Disease relevance of Venules

• Chemerin expression was selectively detected on the luminal side of high endothelial venules in secondary lymphoid organs and in dermal endothelial vessels of lupus erythematosus skin lesions [1].
• Receptor binding sites for substance P, but not substance K or neuromedin K, are expressed in high concentrations by arterioles, venules, and lymph nodules in surgical specimens obtained from patients with ulcerative colitis and Crohn disease [2].
• CD8+ T cells from patients with acute multiple sclerosis display selective increase of adhesiveness in brain venules: a critical role for P-selectin glycoprotein ligand-1 [3].
• Arterioles were appreciably constricted in isocapnic acidosis when NOS, but not COX, was suppressed, whereas venules showed no constrictive response even when both enzymes were inhibited [4].
• Extending the period of these treatments to 90 days resulted in producing hepatic fibrosis developing around individual hepatocytes in the terminal hepatic venule areas and portal areas, accompanied by an increase in hepatic hydroxyproline content [5].

Psychiatry related information on Venules

• Activated MMP-9 (1 microg g(-1)) significantly prolonged the latency period of inducing platelet plug formation in mesenteric venules [6].

High impact information on Venules

• L-selectin mediates lymphocyte homing by facilitating lymphocyte adhesion to addressins expressed in the high endothelial venules (HEV) of secondary lymphoid organs [7].
• Neutrophils roll on this selectin under flow conditions similar to those found in postcapillary venules [8].
• In addition, activation of lymphocytes by physiological stimuli enhanced LAM-1-dependent binding to high endothelial venules [9].
• It is proposed that functional binding of lymphocytes to lymph node high endothelial venules might involve the ubiquitinated region of the receptor; if true, cell surface ubiquitin could play a more general role in cell-cell interaction and adhesion [10].
• In the thymus, CCL19 is predominantly localized in the medulla including endothelial venules [11].

Chemical compound and disease context of Venules

• RESULTS: FNIII14 inhibited the integrin alpha4beta1-mediated B lymphoma Ramos cell adhesion to VCAM-1 on venule endothelial cells, as well as to FN [12].
• A skin biopsy specimen of urticarial and purpuric lesions demonstrated leukocytoclastic vasculitis and granular deposition of C3 and Clq in the basement membrane with IgA, IgM, C3, and Clq in postcapillary venules [13].
• In one of these patients skin biopsies demonstrated granular deposits of IgM, C3, C4, and the hepatitis B surface antigen (HBsAg) and electron-dense deposits of aggregated 20-nm particles resembling HBsAg in postcapillary venules [14].
• Systemic hypoxia (breathing 8% O2 for 3 min) induced a fall in arterial pressure and tachycardia, together with constriction in some arterioles and venules of each section of the vascular tree and dilatation in others [15].
• In this study the effects of SNP and SIN-1 on thrombus formation in rat cerebral arterioles and venules in vivo were assessed using a helium-neon (He-Ne) laser [16].

Biological context of Venules

• Two molecules associated with cell adhesion were studied: MECA-325, a murine lymph node high endothelial venule marker; and MALA-2, the murine homologue of intercellular adhesion molecule 1 [17].
• The objective of this study was to define the nature, magnitude, and mechanisms of histamine-induced leukocyte-endothelial cell interactions in postcapillary venules of the rat mesentery using intravital microscopic techniques [18].
• The density of histamine binding sites was characteristically high in venules; it occurred to a much lesser extent in arterioles, veins, and muscular arteries whereas capillaries and aorta showed the lowest values [19].
• Increasing endogenous H(2)O(2) levels in mice decreases exocytosis and platelet rolling on venules in vivo [20].
• Intravital microscopy was used to examine hemodynamic parameters, leukocyte rolling and adhesion, and microvascular permeability in cremasteric postcapillary venules in wild-type mice and in IL-10-deficient (IL-10(-/-)) mice exposed to lipopolysaccharide (LPS) [21].

Anatomical context of Venules

• alpha(1,3)Fucosylated oligosaccharides represent components of leukocyte counterreceptors for E- and P-selectins and of L-selectin ligands expressed by lymph node high endothelial venules (HEV) [22].
• Application of anti-Ly-22 in the in vitro binding assay shows inhibition of binding of lymphocytes to high endothelial venules (HEVs) [23].
• In addition to attracting B cells, BLC expression led to development of lymph node-like structures that contained B and T cell zones, high endothelial venules, stromal cells, and the chemokine SLC [24].
• Using a parallel plate flow chamber designed to approximate physiologic flow in postcapillary venules, we have characterized a rolling interaction between lymphoid cells and adherent primary and cultured endothelial cells that is not selectin mediated [25].
• The CCR7 ligand elc (CCL19) is transcytosed in high endothelial venules and mediates T cell recruitment [26].

Associations of Venules with chemical compounds

• Intravital microscopy showed that BLT1 signaling induced rapid integrin-mediated arrest of rolling effector and central memory cells in postcapillary venules [27].
• Carbohydrate structural analysis showed that 6-sulfo sialyl Lewis X, a dominant ligand for L-selectin, was almost completely absent from the high endothelial venules of these mutant mice, whereas the amount of unsulfated sialyl Lewis X was much greater [28].
• Like VPF, histamine and serotonin also stimulated ferritin extravasation across venules by way of VVOs [29].
• In the mesenteric venules of the mice treated with anti-PECAM-1 mAb, leukocytes were frequently seen in association with the luminal surface of the vessel, but did not appear to emigrate [30].
• Leukocyte rolling in postcapillary venules of inflamed tissues is reduced in L-selectin-deficient mice and mice treated with L-selectin blocking antibodies, but the glycoprotein ligand for L-selectin in inflamed venules is unknown [31].

Gene context of Venules

• Only the lymphatic endothelia and some high endothelial venules expressed FLT4 mRNA in adult human tissues [32].
• Disparate lymphoid chemokine expression in mice and men: no evidence of CCL21 synthesis by human high endothelial venules [33].
• T-cell homing to secondary lymphoid tissues generally depends on chemokine-induced firm adhesion in high endothelial venules (HEVs) and is primarily mediated through the CC chemokine receptor 7 (CCR7) on lymphocytes [33].
• CLA initiates skin homing by mediating E-selectin-dependent tethering and rolling within cutaneous venules, but the specific roles of CCR4 and CCR10 are unclear [34].
• Similar responses were seen in the central venules, however, in the sinusoids the increased number of stationary leukocytes seen in response to 4 hours of TNF-alpha stimulation in the wild-type mice was not reduced in P-selectin-deficient mice with or without the alpha(4)-integrin antibody [35].

Analytical, diagnostic and therapeutic context of Venules

• After treatment with tumor necrosis factor (TNF)-alpha for 2 h, approximately 24% of all passing leukocytes roll in cremaster venules of wild-type and P-selectin gene-deficient mice [36].
• Chenodeoxycholic acid perfusion caused villous denudation and shortening of and ultrastructural damage to villous venules [37].
• This was accomplished by superfusing a cat mesenteric preparation with inhibitors of NO production, NG-monomethyl-L-arginine (L-NMMA) or NG-nitro-L-arginine methyl ester (L-NAME), and observing single (30-microns diameter) venules by intravital video microscopy [38].
• Molecular cloning and functional analysis of SUT-1, a sulfate transporter from human high endothelial venules [39].
• Norepinephrine (NE) was added to the cremaster bath to produce intermediate reductions in diameter of large arterioles and venules (55% and 38% of maximum constriction, respectively) [40].

References