Iranian journal of kidney diseases · 2017
Upregulation of Cabin1 During Injury to Renal Tubular Epithelial Cells in Rats.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Wen Yueqiang, Li Huiyuan, Zhou Peilan, Liu Lingling, Wang Zebin, Liang Jianbo
Аннотация
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.
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.