Author/Authors :
Wen, Yueqiang Department of Nephrology - The Second Affiliated Hospital - Guangzhou Medical University, Guangzhou, China , Li, Huiyuan Department of Nephrology - The Second Affiliated Hospital - Guangzhou Medical University, Guangzhou, China , Zhou, Peilan Department of Nephrology - The Second Affiliated Hospital - Guangzhou Medical University, Guangzhou, China , Liu, Lingling Department of General Medicine - The Third Affiliated Hospital - Sun Yat-sen University, Guangzhou, China , Wang, Zebin Department of Nephrology - The Second Affiliated Hospital - Guangzhou Medical University, Guangzhou, China , Liang, Jianbo Department of Nephrology - The Second Affiliated Hospital - Guangzhou Medical University, Guangzhou, China
Abstract :
Introduction. Calcineurin-binding protein 1 (Cabin1) interacts with
calcineurin and p53, but its function in renal tubular epithelial cell
(RTEC) is unclear. We established 5/6 nephrectomized rats and
angiotensin II-induced injury to the RTECs in vitro, to observe the
expression of Cabin1 during RTEC injury.
Materials and Methods. Sprague-Dawley rats were sacrificed
at 4 and 8 weeks after 5/6 nephrectomy. Renal pathology and
mitochondrial damage were detected by light and electrical
microscope. The distribution of E-cadherin and α-smad were
detected by indirect immunofluorescence staining. Cabin1 protein
expression was detected by Western blot.
Results. Obvious tubulointerstitial fibrosis was found in the
nephrectomized rats at 8 weeks after 5/6 nephrectomy, accompanied
by the increasing levels of creatinine, as well as the disruption of
E-cadherin and overexpression of α-smad in RTECs. Moreover,
the mitochondria became swollen and mitochondrial cristae were
disrupted and poorly defined in the RTECs. Compared to the
sham-operated rats, Cabin1 protein expression was significantly
increased at 8 weeks after 5/6 nephrectomy, while angiotensin
II-induced Cabin1 protein expression significantly increased 48
hours after stimulation in normal rat kidney epithelial cells.
Conclusions. Injury to the RTEC and Cabin1 protein overexpression
occurred in a time-dependent manner both in vitro and in vivo.
Cabin1 may become a potential molecular target in RTEC injury.
Keywords :
Cabin1 , renal tubular epithelial cell , mitochondrial dysfunction , angiotensin II , p53