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Abstract: SA-PO508

Activation of Vitamin D Receptor Attenuates High Glucose-Induced Cellular Injury Partially Dependent on CYP2J5 in Murine Renal Tubule Epithelial Cell

Session Information

Category: Diabetic Kidney Disease

  • 601 Diabetic Kidney Disease: Basic


  • Liu, Yan, The Third Xiangya Hospital of Central South University, Changsha, HUNAN, China
  • Zhang, Hao, The Third Xiangya Hospital of Central South University, Changsha, HUNAN, China

Vitamin D receptor (VDR), have renoprotection effect against diabetic nephropathy (DN). Paricalcitol is a VDR activator. Epoxyeicosatrienoic acids (EETs) are cytochrome P450 (CYP) protecting against diabetes and DN. Our objective is to investigate whether activation of vitamin D receptor protect nephropathy partially dependent on CYP2J5 in murine renal tubule epithelial cell.


Adult male wile type (WT) and Vdr-/- mice were used,.STZ-induced diabetic nephropathy model was established and paricalcitol was injected. 12 weeks after the STZ injection, mice were sacrificed. Kidneys were collected for histology and immunohistochemistry staining. Murine kidney proximal tubule epithelial cell line (BU.MPT) was used in this study, incubated with high glucose and paricalcitol. supernatent, mRNA and protein were collected.Real-time PCR and Western blot were used to detect the RNA and protein levels.


1.STZ, VDR-/-,VDR-/-+STZ mice tubulointerstitial injury were more severe than WT, the expression of CYP2J5 and VDR decreased.But STZ mice treated with paricalcitol had attenuated tubulointerstitial injury and increased CYP2J5 and VDR than STZ
2.Activation of VDR attenuated high glucose-induced cellular injury in renal tubular epithelial cells partially though up-regulating CYP2J5 expression. High glucose treatment strongly reduced the CYP2J5 expression and the synthesis of 14,15-EET in murine renal tubular epithelial cells. Supplement of 14,15-EET significantly reduced the lactate dehydrogenase (LDH) release induced by high glucose in renal tubular epithelial cells. Treatment with an activator of VDR, paricalcitol, restored the expression of CYP2J5 reduced by high glucose treatment in renal tubular epithelial cells. And we found that paricalcitol attenuated cellular injury induced by high glucose partially dependent on the up-regulation of CYP2J5 in renal tubular epithelial cells
3.WT and a mutant-Cyp2j5 luciferase reporter plasmid were constructed. We found that paricalcitol treatment (0.1 mM) significantly increased relative luciferase activity in the WT plasmid, compared with the pGL3 basic plasmid


Activation of VDR attenuates high glucose-induced cellular injury partially dependent on CYP2J5 in murine renal tubule epithelial cells and paricalcitol may represent a potential therapy for DN.