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Platelet interaction with lymphatics aggravates intestinal inflammation by suppressing lymphangiogenesis. | LitMetric

AI Article Synopsis

  • Lymphatic failure is linked to inflammatory bowel disease (IBD), where interactions between platelets and lymphatic endothelial cells (LECs) hinder the growth of lymphatic vessels (lymphangiogenesis).
  • In a study involving colitis-induced mice, blocking VEGF-R3 worsened colitis and increased platelet movement to lymphatics, but using antiplatelet antibodies improved lymphatic density and colitis symptoms.
  • The research indicates that even with increased levels of lymphangiogenic factors during inflammation, platelet interactions suppress lymphangiogenesis, suggesting a potential new treatment avenue for IBD by targeting these interactions.

Article Abstract

Lymphatic failure is a histopathological feature of inflammatory bowel disease (IBD). Recent studies show that interaction between platelets and podoplanin on lymphatic endothelial cells (LECs) suppresses lymphangiogenesis. We aimed to investigate the role of platelets in the inflammatory process of colitis, which is likely to be through modulation of lymphangiogenesis. Lymphangiogenesis in colonic mucosal specimens from patients with IBD was investigated by studying mRNA expression of lymphangiogenic factors and histologically by examining lymphatic vessel (LV) densities. Involvement of lymphangiogenesis in intestinal inflammation was studied by administering VEGF-receptor 3 (VEGF-R3) inhibitors to the mouse model of colitis using dextran sulfate sodium and evaluating platelet migration to LVs. The inhibitory effect of platelets on lymphangiogenesis was investigated in vivo by administering antiplatelet antibody to the colitis mouse model and in vitro by coculturing platelets with lymphatic endothelial cells. Although mRNA expressions of lymphangiogenic factors such as VEGF-R3 and podoplanin were significantly increased in the inflamed mucosa of patients with IBD compared with those with quiescent mucosa, there was no difference in LV density between them. In the colitis model, VEGF-R3 inhibition resulted in aggravated colitis, decreased lymphatic density, and increased platelet migration to LVs. Administration of an antiplatelet antibody increased LV densities and significantly ameliorated colitis. Coculture with platelets inhibited proliferation of LECs in vitro. Our data suggest that despite elevated lymphangiogenic factors during colonic inflammation, platelet migration to LVs resulted in suppressed lymphangiogenesis, leading to aggravation of colitis by blocking the clearance of inflammatory cells. Modulating the interaction between platelets and LVs could be a new therapeutic means for treating IBD.

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Source
http://dx.doi.org/10.1152/ajpgi.00455.2015DOI Listing

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