Galectin-1 production is elevated in hypertrophic scar
Liam D. Kirkpatrick BA
Firefighters' Burn and Surgical Research Laboratory, MedStar Health Research Institute, Washington, District of Columbia, USA
Search for more papers by this authorJeffrey W. Shupp MD
Firefighters' Burn and Surgical Research Laboratory, MedStar Health Research Institute, Washington, District of Columbia, USA
Department of Biochemistry and Molecular and Cellular Biology, Georgetown University School of Medicine, Washington, District of Columbia, USA
The Burn Center, Department of Surgery, MedStar Washington Hospital Center, Washington, District of Columbia, USA
Department of Surgery, Georgetown University School of Medicine, Washington, District of Columbia, USA
Search for more papers by this authorRobert D. Smith BS
Firefighters' Burn and Surgical Research Laboratory, MedStar Health Research Institute, Washington, District of Columbia, USA
Search for more papers by this authorAbdulnaser Alkhalil PhD
Firefighters' Burn and Surgical Research Laboratory, MedStar Health Research Institute, Washington, District of Columbia, USA
Search for more papers by this authorLauren T. Moffatt PhD
Firefighters' Burn and Surgical Research Laboratory, MedStar Health Research Institute, Washington, District of Columbia, USA
Department of Biochemistry and Molecular and Cellular Biology, Georgetown University School of Medicine, Washington, District of Columbia, USA
Search for more papers by this authorCorresponding Author
Bonnie C. Carney PhD
Firefighters' Burn and Surgical Research Laboratory, MedStar Health Research Institute, Washington, District of Columbia, USA
Department of Biochemistry and Molecular and Cellular Biology, Georgetown University School of Medicine, Washington, District of Columbia, USA
Correspondence
Bonnie C. Carney, PhD, George Hyman Research Building, 108 Irving Street, NW, Room 306, Washington, DC 20010, USA.
Email: [email protected]
Search for more papers by this authorLiam D. Kirkpatrick BA
Firefighters' Burn and Surgical Research Laboratory, MedStar Health Research Institute, Washington, District of Columbia, USA
Search for more papers by this authorJeffrey W. Shupp MD
Firefighters' Burn and Surgical Research Laboratory, MedStar Health Research Institute, Washington, District of Columbia, USA
Department of Biochemistry and Molecular and Cellular Biology, Georgetown University School of Medicine, Washington, District of Columbia, USA
The Burn Center, Department of Surgery, MedStar Washington Hospital Center, Washington, District of Columbia, USA
Department of Surgery, Georgetown University School of Medicine, Washington, District of Columbia, USA
Search for more papers by this authorRobert D. Smith BS
Firefighters' Burn and Surgical Research Laboratory, MedStar Health Research Institute, Washington, District of Columbia, USA
Search for more papers by this authorAbdulnaser Alkhalil PhD
Firefighters' Burn and Surgical Research Laboratory, MedStar Health Research Institute, Washington, District of Columbia, USA
Search for more papers by this authorLauren T. Moffatt PhD
Firefighters' Burn and Surgical Research Laboratory, MedStar Health Research Institute, Washington, District of Columbia, USA
Department of Biochemistry and Molecular and Cellular Biology, Georgetown University School of Medicine, Washington, District of Columbia, USA
Search for more papers by this authorCorresponding Author
Bonnie C. Carney PhD
Firefighters' Burn and Surgical Research Laboratory, MedStar Health Research Institute, Washington, District of Columbia, USA
Department of Biochemistry and Molecular and Cellular Biology, Georgetown University School of Medicine, Washington, District of Columbia, USA
Correspondence
Bonnie C. Carney, PhD, George Hyman Research Building, 108 Irving Street, NW, Room 306, Washington, DC 20010, USA.
Email: [email protected]
Search for more papers by this authorAbstract
Upon healing, burn wounds often leave hypertrophic scars (HTSs) marked by excess collagen deposition, dermal and epidermal thickening, hypervascularity, and an increased density of fibroblasts. The Galectins, a family of lectins with a conserved carbohydrate recognition domain, function intracellularly and extracellularly to mediate a multitude of biological processes including inflammatory responses, angiogenesis, cell migration and differentiation, and cell-ECM adhesion. Galectin-1 (Gal-1) has been associated with several fibrotic diseases and can induce keratinocyte and fibroblast proliferation, migration, and differentiation into fibroproliferative myofibroblasts. In this study, Gal-1 expression was assessed in human and porcine HTS. In a microarray, galectins 1, 4, and 12 were upregulated in pig HTS compared to normal skin (fold change = +3.58, +6.11, and +3.03, FDR <0.01). Confirmatory qRT-PCR demonstrated significant upregulation of Galectin-1 (LGALS1) transcription in HTS in both human and porcine tissues (fold change = +7.78 and +7.90, P <.05). In pig HTS, this upregulation was maintained throughout scar development and remodeling. Immunofluorescent staining of Gal-1 in human and porcine HTS showed significantly increased fluorescence (202.5 ± 58.2 vs 35.2 ± 21.0, P <.05 and 276.1 ± 12.7 vs 69.7 ± 25.9, P <.01) compared to normal skin and co-localization with smooth muscle actin-expressing myofibroblasts. A strong positive correlation (R = .948) was observed between LGALS1 and Collagen type 1 alpha 1 mRNA expression. Gal-1 is overexpressed in HTS at the mRNA and protein levels and may have a role in the development of scar phenotypes due to fibroblast over-proliferation, collagen secretion, and dermal thickening. The role of galectins shows promise for future study and may lead to the development of a pharmacotherapy for treatment of HTS.
CONFLICT OF INTEREST
The authors state no conflict of interest.
Supporting Information
| Filename | Description |
|---|---|
| wrr12869-sup-0001-Figures.zipapplication/x-zip-compressed, 1.2 MB | FIGURE S1 Gal-1 and α-SMA co-staining antibody controls show there is no nonspecific staining. Three controls were utilized for the co-staining experiment: the “No α-SMA 1°” slides received only the rabbit Gal-1 primary antibody; the “No Gal-1 1°” slides received only the mouse α-SMA primary antibody; the “Neither 1°” slides received no primary antibodies. All controls received both the goat anti-mouse CY3 and goat anti-rabbit CY5 secondary antibodies. No nonspecific staining was observed on either the porcine (A) or human (B) slides. DAPI, blue; α-SMA/CY3, red; Gal-1/CY5, green. Scale bar = 100 μm. |
Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.
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