Abstract
The inflammatory reaction influences the deposition of collagen within wound granulation tissue. The aim of the present study is to determine whether histamine acting directly on myofibroblasts derived from wound granulation tissue may influence collagen deposition. It also identifies the histamine receptor involved in this process. The experiments were carried out on cells isolated from the granulation tissue of a wound model (a polypropylene net inserted subcutaneously to rats) or intact rat skin. Collagen content was measured following the addition of different concentrations of histamine and treatment with histamine receptor antagonists (ketotifen – H1 inhibitor, ranitidine – H2 inhibitor) and a histamine receptor H1 agonist (2-pyridylethylamine dihydrochloride).The cells were identified as myofibroblasts: alpha-smooth muscle actin, vimentin, and desmin positive in all experimental conditions. Histamine increased the collagen level within both cell cultures, i.e., those isolated from granulation tissue or intact skin. It did not, however, influence the expression of either the collagen type I or III genes within the cultured myofibroblasts. Histamine activity was reduced by ketotifen (the H1 receptor inhibitor) and increased by the H1 receptor agonist, as demonstrated by changes in the levels of collagen in the myofibroblast culture. Histamine increased collagen content within the cultures, acting directly on myofibroblasts via H1 receptor stimulation.
Highlights
Wound repair is a complex phenomenon comprising several interdependent processes such as hemostasis, inflammation, cell migration and proliferation, and protein synthesis, as well as wound contraction and remodeling
The cells isolated from the granulation tissue of the wound were identified as myofibroblasts based on their type of spread on Petri dishes and the intracellular expression of α-smooth muscle actin, vimentin, and desmin [19]
The mechanisms underlying the effects of both ketotifen and ranitidine on the expression of α-smooth muscle actin, vimentin, and desmin should be investigated in later study
Summary
Wound repair is a complex phenomenon comprising several interdependent processes such as hemostasis, inflammation, cell migration and proliferation, and protein synthesis, as well as wound contraction and remodeling. A fundamental element of the wound environment is constituted by the cells that participate in all repair processes, e.g., fibroblasts, myofibroblasts, epithelial cells, endothelial cells, and. The inflammatory process in a wound is aimed at delivering leukocytes to the site of injury. These cells are responsible for the removal of bacteria and cellular debris, as well as the secretion of mediators involved in wound repair regulation. It is crucial that an appropriate inflammatory signal is produced to facilitate wound healing and scar development. Mast cells play a key role in mediating inflammation by producing histamine.
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