Platelet biology in regenerative medicine of skeletal muscle

Abstract

Platelet-based applications such as platelet-rich plasma (PRP) and platelet releasate have gained unprecedented attention in regenerative medicine across a variety of tissues as of late. The rationale behind utilizing PRP originates in the delivery of key cytokines and growth factors from α-granules to the targeted area, which in turn act as cell cycle regulators and promote the healing process across a variety of tissues. The aim of the present review is to assimilate current experimental evidence on the role of platelets as biomaterials in tissue regeneration, particularly in skeletal muscle, by integrating findings from human, animal and cell studies. This review is composed of 3 parts: firstly, we review key aspects of platelet biology that precede the preparation and use of platelet-related applications for tissue regeneration. Secondly, we critically discuss relevant evidence on platelet-mediated regeneration in skeletal muscle focusing on findings from (i) clinical trials, (ii) experimental animal studies and (iii) cell culture studies; and thirdly, we discuss the application of platelets in the regeneration of several other tissues including tendon, bone, liver, vessels and nerve. Finally, we review key technical variations in platelet preparation that may account for the large discrepancy in outcomes from different studies. This review provides an up-to-date reference tool for biomedical and clinical scientists involved in platelet-mediated tissue regenerative applications.

Development of a label‒free nanolc/ms/ms assay for monitoring the changes in the proteomic landscape of thrombin‒activated human platelets

“…This response is mediated through several signaling pathways acting downstream of receptors for von Willebrand Factor (vWF), thrombin (the PAR receptors) and collagen. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20] Autocrine stimulatory factors such as ADP and thromboxane are important for stimulating further adhesion to fibrinogen, vWF and collagen (through integrin receptors αIIbβ3, α2β1) and for activating circulating platelets. [5][6][7][8][9][10] Platelets play a pivotal role in the pathophysiological mechanisms underlying a wide family of CVDs, especially acute coronary syndromes (ACSs), as key players in thrombus formation after atheroma plaque rupture.…”

“…Platelets are small anucleated blood particles derived from megakaryocytes in the bone marrow, and they play a key role in the control of bleeding and hemostasis. [1][2][3][4][5][6][7][8][9][10] Platelets need to be activated to perform their functions, a process mediated by many physiological activators. The best known and characterized activators at the level of signaling transduction mechanisms are: thrombin, arachidonic acid and its derivatives (thromboxane A2), collagen, and the adenosine nucleotides (ADP and ATP).…”

“…The best known and characterized activators at the level of signaling transduction mechanisms are: thrombin, arachidonic acid and its derivatives (thromboxane A2), collagen, and the adenosine nucleotides (ADP and ATP). [2][3][4][5][6][7][8] Activated platelets undergo vast cytoskeleton, organelles, and secretory protein reorganization accompanied by many posttranslational modifications (PTM). [5][6][7][8][9][10][11][12][13][14] Due to their anucleate nature, platelets have limited protein synthesis, and therefore it is expected that most of the changes encountered at the level of the proteome under different pathophysiological conditions will be determined mostly by changes in protein expression (translational and post-translational regulated), at the level of PTM, proteolysis, or secretion during platelets degranulation processes associated with their activation.…”

“…[11][12][13][14][15] It is well documented that selected platelet messages are translated into proteins after activation, regulating the inflammatory and hemostatic responses of the platelet. [2][3][4][5][6][7][8] Platelets can be affected by many physiological conditions during blood circulation that can ultimately lead to vascular complications initiated by thrombus formation. [12][13][14][15][16] During activation, release of platelet microparticles can generate various pathophysiological effects, such as initiation and exacerbation of stroke.…”

Human Platelet Rich Plasma Alleviates Liver Fibrosis in Murine Schistosomiasis Mansoni

“…Platelet rich plasma (PRP) is a highly concentrated platelets preparation coming to around five times more than their normal blood count. The utilization of PRP as a regenerative medication has quickly developed to incorporate wide varieties of clinical conditions including ulcers, bone diseases and tissue damage [16,17] . PRP releases numerous mediators like cytokines, chemokines and growth factors into the affected areas to initiate their recovery through expanding, proliferation and relocation of vital cells [18] .…”