ArticleJournal of leukocyte biology2012
Receptor cleavage and P-selectin-dependent reduction of leukocyte adhesion in the spontaneously hypertensive rat.
Article in Journal of leukocyte biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it.
- SELP genetic polymorphisms may contribute to the pathogenesis of coronary heart disease and myocardial infarction: a meta-analysis.Molecular biology reports · 2014Pooled it
- Storage Temperature Affects Platelet Activation and Degranulation in Response to Stimuli.International journal of molecular sciences · 2025Article
- Platelet-derived circulating soluble P-selectin is sufficient to induce hematopoietic stem cell mobilization.Stem cell research & therapy · 2023Article
- Endothelial Cells Exhibit Two Waves of P-selectin Surface Aggregation Under Endotoxic and Oxidative Conditions.The protein journal · 2019Article
- Pancreatic source of protease activity in the spontaneously hypertensive rat and its reduction during temporary food restriction.Microcirculation (New York, N.Y. : 1994) · 2019Article
- IGF-1 receptor cleavage in hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2018Article
- Mechanisms of I/R-Induced Endothelium-Dependent Vasodilator Dysfunction.Advances in pharmacology (San Diego, Calif.) · 2018Review
- A high-salt diet enhances leukocyte adhesion in association with kidney injury in young Dahl salt-sensitive rats.Hypertension research : official journal of the Japanese Society of Hypertension · 2017Article
- Arterial Hypertension Aggravates Innate Immune Responses after Experimental Stroke.Frontiers in cellular neuroscience · 2015Article
- Proteolytic receptor cleavage in the pathogenesis of blood rheology and co-morbidities in metabolic syndrome. Early forms of autodigestion.Biorheology · 2015Review
- Cleavage and reduced CD36 ectodomain density on heart and spleen macrophages in the spontaneously hypertensive rat.Microvascular research · 2014Article
- Soluble adhesion molecules as markers for sepsis and the potential pathophysiological discrepancy in neonates, children and adults.Critical care (London, England) · 2014Review
- The autodigestion hypothesis for shock and multi-organ failure.Annals of biomedical engineering · 2014Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
The SHR, a genetic model for hypertension and the metabolic syndrome, has attenuated leukocyte adhesion to the postcapillary endothelium by an unknown mechanism. Based on recent evidence of elevated levels of MMPs in plasma and on microvascular endothelium of the SHR with cleavage of several receptor types, we hypothesize that the reduced leukocyte-endothelial interaction is a result of enhanced proteolytic cleavage of P-selectin on the postcapillary endothelium and PSGL-1 on leukocytes. The attenuated rolling interactions of SHR leukocytes with the endothelium were restored by chronic treatment with a broad-spectrum MMP inhibitor (CGS) for 24 weeks. The SHR MMP levels, in plasma and mesentery, as well as the systolic blood pressure, decreased significantly with treatment. In the SHR mesentery, labeling of P-selectin in the postcapillary venules by immunohistochemistry demonstrated, on average, a 31% lower extracellular P-selectin density compared with the normotensive WKY. A significantly lower extracellular PSGL-1 density on the membranes of SHR neutrophils compared with the WKY also supported our hypothesis. In vivo stimulation of the mesenteric postcapillary venules with histamine demonstrated that the SHR had an attenuated response, as measured by leukocyte rolling velocity on the endothelium. The reduced P-selectin and PSGL-1 density, on SHR postcapillary endothelium and on SHR leukocytes, respectively, was restored significantly by chronic MMP inhibition. The impaired ability of SHR leukocytes to reduce rolling velocity upon inflammatory stimulation led to fewer firmly adhered leukocytes to the endothelium as a contributor to immune suppression.
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