Platelet Purinergic receptors in wound healing:
Any injury to our body is healed by the means of various intricate mechanisms and complex processes. Wound healing is a part of our body’s normal homeostasis. Recent studies show there is a massive release of ATP and UTP in case of inflammation in an area of injury and also expression of platelet purinergic receptors namely P2Y1, P2Y12 and P2X1[20]. These are also present in normal human keratinocytes that are identified by in situ hybridization technique. Mast cells also play a major role in tissue healing and homeostasis. But these cells express a vast heterogeneity depending upon their location. Mast cells from lungs show P2X7 expression in higher amounts. But the activated human cord blood mast cells (CBMCs) are rich in P2X1, P2Y1 and P2Y12 [21]. RT-PCR analysis of mRNA from endothelium-denuded human coronary arteries has demonstrated strong bands for P2Y2 and P2X1, although bands for P2Y1, P2Y4, and P2Y6 receptor mRNA could also be detected [22]. Endothelial cells, vascular smooth muscle cells, and fibroblasts are the structural elements of the blood vessel walls. Blood vessel regeneration is an important component of normal wound healing. This process occurs through both angiogenesis and vasculogenesis. Angiogenesis assays using Human Umbilical vein Endothelial Cells (HUVEC) have shown the expression of P2X4 in higher levels [23]. All cell types involved in wound healing differentially express P2X and P2Y receptors, and the receptor expression patterns vary between cellular types. Moreover, the differential expression of nucleotide receptor subtypes contributes to tissue cell heterogeneity which might be responsible for inducing a variety of responses by nucleotides present in the site of wounding. These studies are yet to prove any functional implications of purinergic receptors. These information with sustained research in future might revolutionize the therapeutics in an optimistic way it might even lead to development of successful antifibrotic agents as well.
Figure 3: Cellular events during different stages of wound healing