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ORIGINAL ARTICLE
Year : 2020  |  Volume : 6  |  Issue : 1  |  Page : 1-9

Protein disulfide isomerase A3: A potential regulatory factor of colon epithelial cells


1 Department of Clinical Nutrition, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong, China
2 Department of Gastrointestinal and Anal Surgery, The Second Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China
3 Department of Gastrointestinal Surgery, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong, China

Correspondence Address:
Haiping Jiang
Department of Gastrointestinal Surgery, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ctm.ctm_33_19

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Aim: This study aimed to investigate the effects of protein disulfide isomerase A3 (PDIA3) on the proliferation and apoptosis of colon epithelial cells, so as to explore its possible role in colon compensation of ultra-short bowel syndrome. Methods: The expression of PDIA3 gene in NCM460 colonic epithelial cells was upregulated and silenced by liposome transient transfection technique. The expression of PDIA3 protein was determined by Western blotting, the proliferation rate of NCM460 cells was detected by CCK8, and the apoptosis rate of NCM460 cells was determined by flow cytometry. Results: DNA sequencing and Western blotting results successfully verified that PDIA3 protein expression in NCM460 cells was upregulated and silenced by liposomal transfection. In the PDIA3 overexpression experiment, the proliferation rate of the experimental group was lower than that of the empty carrier group at 24 h, 48 h, and 72 h, and the apoptosis rate of the experimental group was higher than that of the empty carrier group (P < 0.05, the difference was statistically significant). In the PDIA3-silenced experiment, the proliferation rate of the experimental group was higher than that of the empty carrier group at 24 h, 48 h, and 72 h, and the apoptosis rate of the experimental group was lower than that of the empty carrier group (P < 0.05, the difference was statistically significant). Conclusion: PDIA3 inhibits the proliferation of human colonic epithelial cells (NCM460) and promotes their apoptosis, which may not be a key regulatory protein in colon compensation of ultra-short bowel syndrome.


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