AI Article Synopsis

  • Understanding the roles of keratinocyte matrix adhesions, specifically focal contacts and hemidesmosomes, is crucial for grasping the wound-healing process in skin.
  • Recent research using mouse genetic models and cell cultures is uncovering how these proteins influence the speed and direction of skin cell movement through various signaling pathways.
  • Investigating these adhesion proteins is vital, as impaired wound healing poses significant issues for vulnerable groups like the elderly and diabetics, paving the way for new therapeutic strategies.

Article Abstract

During wound healing of the skin, keratinocytes should move over while still adhering to their underlying matrix. Thus, mechanistic insights into the wound-healing process require an understanding of the forms and functions of keratinocyte matrix adhesions, specifically focal contacts and hemidesmosomes, and their components. Although the structure and composition of focal contacts and hemidesmosomes are relatively well defined, the functions of their components are only now being delineated using mouse genetic models and knockdown approaches in cell culture systems. Remarkably, both focal contact and hemidesmosomal proteins appear involved in determining the speed and directional migration of epidermal cells by modulating several signal transduction pathways. Although many publications are centered on focal contacts, their existence in tissues such as the skin is controversial. Nonetheless, focal contact proteins are central to mechanisms that regulate skin cell motility. Conversely, hemidesmosomes have been identified in intact skin but whether hemidesmosomal components play a positive regulatory function in keratinocyte motility remains debated in the field. Defective wound healing is a developing problem in the aged, hospitalized and diabetic populations. Hence, deriving new insights into the molecular roles of matrix adhesion proteins in wound healing is a prerequisite to the development of novel therapeutics to enhance tissue repair and regeneration.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3955972PMC
http://dx.doi.org/10.1089/wound.2013.0489DOI Listing

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