AUTHOR=Chao Guanqun , Wang Zhaojun , Yang Yi , Zhang Shuo TITLE=LncRNA H19 as a Competing Endogenous RNA to Regulate AQP Expression in the Intestinal Barrier of IBS-D Patients JOURNAL=Frontiers in Physiology VOLUME=11 YEAR=2021 URL=https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2020.602076 DOI=10.3389/fphys.2020.602076 ISSN=1664-042X ABSTRACT=Objective

The study aimed to investigate the role of Long non-coding RNA (LncRNA) H19 in the pathogenesis of Diarrhea Irritable Bowel Syndrome (IBS-D), and further to the regulatory effect of LncRNA H19 on AQP1, 3 in the intestinal mucosa of IBS-D patients, so as to seek a new way to elucidate the mechanism of IBS in clinic.

Methods

The levels of LncRNA H19, AQP1, and AQP3 were detected in colonic tissues of IBS-D patients, compared with that in healthy controls. Through RNA gene interference and activation methods, small activating RNA (saRNA) and small interfering (siRNA) were transfered into Caco-2 cells in vitro experiment, and sub-group for two control group, siH19 empty vector group, siH19 interference group, overexpression H19 vector group, and overexpression H19 empty vector group. Quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot were applied to evaluate the expression levels of LncRNA H19 and the amount of AQP1 and AQP3 protein expression, respectively.

Results

Compared with healthy volunteers, the levels of LncRNA H19, AQP1, and AQP3 in the colonic mucosa of IBS-D patients were significantly decreased (P < 0.05). The results in vitro transfection experiment revealed that the level of LncRNA H19 in the siH19 interference group was significantly declined (P < 0.05), while there was a remarkable increase in the overexpression H19 vector group (P < 0.05), compared with the corresponding control groups. The expression of AQP1 and AQP3 in Caco-2 cells was of positive correlation with the level of LncRNA H19.

Conclusion

That the down-regulation of LncRNA H19 resulted in the expression changes of AQP1 and AQP3 may play an important role in the occurrence and development of IBS-D.