miR-27a-3p promotes inflammatory response in infectious endophthalmitis via targeting TSC1

Yanting Chen1, Shanxiang Li2, Hong He2

  • 1Hainan Eye Hospital and Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, No.19 Xiuhua Road, Xiuying District, Haikou, 570311, Hainan, China. bery1455@126.com.

Scientific Reports
|August 21, 2024
PubMed

Insights

MicroRNA-27a-3p worsens inflammation in infectious endophthalmitis (IE) by targeting TSC1. This finding offers new therapeutic strategies for IE management.

Area of Science:

  • Ophthalmology
  • Molecular Biology
  • Immunology

Background:

  • Infectious endophthalmitis (IE) is a severe ocular condition that threatens vision.
  • MicroRNAs (miRNAs) play crucial roles in regulating inflammatory processes.
  • The specific role of microRNA (miR)-27a-3p in IE pathogenesis remains largely unexplored.

Purpose of the Study:

  • To investigate the impact of miR-27a-3p on inflammation in infectious endophthalmitis (IE).
  • To identify the target gene of miR-27a-3p involved in IE-related inflammation.
  • To explore the potential of targeting miR-27a-3p for IE therapeutic strategies.

Main Methods:

  • Established a rat model of IE using intravitreal lipopolysaccharide (LPS) injection.
  • Quantified miR-27a-3p and inflammatory gene expression using RT-qPCR in rats and human samples.
  • Measured inflammatory cytokine concentrations in human vitreous samples via ELISA and conducted in vitro studies to identify miR-27a-3p targets.

Main Results:

  • miR-27a-3p levels were significantly elevated in LPS-treated rats and IE patients compared to controls.
  • Patients with higher miR-27a-3p expression exhibited increased pro-inflammatory cytokine levels.
  • Tuberous sclerosis complex 1 (TSC1) was identified as a direct target gene of miR-27a-3p, and its inhibition promoted inflammation.

Conclusions:

  • miR-27a-3p exacerbates inflammatory responses in infectious endophthalmitis (IE) through targeting TSC1.
  • Elevated miR-27a-3p is a potential biomarker for IE severity.
  • Targeting miR-27a-3p presents a promising therapeutic avenue for managing IE.