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Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer
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Telomerase Deficiency Causes Alveolar Stem Cell Senescence-associated Low-grade Inflammation in Lungs

Ruping Chen1, Kexiong Zhang2, Hao Chen2

  • 1From the Department of Microbiology/Key Laboratory for Experimental Teratology of Chinese Ministry of Education, School of Medicine, Shandong University, Jinan, Shandong Province 250012, China, the Institute of Aging Research, Hangzhou Normal University, School of Medicine, Hangzhou, Zhejiang Province 311121, China.

The Journal of Biological Chemistry
|November 1, 2015
PubMed

Insights

Telomere component (TERC) or enzyme (TERT) deficiency in mice causes lung stem cell aging and inflammation. This leads to premature lung aging, alveolar sacs, and fibrotic lesions.

Area of Science:

  • Pulmonary Medicine
  • Aging Research
  • Molecular Biology

Background:

  • Mutations in telomerase RNA component (TERC) and telomerase reverse transcriptase (TERT) are linked to lung aging diseases.
  • The precise roles of TERC and TERT in lung disease pathogenesis are not fully understood.

Purpose of the Study:

  • To investigate the functional impact of TERC or TERT deficiency on lung health and aging.
  • To elucidate the molecular mechanisms underlying telomerase's role in lung disease.

Main Methods:

  • Generation of Terc or Tert knockout (KO) mouse models.
  • Analysis of pulmonary phenotypes, including stem cell senescence, epithelial integrity, and inflammation.
  • Quantification of cytokine and chemokine levels in lung tissue and bronchoalveolar lavage fluid.
  • Assessment of myofibroblast differentiation markers and immune cell infiltration.

Main Results:

  • Terc or Tert KO mice exhibit pulmonary alveolar stem cell replicative senescence and epithelial impairment.
  • Telomerase deficiency leads to a significant increase in proinflammatory cytokines (e.g., IL-6, TNF-α) and chemokines (e.g., CCL2).
  • KO mice show decreased TGF-β1 signaling, increased markers of myofibroblast differentiation, and infiltration of inflammatory cells.

Conclusions:

  • Telomerase deficiency triggers replicative senescence in alveolar stem cells, initiating low-grade inflammation.
  • This process drives premature pulmonary aging, alveolar sac formation, and fibrotic lesions.
  • TERC and TERT are critical for maintaining lung homeostasis and preventing age-related lung pathology.
Keywords:
alveolar senescencechronic obstructive pulmonary disease (COPD)lung agingproinflammatory cytokinespulmonary fibrosistelomerasetelomerase reverse transcriptase (TERT)telomeretelomeres

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