scholarly journals Mechanisms of Leukocyte Recruitment Into the Aorta During Atherosclerosis

Atherogenesis ◽  
10.5772/27397 ◽  
2012 ◽  
Author(s):  
Matthew J. ◽  
Elena Galki
Keyword(s):  
Leukocyte Recruitment

Antithrombin III Prevents and Rapidly Reverses Leukocyte Recruitment in Ischemia/Reperfusion

Circulation ◽  
1997 ◽  
Vol 96 (7) ◽  
pp. 2302-2310 ◽  
Author(s):  
Lena Ostrovsky ◽  
Richard C. Woodman ◽  
Derrice Payne ◽  
Diane Teoh ◽  
Paul Kubes
Keyword(s):  
Antithrombin Iii ◽  
Ischemia Reperfusion ◽  
Leukocyte Recruitment

scholarly journals Poldip2 controls leukocyte infiltration into the ischemic brain by regulating focal adhesion kinase-mediated VCAM-1 induction

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Lori N. Eidson ◽  
Qingzeng Gao ◽  
Hongyan Qu ◽  
Daniel S. Kikuchi ◽  
Ana Carolina P. Campos ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cerebral Ischemia ◽  
Focal Adhesion Kinase ◽  
Adhesion Molecules ◽  
Focal Adhesion ◽  
Vascular Inflammation ◽  
Leukocyte Recruitment ◽  
Ischemic Brain ◽  
Inflammatory Monocytes

AbstractStroke is a multiphasic process involving a direct ischemic brain injury which is then exacerbated by the influx of immune cells into the brain tissue. Activation of brain endothelial cells leads to the expression of adhesion molecules such vascular cell adhesion molecule 1 (VCAM-1) on endothelial cells, further increasing leukocyte recruitment. Polymerase δ-interacting protein 2 (Poldip2) promotes brain vascular inflammation and leukocyte recruitment via unknown mechanisms. This study aimed to define the role of Poldip2 in mediating vascular inflammation and leukocyte recruitment following cerebral ischemia. Cerebral ischemia was induced in Poldip2+/+ and Poldip2+/− mice and brains were isolated and processed for flow cytometry or RT-PCR. Cultured rat brain microvascular endothelial cells were used to investigate the effect of Poldip2 depletion on focal adhesion kinase (FAK)-mediated VCAM-1 induction. Poldip2 depletion in vivo attenuated the infiltration of myeloid cells, inflammatory monocytes/macrophages and decreased the induction of adhesion molecules. Focusing on VCAM-1, we demonstrated mechanistically that FAK activation was a critical intermediary in Poldip2-mediated VCAM-1 induction. In conclusion, Poldip2 is an important mediator of endothelial dysfunction and leukocyte recruitment. Thus, Poldip2 could be a therapeutic target to improve morbidity following ischemic stroke.

scholarly journals Protease nexin-1 deficiency increases mouse hindlimb neovascularisation following ischemia and accelerates femoral artery perfusion

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Sonia Selbonne ◽  
Celina Madjene ◽  
Benjamin Salmon ◽  
Yacine Boulaftali ◽  
Marie-Christine Bouton ◽  
...  
Keyword(s):  
Femoral Artery ◽  
Capillary Density ◽  
Leukocyte Recruitment ◽  
Lower Limbs ◽  
Artery Ligation ◽  
Angiogenic Balance ◽  
Important Player ◽  
Protease Nexin ◽  
Artery Perfusion

AbstractWe previously identified the inhibitory serpin protease nexin-1 (PN-1) as an important player of the angiogenic balance with anti-angiogenic activity in physiological conditions. In the present study, we aimed to determine the role of PN-1 on pathological angiogenesis and particularly in response to ischemia, in the mouse model induced by femoral artery ligation. In wild-type (WT) muscle, we observed an upregulation of PN-1 mRNA and protein after ischemia. Angiography analysis showed that femoral artery perfusion was more rapidly restored in PN-1−/− mice than in WT mice. Moreover, immunohistochemistry showed that capillary density increased following ischemia to a greater extent in PN-1−/− than in WT muscles. Moreover, leukocyte recruitment and IL-6 and MCP-1 levels were also increased in PN-1−/− mice compared to WT after ischemia. This increase was accompanied by a higher overexpression of the growth factor midkine, known to promote leukocyte trafficking and to modulate expression of proinflammatory cytokines. Our results thus suggest that the higher expression of midkine observed in PN-1- deficient mice can increase leukocyte recruitment in response to higher levels of MCP-1, finally driving neoangiogenesis. Thus, PN-1 can limit neovascularisation in pathological conditions, including post-ischemic reperfusion of the lower limbs.

scholarly journals Caveolin-1 Increases Proinflammatory Chemoattractants and Blood–Retinal Barrier Breakdown but Decreases Leukocyte Recruitment in Inflammation

2014 ◽  
Vol 55 (10) ◽  
pp. 6224 ◽  
Author(s):  
Xiaoman Li ◽  
Xiaowu Gu ◽  
Timothy M. Boyce ◽  
Min Zheng ◽  
Alaina M. Reagan ◽  
...  
Keyword(s):  
Leukocyte Recruitment ◽  
Blood Retinal Barrier ◽  
Caveolin 1 ◽  
Barrier Breakdown

scholarly journals Loss of p27 phosphorylation at Ser10 accelerates early atherogenesis by promoting leukocyte recruitment via RhoA/ROCK

2015 ◽  
Vol 84 ◽  
pp. 84-94 ◽  
Author(s):  
P. Molina-Sánchez ◽  
R. Chèvre ◽  
C. Rius ◽  
J.J. Fuster ◽  
V. Andrés
Keyword(s):  
Leukocyte Recruitment
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