Laminins: Roles and Utility in Wound Repair
Open accessAbstract
Significance: Laminins are complex extracellular macromolecules that are major players in the control of a variety of core cell processes, including regulating rates of cell proliferation, differentiation, adhesion, and migration. Laminins, and related extracellular matrix components, have essential roles in tissue homeostasis; however, during wound healing, the same proteins are critical players in re-epithelialization and angiogenesis. Understanding how these proteins influence cell behavior in these different conditions holds great potential in identifying new strategies to enhance normal wound closure or to treat chronic/nonhealing wounds. Recent Advances: Laminin-derived bioactive peptides and, more recently, laminin-peptide conjugated scaffolds, have been designed to improve tissue regeneration after injuries. These peptides have been shown to be effective in decreasing inflammation and granulation tissue, and in promoting re-epithelialization, angiogenesis, and cell migration. Critical Issues: Although there is now a wealth of knowledge concerning laminin form and function, there are still areas of some controversy. These include the relative contribution of two laminin-based adhesive devices (focal contacts and hemidesmosomes) to the re-epithelialization process, the impact and implications of laminin proteolytic processing, and the importance of laminin polymer formation on cell behavior. In addition, the roles in wound healing of the laminin-related proteins, netrins, and LaNts are still to be fully defined. Future Directions: The future of laminin-based therapeutics potentially lies in the bioengineering of specific substrates to support laminin deposition for ex vivo expansion of autologous cells for graft formation and transplantation. Significant recent advances suggest that this goal is within sight.
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Keratinocytes activate fibroblasts in a feedback loop through the production of fibronectin, tenascin C, and laminin 332.
“Keratinocytes themselves further activate fibroblasts in a feedback loop through the production of fibronectin, tenascin C, and laminin 332 (Fig. 2) [93].”
From Immunology of Wound Healing (2018) · cites this paper as [93]
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- Authors
- Iorio, V., Troughton, L. D., & Hamill, K. J.
- Affiliations
- University of Liverpool (GB)
- Corresponding author
- Hamill, Kevin J.
- Venue
- Advances in Wound Care
- Publisher
- SAGE Publications
- Published
- 2015-04
- Volume
- 4
- Issue
- 4
- Pages
- 250-263
- ISSN
- 2162-1918 (ISSN-L)
- 2162-1934
- PMC
- PMC4397997
- OpenAlex
- W2315246287
- Cited by
- 169
- References
- 120
- Citations by year
- 2026: 14 · 2025: 11 · 2024: 23 · 2023: 23 · 2022: 13 · 2021: 17 · 2020: 23 · 2019: 8 · 2018: 16 · 2017: 12 · 2016: 6 · 2015: 3
- FWCI
- 0.87
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Advances in Wound Care (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- British Skin Foundation
- University of Liverpool
- Biotechnology and Biological Sciences Research Council (BB/L020513/1)
- Topics
- Health Sciences › Medicine › Rehabilitation › Wound Healing and Treatments
- Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
- Health Sciences › Medicine › Surgery › Tissue Engineering and Regenerative Medicine
- Keywords
- laminin, wound healing, re-epithelialization, angiogenesis, chronic wounds, focal adhesions, hemidesmosomes, netrin, cell migration, cell adhesion, tissue regeneration, ex vivo cell expansion
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