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