full PDF
Read Complete Article
Volume 8 - Feb 2019
Objective: Diabetic kidney disease (DKD) is a severe kidney disease characterized by podocyte apoptosis, injury, and accumulation of extracellular matrices that ultimately lead to end-stage renal disease. Vitamin D3 was reported to provide renal protection in DKD through the Vitamin D receptor (VDR), however there was limited data on whether it has a protective effect on podocytes of DKD induced by high glucose. Methods: The experimental subjects were conditionally immortalized mouse podocytes (MPC-5), which were divided into 4 groups: NG (normal glucose) group, HM (Hypertonic) group, HG (high glucose) group, VD3 (HG +1,25-dihydroxyvitamin D3 (1,25-D3)) group. Western-blot analysis was performed to detect the expression of Bcl-2, Bax and Caspase-3 in podocytes. The mRNA Expression of Bcl-2, Bax and Caspase-3 in the three groups were detected by RT-PCR method. Results: Compared with the NG group, the expression of apoptosis proteins Caspase-3 and Bax in the podocytes of HG group increased, and the expression of Bcl-2 decreased. Pretreatment with vitamin D3 attenuated these abnormalities in podocytes in HG group. Conclusion: Vitamin D can alleviate the apoptosis of podocytes induced by high glucose in vitro.
Diabetic Nephropathy, Vitamin D3, Podocyte, Apoptosis
- 1.Mogensen C E. Microalbuminuria and hypertension with focus on type 1 and type 2 diabetes.[J]. Journal of Internal Medicine, 2010, 254(1):45-66.
- Jim B, Ghanta M, Qipo A, et al. Dysregulated nephrin in diabetic nephropathy of type 2 diabetes: a cross sectional study[J]. Plos One, 2012, 7(5):e36041.
- Yao X M, Liu Y J, Wang Y M, et al. Astragaloside IV prevents high glucose-induced podocyte apoptosis via downregulation of TRPC6[J]. Molecular Medicine Reports, 2016, 13(6):5149.
- Yang H, Zhao B, Liao C, et al. High glucose-induced apoptosis in cultured podocytes involves TRPC6-dependent calcium entry via the RhoA/ROCK pathway[J]. Biochemical & Biophysical Research Communications, 2013, 434(2):394-400.
- Gui D, Guo Y, Wang F, et al. Astragaloside IV, a novel antioxidant, prevents glucose-induced podocyte apoptosis in vitro and in vivo[J]. Plos One, 2012, 7(6):e39824.
- Piwkowska A, Rogacka D, Audzeyenka I, et al. High glucose concentration affects the oxidant‐antioxidant balance in cultured mouse podocytes[J]. Journal of Cellular Biochemistry, 2011, 112(6):1661-1672.
- Ji Z Z, Xu Y C. Melatonin protects podocytes from angiotensin II-induced injury in an in vitro diabetic nephropathy model[J]. Molecular Medicine Reports, 2016, 14(1):920.
- Dusso A S, Brown A J, Slatopolsky E. Vitamin D.[J]. ajp-renal physiology, 2005, 289(1):F8-28.
- Cheng J, Zhang W, Zhang X, et al. Efficacy and safety of paricalcitol therapy for chronic kidney disease: a meta-analysis.[J]. Clinical Journal of the American Society of Nephrology Cjasn, 2012, 7(3):391.
- Agarwal R, Acharya M, Tian J, et al. Antiproteinuric effect of oral paricalcitol in chronic kidney disease[J]. Kidney International, 2005, 68(6):2823-2828.
- Xiao H, Shi W, Liu S, et al. 1,25-Dihydroxyvitamin D3 Prevents Puromycin Aminonucleoside-Induced Apoptosis of Glomerular Podocytes by Activating the Phosphatidylinositol 3-Kinase/Akt-Signaling Pathway[J]. American Journal of Nephrology, 2009, 30(1):34-43.
- Liu B C, Song X, Lu X Y, et al. High glucose induces podocyte apoptosis by stimulating TRPC6 via elevation of reactive oxygen species.[J]. BBA - Molecular Cell Research, 2013, 1833(6):1434-1442.
- Wang Y, Li H, Song SP. Î²-Arrestin 1/2 Aggravates Podocyte Apoptosis of Diabetic Nephropathy via Wnt/Î²-Catenin Pathway[J]. Med Sci Monit, 2018, 24:1724-1732.
- Ilatovskaya D V, Levchenko V, Lowing A, et al. Podocyte injury in diabetic nephropathy: implications of angiotensin II – dependent activation of TRPC channels[J]. Scientific Reports, 2015, 5:17637.
- Susztak K, Raff A C, Schiffer M, et al. Glucose-induced reactive oxygen species cause apoptosis of podocytes and podocyte depletion at the onset of diabetic nephropathy.[J]. Diabetes, 2006, 55(1):225.
- Lee S H, Moon S J, Paeng J, et al. Podocyte hypertrophy precedes apoptosis under experimental diabetic conditions[J]. Apoptosis, 2015, 20(8):1056-1071.
- Wang Y, Zhou J, Minto A W, et al. Altered vitamin D metabolism in type II diabetic mouse glomeruli may provide protection from diabetic nephropathy.[J]. Kidney International, 2006, 70(5):882-891.
- Zhang Z, Sun L, Wang Y, et al. Renoprotective role of the vitamin D receptor in diabetic nephropathy[J]. Kidney International, 2008, 73(2):163-171.
- Deng X, Cheng J, Shen M. Vitamin D improves diabetic nephropathy in rats by inhibiting renin and relieving oxidative stress[J]. Journal of Endocrinological Investigation, 2016, 39(6):657-666.
- Hamden K, Carreau S, Jamoussi K, et al. 1Alpha,25 dihydroxyvitamin D3: therapeutic and preventive effects against oxidative stress, hepatic, pancreatic and renal injury in alloxan-induced diabetes in rats.[J]. Journal of Nutritional Science & Vitaminology, 2009, 55(3):215-222.
- Deb D K, Sun T, Wong K E, et al. Combined vitamin D analog and AT1 receptor antagonist synergistically block the development of kidney disease in a model of type 2 diabetes[J]. Kidney International, 2010, 77(11):1000.
Cite this Article:
International Journal of Sciences is Open Access Journal.
This article is licensed under a Creative Commons Attribution 4.0 International (CC BY 4.0) License.
Author(s) retain the copyrights of this article, though, publication rights are with Alkhaer Publications.