AI Article Synopsis

  • Hypertrophic scar (HTS) formation is a major issue for burn injury patients, with dermal microvascular endothelial cells (DMVECs) playing a key but under-researched role in this process.
  • The study discovered that DMVECs in HTS exhibited significant differences in gene expression and functionality compared to those from normal skin, including altered permeability and a specific profile of 31 differentially expressed genes.
  • Results indicated that HTS DMVECs have a unique response to injury, being less permeable and displaying mixed factors that can affect scar formation, suggesting their important role in understanding and treating HTS development.

Article Abstract

Hypertrophic scar (HTS) formation is a common challenge for patients after burn injury. Dermal microvascular endothelial cells (DMVECs) are an understudied cell type in HTS. An increase in angiogenesis and microvessel density can be observed in HTS. Endothelial dysfunction may play a role in scar development. This study aims to generate a functional and expression profile of HTS DMVECs. We hypothesize that transcript and protein-level responses in HTS DMVECs differ from those in normal skin (NS). HTSs were created in red Duroc pigs. DMVECs were isolated using magnetic-activated cell sorting with ulex europaeus agglutinin 1 (UEA-1) lectin. Separate transwell inserts were used to form monolayers of HTS DMVECs and NS DMVECs. Cell injury was induced and permeability was assessed. Gene expression in HTS DMVECS versus NS DMVECs was measured. Select differentially expressed genes were further investigated. HTS had an increased area density of dermal microvasculature compared to NS. HTS DMVECs were 17.59% less permeable than normal DMVECs (p < 0.05). After injury, NS DMVECs were 28.4% and HTS DMVECs were 18.8% more permeable than uninjured controls (28.4 ± 4.8 vs 18.8 ± 2.8; p = 0.11). PCR array identified 31 differentially expressed genes between HTS and NS DMVECs, of which 10 were upregulated and 21 were downregulated. qRT-PCR and ELISA studies were in accordance with the array. DMVECs expressed a mixed profile of factors that can contribute to and inhibit scar formation. HTS DMVECs have both a discordant response to cellular insults and baseline differences in function, supporting their proposed role in scar pathology. Further investigation of DMVECs is warranted to elucidate their contribution to HTS pathogenesis.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9293893PMC
http://dx.doi.org/10.1038/s41598-022-16376-zDOI Listing

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