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Monocytes/macrophages are recruited from post‐capillary venules during microvascular arteriogenesis (670.7)
Author(s) -
Bruce Anthony,
KellyGoss Molly,
Meisner Joshua,
Price Richard,
Peirce Shayn
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.670.7
Subject(s) - arteriogenesis , arteriole , venule , microvessel , anatomy , microbiology and biotechnology , cx3cr1 , pathology , endothelium , medicine , inflammation , chemistry , microcirculation , biology , immunology , angiogenesis , immunohistochemistry , chemokine , chemokine receptor
It has previously been shown that circulating monocytes are essential to arteriogenesis in collateral arteries/arterioles following elevated shear stress induced by occlusion. Once recruited to the stimulated collateral vessel, these cells promote smooth muscle cell and endothelial cell proliferation through secreted cytokines. However, questions remain regarding the route by which circulating monocytes extravasate (egress from arteriole vs. venule) during microvascular arteriogenesis. We utilize confocal microscopy to evaluate recruitment of CX3CR1‐GFP positive monocytes/macrophages to collateral arterioles and post‐capillary venules at multiple time points following feeder arteriole ligation in the mouse spinotrapezius. We find arterioles and venules in ligated muscles to have significantly increased CX3CR1‐GFP cell recruitment compared to sham‐operated muscles. However, these increases occur at different times depending on microvessel type. We document a shift in the position of CX3CR1‐GFP high cells from venule‐associated to arteriole‐associated over the course of three days. We find that accumulation of adhered monocytes occurs only in venular lumina for all time points examined. Our results indicate that monocytes recruited during microvascular arteriogenesis extravasate from post‐capillary venules and that macrophages recruited to remodeling collateral arterioles express high levels of CX3CR1. Grant Funding Source : NIH‐HL082838‐02