scholarly journals F-actin-rich contractile endothelial pores prevent vascular leakage during leukocyte diapedesis through local RhoA signalling

2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Niels Heemskerk ◽  
Lilian Schimmel ◽  
Chantal Oort ◽  
Jos van Rijssel ◽  
Taofei Yin ◽  
...  
Keyword(s):  
Vascular Leakage ◽  
Endothelial Pores

Relation between intestinal iNOS activation, epithelial cell viability and vascular leakage following Helicobacter pylori endotoxin challenge

2004 ◽  
Vol 42 (05) ◽  
Author(s):  
Z Szepes ◽  
É Morschl ◽  
J Egresits ◽  
F László ◽  
J Lonovics
Keyword(s):  
Helicobacter Pylori ◽  
Epithelial Cell ◽  
Cell Viability ◽  
Vascular Leakage ◽  
Endotoxin Challenge

Delayed and prolonged vascular leakage in inflammation: the effects of dehydromonocrotaline on blood vessels in the rat cremaster

Pathology ◽  
1976 ◽  
Vol 8 (1) ◽  
pp. 7-20 ◽  
Author(s):  
J.V. Hurley ◽  
Marjorie V. Jago
Keyword(s):  
Blood Vessels ◽  
Vascular Leakage

Roles of the Hypoximir microRNA-424/322 on Acute Hypoxia and Hypoxia-Induced Pulmonary Vascular Leakage

2018 ◽  
Author(s):  
Shih-Hung Tsai ◽  
Po-Hsun Huang ◽  
Yu-Juei Hsu ◽  
Yen-Wen Chen ◽  
Jen-Chun Wang ◽  
...  
Keyword(s):  
Acute Hypoxia ◽  
Vascular Leakage

Creation of retinal vein occlusion model in cynomolgusmonkeys and determination of its pathological features

2020 ◽  
Vol 17 ◽  
Author(s):  
Satoshi Inagaki ◽  
Masamitsu Shimazawa ◽  
Wataru Otsu ◽  
Tomoaki Araki ◽  
Yosuke Numata ◽  
...  
Keyword(s):  
Growth Factors ◽  
Retinal Vein Occlusion ◽  
Vascular System ◽  
Retinal Thickness ◽  
Chronic Phase ◽  
Vascular Leakage ◽  
Foveal Avascular Zone ◽  
Retinal Edema ◽  
Vein Occlusion ◽  
Angiopoietin 2

Objective: A retinal vein occlusion (RVO) is a relatively common retinal vascular disorder especially in the elder-ly. Many experiments have been performed on patients with a RVO but performing any type of experiments and especially longitudinal experiments on humans is difficult if not impossible on ethical grounds. Therefore, we have created a retinal vein occlusion (RVO) model by laser irradiation of cynomolgus monkeysafter an intravenous injection of rose bengal. Weevaluated the pathological changes of the retina, and the effects of ranibizumab, an anti-vascular endothelial growth factor (VEGF) antibody, on the characteristics of the RVO. Methods: The integrity of the vascular system was evaluated by fluorescein angiography (FA), and the retinal thickness and volume were determined by optical coherence tomography (OCT). The cytokines and growth factors in the aqueous humor were identified by multiplex profiling. Results: Our results showed that ranibizumab decreased the degree of vascular leakage and retinal edema at 1-3 days (acute phase) and 3-7 days (subacute phase), and suppressed foveal thinning at 28-42 days (chronic phase) after the laser irradia-tion. Ranibizumab also decreased the area of the foveal avascular zone, and the area was negatively and significantly corre-lated with the thickness of the ganglion cell layer (GCL) complex. Furthermore, ranibizumab reduced the increased expres-sion of VEGF in the aqueous humour, but did not affect the expressions of interleukin-6 (IL-6), monocyte chemotactic pro-tein-1 (MCP-1), angiopoietin-1 (ANG-1), or angiopoietin-2 (ANG-2).Thesefindings suggest that ranibizumab attenuates the retinal edema and subsequent retinal atrophy in partby neutralizing VEGF. However, other cytokines and growth factors were also affected by the ranibizumab which suggests that not only VEGF but also other unidentified agents might play a role in the pathogenesis of the RVO. Conclusion: We have created a non-human primate RVO model, which resembles the clinical RVO pathology. In this model, an injection of ranibizumab leads to a reduction in the vascular leakage and the retinal thickness and volume by blockingthe expression of VEGF. Our model might be useful for investigating the pathological mechanisms of RVOs and explore new therapeutic agents for RVO.

