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Updated: Dec 5, 2025

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In Vitro Model of Human Cutaneous Hypertrophic Scarring using Macromolecular Crowding
Published on: May 1, 2020
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Galectin-1 production is elevated in hypertrophic scar.
Liam D Kirkpatrick1, Jeffrey W Shupp1,2,3,4, Robert D Smith1
1Firefighters' Burn and Surgical Research Laboratory, MedStar Health Research Institute, Washington, District of Columbia, USA.
Summary
Galectin-1 (Gal-1) is significantly upregulated in hypertrophic scars (HTSs), contributing to fibroblast proliferation and collagen deposition. This finding suggests Gal-1 as a potential therapeutic target for HTS treatment.
Area of Science:
- Biochemistry
- Dermatology
- Molecular Biology
Background:
- Hypertrophic scars (HTSs) result from abnormal wound healing, characterized by excess collagen and fibroblast activity.
- Galectins are lectins involved in various biological processes, including cell proliferation and extracellular matrix interactions.
- Galectin-1 (Gal-1) has been implicated in fibrotic diseases and can promote fibroblast differentiation.
Purpose of the Study:
- To investigate the expression and role of Galectin-1 (Gal-1) in human and porcine hypertrophic scars (HTSs).
- To determine if Gal-1 is associated with key features of HTS, such as fibroblast proliferation and collagen production.
Main Methods:
- Gene expression analysis using microarrays and quantitative real-time PCR (qRT-PCR) in HTS and normal skin tissues.
- Immunofluorescent staining to assess Gal-1 protein levels and its co-localization with myofibroblasts.
- Correlation analysis between Gal-1 expression and collagen type 1 alpha 1 mRNA levels.
Main Results:
- Galectins 1, 4, and 12 were upregulated in porcine HTS.
- Galectin-1 (LGALS1) transcription was significantly upregulated in both human and porcine HTS compared to normal skin.
- Increased Gal-1 protein expression was observed in HTS, co-localizing with myofibroblasts.
- A strong positive correlation was found between LGALS1 and Collagen type 1 alpha 1 mRNA expression.
Conclusions:
- Galectin-1 is overexpressed at both mRNA and protein levels in hypertrophic scars.
- Gal-1 may play a crucial role in HTS development by promoting fibroblast over-proliferation and collagen secretion.
- Targeting Gal-1 presents a promising avenue for future pharmacotherapy development for HTS.
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