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Related Concept Videos

Gene Regulation in Microbial Communities: Quorum Sensing01:28

Gene Regulation in Microbial Communities: Quorum Sensing

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Quorum sensing is a mechanism of bacterial communication that enables coordinated gene expression in response to changes in population density. This facilitates collective behaviors that enhance survival, resource acquisition, and ecological adaptation. This process relies on small signaling molecules called autoinducers that accumulate as bacterial populations grow. When a critical threshold concentration of autoinducers is reached, bacterial cells collectively modify gene expression,...
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Aquaporins01:25

Aquaporins

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Aquaporins or AQPs are a family of integral membrane proteins whose primary function is to transport water, while some called aquaglyceroporins also transport glycerol. In addition, aquaporins have also been suspected to be involved in transporting volatile substances, such as carbon dioxide and ammonia, across membranes. Such AQPs that act as gas channels are often highly expressed in cells involved in the gaseous exchange, such as red blood cells, epithelial cells, and pulmonary capillaries.
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Related Experiment Video

Updated: Oct 21, 2025

Bronchoalveolar Lavage Exosomes in Lipopolysaccharide-induced Septic Lung Injury
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Long non‑coding RNA FGD5‑AS1/microRNA‑133a‑3p upregulates aquaporin 1 to decrease the inflammatory response in

Yuru Chu1, Xu Wang2, Naihao Yu1

  • 1Intensive Care Unit, Tianjin Academy of Traditional Chinese Medicine Affiliated Hospital, Tianjin 300120, P.R. China.

Molecular Medicine Reports
|September 9, 2021
PubMed
Summary

Long non-coding RNA FGD5-AS1 may inhibit sepsis-induced inflammation by regulating miR-133a-3p and aquaporin 1. Overexpression of FGD5-AS1 reduced inflammatory cytokines, suggesting a therapeutic potential for sepsis.

Keywords:
FGD5‑AS1aquaporin 1competitive endogenous RNAmicroRNA‑133a‑3psepsis

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Area of Science:

  • Molecular Biology
  • Immunology
  • Cardiology

Background:

  • Sepsis is a life-threatening systemic inflammatory response to infection.
  • Understanding the molecular mechanisms underlying sepsis is crucial for developing effective treatments.
  • Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in inflammatory diseases.

Purpose of the Study:

  • To investigate the role of FGD5-AS1 in sepsis and lipopolysaccharide (LPS)-induced inflammation.
  • To elucidate the interaction between FGD5-AS1, miR-133a-3p, and aquaporin 1 (AQP1) in sepsis.

Main Methods:

  • Constructed sepsis and LPS-induced cardiomyocyte models in animals and cells.
  • Utilized FGD5-AS1 overexpression to assess its effect on inflammatory responses.
  • Measured inflammatory cytokine levels (TNF-α, IL-1β, IL-6) using ELISA and RT-qPCR.
  • Confirmed molecular interactions via dual-luciferase reporter and miRNA pull-down assays.

Main Results:

  • Sepsis and LPS induced decreased FGD5-AS1 and increased miR-133a-3p expression.
  • FGD5-AS1 overexpression upregulated AQP1 and downregulated miR-133a-3p.
  • FGD5-AS1 overexpression inhibited the expression of TNF-α, IL-6, and IL-1β.
  • Confirmed FGD5-AS1 acts as a competing endogenous RNA (ceRNA) for miR-133a-3p, targeting AQP1.

Conclusions:

  • FGD5-AS1 functions as a ceRNA for miR-133a-3p, modulating AQP1 expression.
  • FGD5-AS1 overexpression demonstrates anti-inflammatory effects in sepsis models.
  • FGD5-AS1 represents a potential therapeutic target for sepsis treatment.