Acceleration of Lung Regeneration by Platelet-Rich Plasma Extract through the Low-Density Lipoprotein Receptor–Related Protein 5–Tie2 Pathway

Mammoto, Tadanori; Zhao, Chen; Jiang, Amanda; Jiang, Elisabeth; Ingber, Donald E.; Mammoto, Akiko

doi:10.1165/rcmb.2015-0045oc

Cited by 27 publications

(72 citation statements)

References 49 publications

(32 reference statements)

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“…This important result demonstrates that ASA alone inhibits some components of acute lung inflammation in humans and human tissues under some conditions, but it may not be sufficient to alter the natural history of ARDS. An additional possibility regarding the negative LIPS-A outcome is that platelets have barrier-protective activities (Figure 4) and alveolar reparative potential in the injured lung (14,(188)(189)(190) that might be blunted by antiplatelet agents such as ASA (12). As a corollary, evidence that platelets have defensive activities against pathogens continues to evolve (7,15,26,28,191); these functions could also be reduced by inhibitory drugs.…”

Section: Antiplatelet Agents In Prevention and Therapy Of Ardsmentioning

confidence: 99%

Amicus or Adversary Revisited: Platelets in Acute Lung Injury and Acute Respiratory Distress Syndrome

Middleton

Rondina

Schwertz

et al. 2018

Am J Respir Cell Mol Biol

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Platelets are essential cellular effectors of hemostasis and contribute to disease as circulating effectors of pathologic thrombosis. These are their most widely known biologic activities. Nevertheless, recent observations demonstrate that platelets have a much more intricate repertoire beyond these traditional functions and that they are specialized for contributions to vascular barrier integrity, organ repair, antimicrobial host defense, inflammation, and activities across the immune continuum. Paradoxically, on the basis of clinical investigations and animal models of disease, some of these newly discovered activities of platelets appear to contribute to tissue injury. Studies in the last decade indicate unique interactions of platelets and their precursor, the megakaryocyte, in the lung and implicate platelets as essential effectors in experimental acute lung injury and clinical acute respiratory distress syndrome. Additional discoveries derived from evolving work will be required to precisely define the contributions of platelets to complex subphenotypes of acute lung injury and to determine if these remarkable and versatile blood cells are therapeutic targets in acute respiratory distress syndrome.

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Section: Antiplatelet Agents In Prevention and Therapy Of Ardsmentioning

confidence: 99%

Amicus or Adversary Revisited: Platelets in Acute Lung Injury and Acute Respiratory Distress Syndrome

Middleton

Rondina

Schwertz

et al. 2018

Am J Respir Cell Mol Biol

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“…Mammoto et al (2016) [67] reported that PRP accelerates lung regeneration since it contains abundant angiopoietin-1 which stimulates new blood vessels formation, maintains vascular integrity in vitro and in vivo and increases phosphorylation levels of lowdensity lipoprotein receptor-related protein 5 (LRP5) and thus activates angiogenic factor receptor Tie2 in endothelial cells (ECs) and accelerates endothelial cell sprouting. What's more, PRP promotes Achilles tendon healing [68] epithelialization and angiogenesis of splitthickness skin graft donor sites [69] .…”

Section: Additionally Wright Carpenter Et Al(2004)mentioning

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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“…We and other groups have shown that the Wnt ligand co-receptor, low-density lipoprotein receptor-related protein 5 (LRP5) controls various angiogenic pathways (e.g., angiopoietins (Angs)-Tie2 [15,17], VEGF-VEGFR2 [27,28], neuropilin (NRP2) [29]), and stimulates retinal [27,30–32] and lung vascular development in neonatal mice [14–17]. LRP5 also mediates compensatory lung growth after PNX in young adult mice through Ang-Tie2 signaling [33]. Thus, LRP5 signaling may be the key control point for the impairment of vascular and alveolar morphogenesis in the aged lung.…”

Section: Introductionmentioning

confidence: 99%

LRP5 in age-related changes in vascular and alveolar morphogenesis in the lung

Mammoto

Muyleart

Mammoto

2019

Aging

Self Cite

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Aging is associated with impaired angiogenesis and lung alveolar regeneration, which contributes to the increased susceptibility to chronic lung diseases (CLD). We have reported that the Wnt ligand co-receptor, low-density lipoprotein receptor-related protein 5 (LRP5), stimulates angiogenesis and lung alveolar regeneration. However, the role of LRP5 in age-related decline in vascular and alveolar morphogenesis remains unclear. In this report, we have demonstrated that vascular and alveolar structures are disrupted in the 24-month (24M) old mouse lungs. The expression of LRP5 and the major angiogenic factors, VEGFR2 and Tie2, is lower in endothelial cells (ECs) isolated from 24M old mouse lungs compared to those from 2M old mouse lungs. Vascular and alveolar formation is attenuated in the hydrogel implanted on the 24M old mouse lungs, while overexpression of LRP5, which restores angiogenic factor expression, reverses vascular and alveolar morphogenesis in the gel. Compensatory lung growth after unilateral pneumonectomy is inhibited in 24M old mice, which is reversed by overexpression of LRP5. These results suggest that LRP5 mediates age-related inhibition of angiogenesis and alveolar morphogenesis. Modulation of LRP5 may be a novel intervention to rejuvenate regenerative ability in aged lung and will lead to the development of efficient strategies for aging-associated CLD.

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Acceleration of Lung Regeneration by Platelet-Rich Plasma Extract through the Low-Density Lipoprotein Receptor–Related Protein 5–Tie2 Pathway

Cited by 27 publications

References 49 publications

Amicus or Adversary Revisited: Platelets in Acute Lung Injury and Acute Respiratory Distress Syndrome

Amicus or Adversary Revisited: Platelets in Acute Lung Injury and Acute Respiratory Distress Syndrome

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

LRP5 in age-related changes in vascular and alveolar morphogenesis in the lung

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