caa a22 4500 606234195 CHVBK 20210128101236.0 cr unu---uuuuu 210128e20150101xx s 000 0 eng 10.1007/s11010-014-2242-9 doi (NATIONALLICENCE)springer-10.1007/s11010-014-2242-9 The novel role of TRPC6 in vitamin D ameliorating podocyte injury in STZ-induced diabetic rats [Elektronische Daten] [Xiaoliang Zhang, Zhixia Song, Yinfeng Guo, Min Zhou] Podocyte injury plays a critical role in the development and progression of diabetic nephropathy (DN). Over expression of TRPC6 on the podocytes has been revealed to cause podocyte injury in non-diabetic states. Besides, the emerging evidence from clinic revealed that vitamin D could reduce albuminuria and improve renal function, which was associated with podocyte protection. Our study aimed to investigate whether calcitriol ameliorating podocyte impairment is associated with regulation of the expression of TRPC6 in STZ-induced rats. Sprague-Dawley rats were randomly divided into three groups: normal control, DN, and DN treated with calcitriol (DN+VD); VD rats were treated with 0.1μg/kg/d calcitriol by gavage. DN model rats were established by intraperitoneal injections of streptozocin. The rats were sacrificed after 18weeks treatment. DN rats exhibited increased proteinuria accompanied by elevated TRPC6 expression. Treatment with calcitriol not only reduced proteinuria, but also normalized TRPC6 expression. Meanwhile, in DN rats, the expression of podocyte specific markers including nephrin and podocin was significantly decreased, accompanied by increased desmin, a marker of podocyte injury. Treatment with calcitriol reversed above changes. In addition, vitamin D receptor (VDR) was significantly decreased, whereas this reduction was attenuated by the calcitriol treatment. Moreover, TRPC6 was positively correlated with both 24h urinary protein and desmin. In contrast, TRPC6 was negatively correlated with both VDR and nephrin expression in podocytes. Calcitriol can ameliorate podocyte injury, which is contributed by the inhibition of enhanced TRPC6 expression in the early stages of DN rats. Springer Science+Business Media New York, 2014 Calcitriol nationallicence Vitamin D receptor nationallicence TRPC6 nationallicence Podocyte nationallicence Diabetic nephropathy nationallicence Zhang Xiaoliang Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, 210009, Nanjing, Jiangsu, China aut Song Zhixia Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, 210009, Nanjing, Jiangsu, China aut Guo Yinfeng Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, 210009, Nanjing, Jiangsu, China aut Zhou Min Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, 210009, Nanjing, Jiangsu, China aut Molecular and Cellular Biochemistry Springer US; http://www.springer-ny.com 399/1-2(2015-01-01), 155-165 0300-8177 399:1-2<155 2015 399 11010 https://doi.org/10.1007/s11010-014-2242-9 text/html Onlinezugriff via DOI BK010053 XK010053 XK010000 Metadata rights reserved Springer special CC-BY-NC licence nationallicence 1 research-article jats NATIONALLICENCE NATIONALLICENCE NL-springer NATIONALLICENCE 856 40 https://doi.org/10.1007/s11010-014-2242-9 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Zhang Xiaoliang Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, 210009, Nanjing, Jiangsu, China aut NATIONALLICENCE 700 1- Song Zhixia Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, 210009, Nanjing, Jiangsu, China aut NATIONALLICENCE 700 1- Guo Yinfeng Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, 210009, Nanjing, Jiangsu, China aut NATIONALLICENCE 700 1- Zhou Min Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, 210009, Nanjing, Jiangsu, China aut NATIONALLICENCE 773 0- Molecular and Cellular Biochemistry Springer US; http://www.springer-ny.com 399/1-2(2015-01-01), 155-165 0300-8177 399:1-2<155 2015 399 11010