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A study on regulatory mechanism of miR-223 in ulcerative colitis through PI3K/Akt-mTOR signaling pathway

W Jiang1, Y-P Han, M Hu

  • 1Department of Gastroenterology, First Affiliated Hospital of Jiamusi University, Jiamusi, China. dncc_321@163.com.

European Review for Medical and Pharmacological Sciences
|June 19, 2019
PubMed
Abstract

Insights

MicroRNA-223 (miR-223) exacerbates ulcerative colitis (UC) by activating the PI3K/Akt-mTOR pathway, leading to increased inflammation and cell apoptosis. Inhibiting miR-223 shows therapeutic potential in UC models.

Area of Science:

  • Molecular Biology
  • Gastroenterology
  • Immunology

Background:

  • Ulcerative colitis (UC) is a chronic inflammatory bowel disease with complex regulatory mechanisms.
  • MicroRNAs (miRNAs) play crucial roles in inflammatory diseases, but their specific roles in UC require further elucidation.
  • The phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)-mammalian target of rapamycin (mTOR) signaling pathway is implicated in cell proliferation, survival, and inflammation.

Purpose of the Study:

  • To investigate the regulatory role of microRNA-223 (miR-223) in ulcerative colitis (UC).
  • To explore the involvement of the PI3K/Akt-mTOR signaling pathway in miR-223-mediated UC pathogenesis.
  • To assess the therapeutic potential of targeting miR-223 in a rat model of UC.

Main Methods:

  • Establishment of a UC rat model.
  • Treatment with a miR-223 inhibitor in a subset of UC rats.
  • Assessment of mTOR expression via immunohistochemistry.
  • Quantification of PI3K/Akt pathway proteins (P85, P110, p-Akt) using Western blotting.
  • Measurement of miR-223 mRNA levels via quantitative polymerase chain reaction (qPCR).
  • Evaluation of cell apoptosis using TUNEL assay.
  • Determination of inflammatory cytokine levels (IL-1β, IL-6) via ELISA.

Main Results:

  • UC induction led to increased mTOR, P85, P110, p-Akt, miR-223, IL-1β, IL-6, and cell apoptosis.
  • Inhibition of miR-223 significantly reduced mTOR, P85, P110, p-Akt, IL-1β, IL-6, and cell apoptosis.
  • While miR-223 expression was elevated in UC, its levels did not significantly change between UC and miR-223 inhibitor groups, suggesting miR-223 acts upstream or parallel to the inhibitor's direct effect on the pathway.

Conclusions:

  • MiR-223 promotes cell apoptosis and inflammation in ulcerative colitis.
  • These effects are mediated through the up-regulation of the PI3K/Akt-mTOR signaling pathway.
  • Targeting miR-223 demonstrates therapeutic promise for managing UC.

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