Cabin1 is upregulated during renal tubular epithelial cells injury in 5/6 nephrectomized rats
10.3969/j.issn.1006-5725.2017.17.008
- VernacularTitle:钙调磷酸酶结合蛋白1在5/6肾切除大鼠肾小管上皮细胞损伤时高表达
- Author:
Huiyuan LI
1
;
Peilan ZHOU
;
Kaiyuan HU
;
Dijing WANG
;
Zebin WANG
;
Jianbo LIANG
;
Yueqiang WEN
Author Information
1. 广州医科大学附属第二医院
- Keywords:
renal tubular epithelial cells;
mitochondrial injury;
cabin1
- From:
The Journal of Practical Medicine
2017;33(17):2838-2842
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the role of Calcineurin binding protein 1(Cabin1)in renal tubular epithelial cells(RTECs)injury. Methods The male Sprague-Dawley rats were randomly divided into Sham-oper-ated and 5/6 nephrectomized group. Nephrectomized rats were further divided into two groups ,which were 4 and 8 weeks after operation,including 6 rats in each group. Rats were sacrificed at 4 or 8 weeks after nephrectomy,then control or remnant kidneys were harvested. 2μm sections of kidney tissues were collected and stained with Masson's trichrome and were graded for tubulointerstitial lesion score (TILS). RTECs mitochondrial morphology changes were detected by electron microscope. Western blot was applied to detect Cabin1 protein level in the renal tissue. Results At 8 weeks after the operation,plenty of RTECs fell off from the basement membrane,accompanied with interstitial fibrosis and the infiltration of inflammatory cells. Moreover ,TILS were significantly increased in rats at 8 weeks after operation while compared to sham-operated rats(7.16 ± 0.52 vs. 0.00 ± 0.00,P<0.05). RTECs mi-tochondria begun to swell at 4 weeks after 5/6 nephrectomy,while the disruption of cristae could be found in rats at 8 weeks. Cabin1 protein expression apparently increased in the remnant kidney. Cabin1 protein obviously increased in rats at 8 weeks after the surgery compared to sham-operated rats(0.97 ± 0.09 vs. 0.22 ± 0.07,P<0.05)and rats at 4 weeks after nephrectomy(0.97 ± 0.09 vs. 0.45 ± 0.03,P<0.05). Conclusions Cabin1 is overexpressed during RTECs injury in 5/6 nephrectomized rats. It can be a crucial factor regulating the damage of RTECs.
