Abstract
Wound healing is a complex process regulated by multiple signals and consisting of several phases known as haemostasis, inflammation, proliferation, and remodelling. Keratinocytes, endothelial cells, macrophages, and fibroblasts are the major cell populations involved in wound healing process. Hypoxia plays a critical role in this process since cells sense and respond to hypoxic conditions by changing gene expression. This study assessed the in vitro expression of 77 genes involved in angiogenesis, metabolism, cell growth, proliferation and apoptosis in human keratinocytes (HaCaT), microvascular endothelial cells (HMEC-1), differentiated macrophages (THP-1), and dermal fibroblasts (HDF). Results indicated that the gene expression profiles induced by hypoxia were cell-type specific. In HMEC-1 and differentiated THP-1, most of the genes modulated by hypoxia encode proteins involved in angiogenesis or belonging to cytokines and growth factors. In HaCaT and HDF, hypoxia mainly affected the expression of genes encoding proteins involved in cell metabolism. This work can help to enlarge the current knowledge about the mechanisms through which a hypoxic environment influences wound healing processes at the molecular level.
Highlights
Wound healing is a complex multistep and multicellular biological process, traditionally divided into four overlapping phases known as haemostasis, inflammation, proliferation, and remodelling [1]
Cells undergo a metabolic reprogramming orchestrated by hypoxia-inducible factors (HIFs) which translocate to the nucleus and activate the transcription of hundreds of target genes
The changes in gene expression in response to hypoxic condition in cell populations involved in wound healing have been described
Summary
Wound healing is a complex multistep and multicellular biological process, traditionally divided into four overlapping phases known as haemostasis, inflammation, proliferation, and remodelling [1]. The healing process is regulated by multiple signals such as growth factors, cytokines, chemokines, matrix metalloproteinases (MMPs) and extracellular macromolecules [4, 5]. Angiogenesis is crucial to ensure an adequate supply of blood for tissue repair and wound healing [6]. Endothelial cells proliferate, demolish basement membrane and migrate to form new blood vessels starting from the ones located at wound edges. Keratinocytes proliferate and migrate from the edges of the wound to restore a confluent epithelium. Migration and proliferation of all the cell types is regulated by complex mechanisms of inhibition and stimulation by growth factors and chemoattractants
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