Inhibition of Homeobox D10 Alleviates Acute Kidney Injury by Upregulating PI3K/AKT Signaling Proteins

Author:

Liu Siqi1,Sun Huixin2,Guo Jingjie2,Ma Linlin3ORCID

Affiliation:

1. Department of Clinical Laboratory, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang 150081, China

2. Institute of Cancer Prevention and Treatment, Harbin Medical University, Harbin, Heilongjiang 150081, China

3. Department of Nephrology, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150086, China

Abstract

Purpose. To observe the protective effect of homeobox D10 (HOXD10) on acute kidney injury (AKI) by regulating PI3K/AKT signaling pathway is the purpose of this study.Methods. 30 rats were randomly divided into three groups: blank control group, model group, and HOXD10 interference group. The kidney function indexes, HOXD10 protein expression, histopathological features, tubulointerstitial injury, and PI3K and AKT protein expression levels of the three groups were analyzed. Results. Compared with the blank control group, the kidney weight, BUN and SCr in model group increased significantly, and TIL score was higher ( P > 0.05 ). The expression of HOXD10 in model group and HOXD10 interference group were higher than blank control group, and the expression of HOXD10 in HOXD10 interference group was lower than model group ( P < 0.05 ). After we administered HOXD10 blocker to AKI rats, pathological sections by HE staining showed that the kidney tissue damage was significantly reduced compared with the model group, and the expression levels of BUN and SCr in kidney tissue decreased, and the TIL score decreased. The expression of p-PI3K and p-AKT decreased after kidney injury. Compared with the model group, the phosphorylation levels of PI3K and AKT in HOXD10 interference group were significantly increased ( P < 0.05 ). Conclusion. Downregulation of HOXD10 can play a protective role on AKI by activating PI3K/AKT signaling pathway, which can reduce tubulointerstitial injury and improve kidney function.

Funder

Foundation of Heilongjiang Academy of Medical Sciences

Publisher

Hindawi Limited

Subject

Virology,Immunology,Microbiology

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