ArticleThe Journal of biological chemistry2020
Secretory galectin-3 induced by glucocorticoid stress triggers stemness exhaustion of hepatic progenitor cells.
Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- The Sugar-Coated Truth of Alcohol-Associated Liver Disease: Galectins as Multifaceted Regulators of Alcohol-Induced Liver Injury.The American journal of pathology · 2026Review
- Mediating role of proteomics in the association between per- and polyfluoroalkyl substance exposure and blood pressure in youth.Environmental pollution (Barking, Essex : 1987) · 2025Article
- Elevated glucocorticoid alters the developmental dynamics of hypothalamic neurogenesis in zebrafish.Communications biology · 2024Article
- Glucocorticoid effects on the brain: from adaptive developmental plasticity to allostatic overload.The Journal of experimental biology · 2024Review
- Secretory GFP reconstitution labeling of neighboring cells interrogates cell-cell interactions in metastatic niches.Nature communications · 2023Article
- Reply to the Letter to the Editor Titled "The Effects of Dexamethasone on Cardiovascular Disease: Friend or Foe?" by Han et al.Cardiovascular drugs and therapy · 2023Article
- Long-term Dexamethasone Treatment Increases Cardiac Galectin-3 Levels.Cardiovascular drugs and therapy · 2023Article
- The Therapeutic Potential of Galectin-3 in the Treatment of Intrahepatic Cholangiocarcinoma Patients and Those Compromised With COVID-19.Frontiers in molecular biosciences · 2021Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adult progenitor cell populations typically exist in a quiescent state within a controlled niche environment. However, various stresses or forms of damage can disrupt this state, which often leads to dysfunction and aging. We built a glucocorticoid (GC)-induced liver damage model of mice, found that GC stress induced liver damage, leading to consequences for progenitor cells expansion. However, the mechanisms by which niche factors cause progenitor cells proliferation are largely unknown. We demonstrate that, within the liver progenitor cells niche, Galectin-3 (Gal-3) is responsible for driving a subset of progenitor cells to break quiescence. We show that GC stress causes aging of the niche, which induces the up-regulation of Gal-3. The increased Gal-3 population increasingly interacts with the progenitor cell marker CD133, which triggers focal adhesion kinase (FAK)/AMP-activated kinase (AMPK) signaling. This results in the loss of quiescence and leads to the eventual stemness exhaustion of progenitor cells. Conversely, blocking Gal-3 with the inhibitor TD139 prevents the loss of stemness and improves liver function. These experiments identify a stress-dependent change in progenitor cell niche that directly influence liver progenitor cell quiescence and function.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.