Autophagy‑related 16‑like 1 is influenced by human&nbsp;herpes virus 1‑encoded microRNAs in biopsy samples from the lower esophageal sphincter muscle during per‑oral endoscopic myotomy for esophageal achalasia

Kanda,Tsutomu; Yoshida,Akira; Ikebuchi,Yuichiro; Ikeda,Haruo; Sakaguchi,Takuki; Urabe,Shigetoshi; Minami,Hitomi; Nakao,Kazuhiko; Inoue,Haruhiro; Isomoto,Hajime

doi:10.3892/br.2020.1383

Autophagy‑related 16‑like 1 is influenced by human herpes virus 1‑encoded microRNAs in biopsy samples from the lower esophageal sphincter muscle during per‑oral endoscopic myotomy for esophageal achalasia

Authors:
- Tsutomu Kanda
- Akira Yoshida
- Yuichiro Ikebuchi
- Haruo Ikeda
- Takuki Sakaguchi
- Shigetoshi Urabe
- Hitomi Minami
- Kazuhiko Nakao
- Haruhiro Inoue
- Hajime Isomoto
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Affiliations: Division of Medicine and Clinical Science, Faculty of Medicine, Tottori University, Yonago, Tottori 683‑8504, Japan, Digestive Center, Showa University Koto‑Toyusu Hospital, Tokyo 135‑8577, Japan, Department of Gastroenterology and Hepatology, Nagasaki University Hospital, Nagasaki 852‑8501, Japan
Published online on: October 30, 2020 https://doi.org/10.3892/br.2020.1383
Article Number: 7

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Abstract

Esophageal achalasia is characterized by abnormal peristalsis of the esophageal body and impaired relaxation of the lower esophageal sphincter (LES); however, its etiology remains unknown. One of the potential causes of esophageal achalasia is herpes simplex virus type 1 (HSV‑1). Following infection with HSV‑1, a complex interaction between the autoimmune and inflammatory responses is initiated. Viral microRNAs (miRNAs/miRs) serve a crucial role in this interaction. In the present study, the expression of E3 ubiquitin‑protein ligase component n‑recognition 1 (UBR1) and autophagy‑related 16‑like 1 (ATG16L1) was assessed in patients with sporadic and classic achalasia as potential targets of the viral miRNAs. We assessed the mRNA levels of target transcripts using reverse transcription‑quantitative PCR. UBR1 expression was slightly decreased, although the difference was not significant. However, ATG16L1 expression was significantly decreased in the LES. In conclusion, ATG16L1 expression was reduced in the LES of achalasia patients; therefore, ATG16L1 might be a target of HSV1‑miR‑H1, and its reduction could be related to the disease mechanism.

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