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Ardali R, Kazemipour N, Nazifi S, et al. Pathophysiological role of Atg5 in human ulcerative colitis. Intest Res. 2020;18(4):421-429doi: 10.5217/ir.2019.00120.
Ardali, R., Kazemipour, N., Nazifi, S., Bagheri Lankarani, K., Razeghian Jahromi, I., & Sepehrimanesh, M. (2020). Pathophysiological role of Atg5 in human ulcerative colitis. Intestinal research, 18(4), 421-429. https://doi.org/10.5217/ir.2019.00120
Ardali, Razieh, et al. "Pathophysiological role of Atg5 in human ulcerative colitis." Intestinal research vol. 18,4 (2020): 421-429. doi: https://doi.org/10.5217/ir.2019.00120
Ardali R, Kazemipour N, Nazifi S, Bagheri Lankarani K, Razeghian Jahromi I, Sepehrimanesh M. Pathophysiological role of Atg5 in human ulcerative colitis. Intest Res. 2020 Oct;18(4):421-429. doi: 10.5217/ir.2019.00120. Epub 2020 May 08. PMID: 32380583; PMCID: PMC7609390.
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Intest Res. 2020 Oct;18(4):421-429. doi: 10.5217/ir.2019.00120. Epub 2020 May 08.

Pathophysiological role of Atg5 in human ulcerative colitis.

Intestinal research

Razieh Ardali, Nasrin Kazemipour, Saeed Nazifi, Kamran Bagheri Lankarani, Iman Razeghian Jahromi, Masood Sepehrimanesh

Affiliations

  1. Biochemistry Division, Department of Basic Sciences, School of Veterinary Medicine, Shiraz University, Shiraz, Iran.
  2. Clinical Pathology Division, Department of Clinical Sciences, School of Veterinary Medicine, Shiraz University, Shiraz, Iran.
  3. Health Policy Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
  4. Cardiovascular Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
  5. New Iberia Research Center, University of Louisiana at Lafayette, Lafayette, LA, USA.

PMID: 32380583 PMCID: PMC7609390 DOI: 10.5217/ir.2019.00120

Abstract

BACKGROUND/AIMS: Ulcerative colitis (UC), along with Crohn's disease, is one of the main types of inflammatory bowel disease (IBD). On the other hand, deregulated autophagy is involved in many chronic diseases, including IBD. In this study, we aimed to investigate the role of Atg5 and microRNA-181a (miR-181a) in the pathophysiology of UC.

METHODS: Colon biopsy, stool, and blood samples of 6 men and 9 women were confirmed for UC. Also, 13 men and 17 women were selected as healthy control (HC). Enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry were used to measure the Atg-5 content of the colon biopsies. Besides, the serum and stool levels of Atg5 were measured using ELISA. Moreover, the total RNA of blood cells was extracted and evaluated for the expression of miR-181a.

RESULTS: We found 1.2 ng/mL versus 0.46 ng/mL, 0.34 ng/mL versus 0.24 ng/mL, and 0.082 ng/mL versus 0.062 ng/mL of Atg5 in stool, intestinal tissue, and serum of UC and HCs, respectively. There was no significant difference in the expression of miR-181a in the blood samples of UC and HCs. Immunohistochemistry showed high positivity without any significant difference between the 2 groups in the quantitative analysis.

CONCLUSIONS: The significant difference observed between the stool Atg5 content of the HCs and UC patients may provide new insight into using this protein as a diagnostic biomarker, however, considering the small size of our studied population further studies are needed.

Keywords: Atg5; Autophagy; Colitis, ulcerative; Immunohistochemistry; mi-RNA

References

  1. Front Immunol. 2018 Apr 05;9:693 - PubMed
  2. Gut. 2015 Mar;64(3):504-17 - PubMed
  3. Therap Adv Gastroenterol. 2015 Jan;8(1):4-22 - PubMed
  4. Int J Clin Exp Med. 2015 Nov 15;8(11):21098-105 - PubMed
  5. Carcinogenesis. 2012 Nov;33(11):2018-25 - PubMed
  6. Cell. 2011 Nov 11;147(4):728-41 - PubMed
  7. Clin Transl Gastroenterol. 2017 Nov 30;8(11):e127 - PubMed
  8. Curr Top Microbiol Immunol. 2009;335:33-70 - PubMed
  9. J Gastroenterol Hepatol. 2015 Aug;30(8):1265-74 - PubMed
  10. Inflamm Bowel Dis. 2016 Feb;22(2):315-26 - PubMed
  11. Anticancer Res. 2013 Dec;33(12):5611-6 - PubMed
  12. Gastroenterol Res Pract. 2018 Jun 4;2018:7565076 - PubMed
  13. Mol Cell. 2012 Mar 9;45(5):629-41 - PubMed
  14. Exp Ther Med. 2016 Dec;12(6):3885-3892 - PubMed
  15. Front Immunol. 2013 Sep 30;4:301 - PubMed
  16. Gastroenterology. 2014 Feb;146(2):508-19 - PubMed
  17. Nature. 2012 Nov 1;491(7422):119-24 - PubMed
  18. Dig Dis. 2016;34(1-2):27-34 - PubMed
  19. Gastroenterology. 2008 Nov;135(5):1624-1635.e24 - PubMed
  20. Cancer Lett. 2015 Jan 28;356(2 Pt B):332-8 - PubMed
  21. Nature. 2008 Nov 13;456(7219):259-63 - PubMed
  22. Gastroenterology. 2011 May;140(6):1785-94 - PubMed
  23. World J Gastroenterol. 2006 May 28;12(20):3204-12 - PubMed
  24. Nat Genet. 2007 Feb;39(2):207-11 - PubMed
  25. Cell Death Dis. 2017 Mar 23;8(3):e2699 - PubMed
  26. Cell Cycle. 2012 Mar 15;11(6):1247-59 - PubMed
  27. Gut. 2011 Nov;60(11):1580-8 - PubMed
  28. Front Immunol. 2017 Jan 09;7:695 - PubMed
  29. Scand J Gastroenterol. 2017 Apr;52(4):468 - PubMed
  30. Expert Rev Mol Med. 2012 Feb 21;14:e5 - PubMed
  31. Nat Genet. 2007 May;39(5):596-604 - PubMed
  32. Dig Dis Sci. 2017 Jun;62(6):1426-1438 - PubMed
  33. Autophagy. 2018;14(2):207-215 - PubMed
  34. Autophagy. 2013 Mar;9(3):374-85 - PubMed
  35. Autophagy. 2014 Mar;10(3):468-79 - PubMed
  36. Sci Rep. 2018 Feb 8;8(1):2619 - PubMed
  37. Nat Commun. 2017 Jul 24;8(1):98 - PubMed
  38. Anticancer Res. 2012 Sep;32(9):4091-6 - PubMed
  39. PLoS One. 2013;8(3):e58639 - PubMed
  40. World J Gastroenterol. 2017 Mar 21;23(11):1944-1953 - PubMed

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