Is the Use of Autologous Platelet-Rich Plasma Gels in Gynecologic, Cardiac, and General, Reconstructive Surgery Beneficial?

Everts, Peter A.; Hoogbergen, Maarten M.; A.Weber, Tjaarda; Devilee, Roger J.J.; Monftort, Gust van; Hingh, Ignace H. J. T. de

doi:10.2174/138920112800624346

Cited by 50 publications

(54 citation statements)

References 53 publications

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“…The relevance of platelets and their products for successful tissue reconstitution is reflected in the use of platelet-rich plasma (PRP) to promote healing (53)(54)(55). However, rendering mice thrombocytopenic leads to increased wound inflammation without affecting the reparative aspects of wound repair (56).…”

Section: Figurementioning

confidence: 99%

Gray platelet syndrome and defective thrombo-inflammation in Nbeal2-deficient mice

Deppermann¹,

Cherpokova²,

Nurden³

et al. 2013

J. Clin. Invest.

161

159

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Platelets are anuclear organelle-rich cell fragments derived from bone marrow megakaryocytes (MKs) that safeguard vascular integrity. The major platelet organelles, α-granules, release proteins that participate in thrombus formation and hemostasis. Proteins stored in α-granules are also thought to play a role in inflammation and wound healing, but their functional significance in vivo is unknown. Mutations in NBEAL2 have been linked to gray platelet syndrome (GPS), a rare bleeding disorder characterized by macrothrombocytopenia, with platelets lacking α-granules. Here we show that Nbeal2-knockout mice display the characteristics of human GPS, with defective α-granule biogenesis in MKs and their absence from platelets. Nbeal2 deficiency did not affect MK differentiation and proplatelet formation in vitro or platelet life span in vivo. Nbeal2-deficient platelets displayed impaired adhesion, aggregation, and coagulant activity ex vivo that translated into defective arterial thrombus formation and protection from thrombo-inflammatory brain infarction following focal cerebral ischemia. In a model of excisional skin wound repair, Nbeal2-deficient mice exhibited impaired development of functional granulation tissue due to severely reduced differentiation of myofibroblasts in the absence of α-granule secretion. This study demonstrates that platelet α-granule constituents are critically required not only for hemostasis but also thrombosis, acute thrombo-inflammatory disease states, and tissue reconstitution after injury.

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Section: Figurementioning

confidence: 99%

Gray platelet syndrome and defective thrombo-inflammation in Nbeal2-deficient mice

Deppermann¹,

Cherpokova²,

Nurden³

et al. 2013

J. Clin. Invest.

161

159

View full text Add to dashboard Cite

show abstract

“…In addition, increasing data indicate that platelets are also involved in fundamental processes of vascular biology, such as angiogenesis, tissue regeneration, and tumor metastasis. [1][2][3][4] Platelets promote new blood vessel growth via numerous stimulators of angiogenesis. For example, vascular endothelial growth factor, fibroblast growth factor, and platelet-derived growth factor can induce endothelial cell proliferation and cell migration, stimulate chemotaxis, and increase tubule formation.…”

Section: Introductionmentioning

confidence: 99%

Phagocytosis of platelets enhances endothelial cell survival under serum deprivation

Ping

Ren

Lan

et al. 2015

Exp Biol Med (Maywood)

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Platelets are key players in fundamental processes of vascular biology, such as angiogenesis, tissue regeneration, and tumor metastasis. However, the underlying mechanisms remain unclear. In this study, some tumor vascular endothelial cells were positively stained by antiplatelet antibodies. Further investigation revealed that platelets were taken up by endothelial cells in vitro and in vivo. Human umbilical vascular endothelial cells were rendered apoptotic under conditions of serum deprivation. However, endothelial apoptosis was suppressed and cell viability was enhanced when platelets were added to the cultures. Endothelial survival was paralleled by an upregulation of phosphorylated Akt and p70 S6K. In conclusion, this study demonstrated that platelets can be phagocytosed by endothelial cells, and the phagocytosed platelets could suppress endothelial apoptosis and promote cell viability level. The mechanism underlying this process involves the activation of Akt signaling.

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“…These findings were in agreement with the study of Harris et al(2012) [40] who injected PRP or saline solution into a variety of none injured muscle tissues of healthy rabbits and histologically evaluated the specimens after 2, 6 and 12 weeks. They reported that PRP initially promotes intensification of the inflammatory process in muscle injuries because this inflammatory phase is a very important step during muscle healing as it triggers the wound healing cascade leading to the cellular migration and proliferation, glycosaminoglycan and collagen deposition, collagen maturation and remodeling of the tissue [41] .The neutrophils and monocytes have granules filled with myeloperoxidase that contributes to the antimicrobial action of PRP [42] . [42] who used platelet-rich fibrin matrix did not detect any effect on inflammation.…”

Section: Discussionmentioning

confidence: 99%

Autologous platelet rich plasma enhances satellite cells expression of MyoD and exerts angiogenic and antifibrotic effects in experimental rat model of traumatic skeletal muscle injury

Attia

Atef

Elmansy

2017

Egyptian Journal of Histology

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Introduction: Skeletal muscle injuries comprise the greater part of sports-related injuries. Role of growth factors in healing of injured tissue encouraged the use of platelet-rich plasma (PRP). Aim of the work: We aimed to study the effect of PRP on skeletal muscle injury. Materials & Methods: Forty adult male rats were divided into four equal groups; control and 2, 7, 14 days after the injury. The injured muscles were either treated with PRP or left without treatment. The rats were sacrificed and the muscle specimens were processed for histological and immunohistochemical staining for detection of Anti-MyoD, anti-CD34 and anti TGFβ1 followed by morphometric study. Results: PRP treatment induced initial intense inflammatory response with neutrophils and macrophages cell infiltrate subsided in the 7th day. When compared to untreated groups, PRP treated ones showed significant increases in the mean number of regenerating muscle fibers (22.03±4.08) and angiogenesis (10.83±2.46) on the 7th day. The median number of MyoD immunopositive stellate cells showed a significant increase on the 2nd day ,72 (62-78) and then decrease on the 7th day; 28(22-33) to be non significant after 14th days; 4(3-5) of injury. A significant decrease in the mean area % of collagen deposition (2.27±.0.59, 3.68±0.72 and 4.76±0.82) and TGF β1 immunoexpression, medians; 5 (4.20-5.70), 2.50 (2.10-3.50) and 2.30( 1.60-3.20) after 2, 7 and 14 days, respectively, were observed. Conclusions: PRP could exert a promising effect on skeletal muscle injuries via enhancing myogenesis, neovascularization and reduction of fibrosis. Since autologous blood preparations are safe, PRP may serve as a valuable adjunct in management of such injuries.

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Is the Use of Autologous Platelet-Rich Plasma Gels in Gynecologic, Cardiac, and General, Reconstructive Surgery Beneficial?

Cited by 50 publications

References 53 publications

Gray platelet syndrome and defective thrombo-inflammation in Nbeal2-deficient mice

Gray platelet syndrome and defective thrombo-inflammation in Nbeal2-deficient mice

Phagocytosis of platelets enhances endothelial cell survival under serum deprivation

Autologous platelet rich plasma enhances satellite cells expression of MyoD and exerts angiogenic and antifibrotic effects in experimental rat model of traumatic skeletal muscle injury

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