scholarly journals Capsaicin-Sensitive Peptidergic Sensory Nerves Are Anti-Inflammatory Gatekeepers in the Hyperacute Phase of a Mouse Rheumatoid Arthritis Model

2021 ◽  
Vol 22 (4) ◽  
pp. 1682
Author(s):  
Bálint Botz ◽  
Gábor Kriszta ◽  
Kata Bölcskei ◽  
Ádám István Horváth ◽  
Attila Mócsai ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Morphological Changes ◽  
Vascular Leakage ◽  
Sensory Nerves ◽  
Clinical Severity ◽  
Severity Scores ◽  
Clinical Scoring ◽  
Anti Inflammatory ◽  
Ros Burst

Capsaicin-sensitive peptidergic sensory nerves play complex, mainly protective regulatory roles in the inflammatory cascade of the joints via neuropeptide mediators, but the mechanisms of the hyperacute arthritis phase has not been investigated. Therefore, we studied the involvement of these afferents in the early, “black box” period of a rheumatoid arthritis (RA) mouse model. Capsaicin-sensitive fibres were defunctionalized by pretreatment with the ultrapotent capsaicin analog resiniferatoxin and arthritis was induced by K/BxN arthritogenic serum. Disease severity was assessed by clinical scoring, reactive oxygen species (ROS) burst by chemiluminescent, vascular permeability by fluorescent in vivo imaging. Contrast-enhanced magnetic resonance imaging was used to correlate the functional and morphological changes. After sensory desensitization, both early phase ROS-burst and vascular leakage were significantly enhanced, which was later followed by the increased clinical severity scores. Furthermore, the early vascular leakage and ROS-burst were found to be good predictors of later arthritis severity. We conclude that the anti-inflammatory role of peptidergic afferents depends on their activity in the hyperacute phase, characterized by decreased cellular and vascular inflammatory components presumably via anti-inflammatory neuropeptide release. Therefore, these fibres might serve as important gatekeepers in RA.

scholarly journals Platelet and Erythrocyte Extravasation across Inflamed Corneal Venules Depend on CD18, Neutrophils and Mast Cell Degranulation

2021 ◽  
Vol 22 (14) ◽  
pp. 7360
Author(s):  
Angie De La Cruz ◽  
Aubrey Hargrave ◽  
Sri Magadi ◽  
Justin A. Courson ◽  
Paul T. Landry ◽  
...  
Keyword(s):  
Mast Cell ◽  
Cell Types ◽  
Mast Cell Degranulation ◽  
Wild Type ◽  
Delayed Wound Healing ◽  
Corneal Epithelial ◽  
Corneal Abrasion ◽  
Low Levels ◽  
Endothelial Pores

Platelet extravasation during inflammation is under-appreciated. In wild-type (WT) mice, a central corneal epithelial abrasion initiates neutrophil (PMN) and platelet extravasation from peripheral limbal venules. The same injury in mice expressing low levels of the β2-integrin, CD18 (CD18hypo mice) shows reduced platelet extravasation with PMN extravasation apparently unaffected. To better define the role of CD18 on platelet extravasation, we focused on two relevant cell types expressing CD18: PMNs and mast cells. Following corneal abrasion in WT mice, we observed not only extravasated PMNs and platelets but also extravasated erythrocytes (RBCs). Ultrastructural observations of engorged limbal venules showed platelets and RBCs passing through endothelial pores. In contrast, injured CD18hypo mice showed significantly less venule engorgement and markedly reduced platelet and RBC extravasation; mast cell degranulation was also reduced compared to WT mice. Corneal abrasion in mast cell-deficient (KitW-sh/W-sh) mice showed less venule engorgement, delayed PMN extravasation, reduced platelet and RBC extravasation and delayed wound healing compared to WT mice. Finally, antibody-induced depletion of circulating PMNs prior to corneal abrasion reduced mast cell degranulation, venule engorgement, and extravasation of PMNs, platelets, and RBCs. In summary, in the injured cornea, platelet and RBC extravasation depends on CD18, PMNs, and mast cell degranulation.

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