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Related Experiment Video

Updated: May 11, 2025

Efficient Transcriptionally Controlled Plasmid Expression System for Investigation of the Stability of mRNA Transcripts in Primary Alveolar Epithelial Cells
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Blocking triggering receptors expressed on myeloid cell-1 alleviates alveolar epithelial cell senescence by

Wen-Jing Zhong1, Jian-Bing Xiong2,3, Chen-Yu Zhang1

  • 1Department of Physiology, School of Basic Medical Science, Central South University, Changsha, 410078, Hunan, China.

Histochemistry and Cell Biology
|April 16, 2025
PubMed
Summary

Blocking triggering receptor expressed on myeloid cells-1 (TREM-1) reduces oxidative stress and alveolar epithelial cell senescence, offering a new therapeutic target for pulmonary fibrosis.

Keywords:
Alveolar epithelial cellNrf2Pulmonary fibrosisSenescenceTREM-1

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Area of Science:

  • Pulmonary Medicine
  • Cellular Biology
  • Immunology

Background:

  • Pulmonary fibrosis (PF) is a fatal, age-associated disease driven by alveolar epithelial cell (AEC) senescence.
  • Reactive oxygen species (ROS) accumulation exacerbates cellular senescence.
  • The role of triggering receptor expressed on myeloid cells-1 (TREM-1) in PF-associated oxidative stress and AEC senescence is unclear.

Purpose of the Study:

  • To investigate the role of TREM-1 in PF pathogenesis.
  • To determine if TREM-1 blockade mitigates PF by reducing oxidative stress and AEC senescence.
  • To elucidate the molecular mechanisms linking TREM-1, oxidative stress, and AEC senescence.

Main Methods:

  • Mice were induced with bleomycin (BLM)-induced PF and treated with TREM-1 blockade.
  • Senescence-related proteins (p16, p21, p53, γ-H2AX) and antioxidant markers (Nrf2, HO-1) were assessed in lung tissue.
  • In vitro studies utilized AECs treated with BLM and TREM-1 blockade, with subsequent analysis of ROS levels and senescence.
  • The Nrf2/HO-1 pathway's role was examined by inhibiting these markers.

Main Results:

  • TREM-1 blockade attenuated BLM-induced PF in mice, decreasing senescence markers in lung tissue.
  • TREM-1 blockade restored antioxidant levels by increasing Nrf2- and HO-1-positive cells.
  • TREM-1 was highly expressed in surfactant-associated protein (SPC)-positive AECs.
  • In vitro, TREM-1 blockade reduced ROS and BLM-induced AEC senescence, an effect partially reversed by Nrf2/HO-1 inhibition.

Conclusions:

  • TREM-1 blockade ameliorates pulmonary fibrosis by reducing oxidative stress and AEC senescence.
  • The Nrf2/HO-1 signaling pathway is crucial in mediating TREM-1-induced AEC senescence.
  • Targeting TREM-1 represents a potential therapeutic strategy for pulmonary fibrosis.