بیان ژن در جمعیت سلولی درگیر در ترمیم زخم
1- Introduction
2- Materials and Methods
3- Results and Discussion
4- Conclusions
References
Introduction
Wound healing is a complex multistep and multicellular biological process, traditionally divided into four overlapping phases known as haemostasis, infammation, proliferation, and remodelling [1]. Infammation and hypoxia are mutually interdependent: hypoxia-elicited infammation is implicated in the outcomes of a wide range of human diseases. Te delay in wound healing and wound chronicity are directly linked to persistent infammation. On the other hand, infammatory states are frequently characterised by tissue hypoxia, or by the stabilisation of hypoxia-dependent transcription factors [2, 3]. Te healing process is regulated by multiple signals such as growth factors, cytokines, chemokines, matrix metalloproteinases (MMPs) and extracellular macromolecules [4, 5]. Upon skin injury, innate immune cells (neutrophils and macrophages) are recruited to the site of injury to remove cellular debris and to secrete mediators able to activate keratinocytes, endothelial cells and fbroblasts. 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. Fibroblasts produce collagen, elastin, proteoglycans and other glycoproteins of the extracellular matrix, which then mature outside the cells. Some fbroblasts develop into myofbroblasts that cause contraction of the wound. Keratinocytes proliferate and migrate from the edges of the wound to restore a confuent epithelium. Migration and proliferation of all the cell types is regulated by complex mechanisms of inhibition and stimulation by growth factors and chemoattractants.