Platelet glycoprotein VI and C-type lectin-like receptor 2 deficiency accelerates wound healing by impairing vascular integrity in mice
Wichaiyo S., Lax S., Montague S. J., Li Z., Grygielska B., Pike J. A., Haining E. J., Brill` A., Watson S. P., Rayes J.
Haematologica
Vol.104, Issue8, P. 1648-1660
Опубликовано: 2019
Тип ресурса: Статья
DOI:10.3324/haematol.2018.208363
Аннотация:
Platelets promote wound healing by forming a vascular plug and by secreting growth factors and cytokines. Glycoprotein (GP)VI and C-type lectin-like receptor (CLEC)-2 signal through a (hem)-immunore-ceptor tyrosine-based activation motif, which induces platelet activation. GPVI and CLEC-2 support vascular integrity during inflammation in the skin through regulation of leukocyte migration and function, and by sealing sites of vascular damage. In this study, we investigated the role of impaired vascular integrity due to GPVI and/or CLEC-2 deficiency in wound repair using a full-thickness excisional skin wound model in mice. Transgenic mice deficient in both GPVI and CLEC-2 exhibited accelerated skin wound healing, despite a marked impairment in vascular integrity. The local and temporal bleeding in the skin led to greater plasma protein entry, including fibrinogen and clotting factors, was associated with increased fibrin generation, reduction in wound neutrophils and M1 macrophages, dec
Ключевые слова:
biological marker; CLEC2B protein, human; fibrinogen receptor; lectin; membrane protein; platelet membrane glycoprotein VI; blood clotting factor; c type lectin like receptor 2; collagen; CXCL1 chemokine; fibrin; fibrinogen; formylmethionylleucylphenylalanine; glycoprotein VI; immunoglobulin G; lectin receptor; platelet endothelial cell adhesion molecule 1; podoplanin; thromboplastin; tumor necrosis factor; unclassified drug; vimentin; angiogenesis; animal; female; fluorescent antibody technique; genetics; immunohistochemistry; immunology; knockout mouse; macrophage; male; metabolism; mouse; neutrophil; pathology; skin; wound healing; animal cell; animal experiment; animal model; animal tissue; Article; bleeding; blood clotting; blood vessel injury; blood vessel permeability; controlled study; epithelization; extravasation; fibrin deposition; gene deletion; gene knockout; granulation tissue; immunoreceptor tyrosine based activation motif; inflammation; keratinocyte; leukocyte migration
Язык текста: Английский
ISSN: 1592-8721
Wichaiyo S.
Lax S.
Montague S. J.
Li Z.
Grygielska B.
Pike J. A.
Haining E. J.
Brill` A. Aleksandr 1972-
Watson S. P.
Rayes J.
Wичаиё С.
Лах С.
Монтагуе С. Й.
Ли З.
Грyгиелска Б.
Пике Й. А.
Хаининг Е. Й.
Брилль А. Александр 1972-
Wацон С. П.
Райес Й.
Platelet glycoprotein VI and C-type lectin-like receptor 2 deficiency accelerates wound healing by impairing vascular integrity in mice
Текст визуальный непосредственный
Haematologica
Ferrata Storti Foundation
Vol.104, Issue8 P. 1648-1660
2019
Статья
biological marker CLEC2B protein, human fibrinogen receptor lectin membrane protein platelet membrane glycoprotein VI blood clotting factor c type lectin like receptor 2 collagen CXCL1 chemokine fibrin fibrinogen formylmethionylleucylphenylalanine glycoprotein VI immunoglobulin G lectin receptor platelet endothelial cell adhesion molecule 1 podoplanin thromboplastin tumor necrosis factor unclassified drug vimentin angiogenesis animal female fluorescent antibody technique genetics immunohistochemistry immunology knockout mouse macrophage male metabolism mouse neutrophil pathology skin wound healing animal cell animal experiment animal model animal tissue Article bleeding blood clotting blood vessel injury blood vessel permeability controlled study epithelization extravasation fibrin deposition gene deletion gene knockout granulation tissue immunoreceptor tyrosine based activation motif inflammation keratinocyte leukocyte migration
Platelets promote wound healing by forming a vascular plug and by secreting growth factors and cytokines. Glycoprotein (GP)VI and C-type lectin-like receptor (CLEC)-2 signal through a (hem)-immunore-ceptor tyrosine-based activation motif, which induces platelet activation. GPVI and CLEC-2 support vascular integrity during inflammation in the skin through regulation of leukocyte migration and function, and by sealing sites of vascular damage. In this study, we investigated the role of impaired vascular integrity due to GPVI and/or CLEC-2 deficiency in wound repair using a full-thickness excisional skin wound model in mice. Transgenic mice deficient in both GPVI and CLEC-2 exhibited accelerated skin wound healing, despite a marked impairment in vascular integrity. The local and temporal bleeding in the skin led to greater plasma protein entry, including fibrinogen and clotting factors, was associated with increased fibrin generation, reduction in wound neutrophils and M1 macrophages, dec