Int J Biol Sci 2022; 18(15):5897-5912. doi:10.7150/ijbs.74431 This issue Cite

Research Paper

Anp32e promotes renal interstitial fibrosis by upregulating the expression of fibrosis-related proteins

Ju Wei1,2*, Yi Shan1,2*, Zheng Xiao1,2, Lu Wen1,2, Yilin Tao1,2, Xi Fang1,2, Hanwen Luo1,2, Chengyuan Tang1,2, Ying Li1,2✉

1. Department of Nephrology, The Second Xiangya Hospital of Central South University, Changsha, 410011, Hunan, China.
2. Hunan Key Laboratory of Kidney Disease and Blood Purification, Changsha, 410011, Hunan, China.
* These authors have contributed equally to this work

Citation:
Wei J, Shan Y, Xiao Z, Wen L, Tao Y, Fang X, Luo H, Tang C, Li Y. Anp32e promotes renal interstitial fibrosis by upregulating the expression of fibrosis-related proteins. Int J Biol Sci 2022; 18(15):5897-5912. doi:10.7150/ijbs.74431. https://www.ijbs.com/v18p5897.htm
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Abstract

Graphic abstract

Acidic nuclear phosphoprotein 32 family member e (Anp32e) has been reported to contribute to early mammalian development and cancer metastasis. However, the pathophysiological role of Anp32e in renal interstitial fibrosis (RIF) is poorly understood. Here, we demonstrated that Anp32e was highly expressed in the region of RIF in patients with IgA nephropathy, unilateral ureteral obstruction (UUO) mouse kidneys, and Boston University mouse proximal tubular (BUMPT) cells when treated with TGF-β1; this upregulation was positively correlated with the total fibrotic area of the kidneys. The overexpression of Anp32e enhanced the TGF-β1-induced production of fibrosis-related proteins (fibronectin (Fn) and collagen type I (Col-I)) in BUMPT cells whereas the knockdown of Anp32e suppressed the deposition of these fibrosis-related proteins in UUO mice and TGF-β1-stimulated BUMPT cells. In particular, Anp32e overexpression alone induced the deposition of Fn and Col-I in both mouse kidneys and BUMPT cells without TGF-β1 stimulation. Furthermore, we revealed that the overexpression of Anp32e induced the expression of TGF-β1 and p-Smad3 while TGF-β1 inhibitor SB431542 reversed the Anp32e-induced upregulation of Fn and Col-I in BUMPT cells without TGF-β1 stimulation. Collectively, our data demonstrate that Anp32e promotes the deposition of fibrosis-related proteins by regulating the TGF-β1/Smad3 pathway.

Keywords: Anp32e, renal interstitial fibrosis, CKD, fibrosis-related protein, pro-fibrotic factor, TGF-β1/Smad3


Citation styles

APA
Wei, J., Shan, Y., Xiao, Z., Wen, L., Tao, Y., Fang, X., Luo, H., Tang, C., Li, Y. (2022). Anp32e promotes renal interstitial fibrosis by upregulating the expression of fibrosis-related proteins. International Journal of Biological Sciences, 18(15), 5897-5912. https://doi.org/10.7150/ijbs.74431.

ACS
Wei, J.; Shan, Y.; Xiao, Z.; Wen, L.; Tao, Y.; Fang, X.; Luo, H.; Tang, C.; Li, Y. Anp32e promotes renal interstitial fibrosis by upregulating the expression of fibrosis-related proteins. Int. J. Biol. Sci. 2022, 18 (15), 5897-5912. DOI: 10.7150/ijbs.74431.

NLM
Wei J, Shan Y, Xiao Z, Wen L, Tao Y, Fang X, Luo H, Tang C, Li Y. Anp32e promotes renal interstitial fibrosis by upregulating the expression of fibrosis-related proteins. Int J Biol Sci 2022; 18(15):5897-5912. doi:10.7150/ijbs.74431. https://www.ijbs.com/v18p5897.htm

CSE
Wei J, Shan Y, Xiao Z, Wen L, Tao Y, Fang X, Luo H, Tang C, Li Y. 2022. Anp32e promotes renal interstitial fibrosis by upregulating the expression of fibrosis-related proteins. Int J Biol Sci. 18(15):5897-5912.

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