scholarly journals Postcapillary Venule

2020 ◽  
Author(s):  
Keyword(s):  
Postcapillary Venule

scholarly journals The Mel 14 antibody binds to the lectin domain of the murine peripheral lymph node homing receptor.

1990 ◽  
Vol 110 (1) ◽  
pp. 147-153 ◽  
Author(s):  
B R Bowen ◽  
C Fennie ◽  
L A Lasky
Keyword(s):  
Monoclonal Antibody ◽  
Postcapillary Venule ◽  
Adhesive Interaction ◽  
Lectin Domain ◽  
Antibody Recognition ◽  
Peripheral Lymph ◽  
Chimeric Molecules ◽  
Carbohydrate Ligand

Murine and human leukocytes express surface glycoproteins, termed homing receptors (HRs), containing lectin-like, EGF-like (egf), and complement binding-like domains, that apparently endow these cells with the ability to home to peripheral lymph nodes (pln's) by virtue of an adhesive interaction with the pln postcapillary venule endothelium. The murine pln HR was initially characterized with a rat monoclonal antibody, Mel 14, that was specific for the murine form of the receptor. This work demonstrated that Mel 14 blocked the binding of murine lymphocytes to pln endothelium both in vitro and in vivo, a result consistent with the possibility that this monoclonal antibody recognizes a region of the HR that is involved with endothelium recognition and adhesion. In addition, this antibody also blocked the binding to the HR of PPME, a polyphosphomannan carbohydrate known to inhibit lymphocyte-pln endothelium interactions, suggesting that Mel 14 may recognize the lectin domain of the pln HR. Here we show that, while Mel 14 recognized truncated HR containing both the lectin and egf domains, antibody recognition was lost when the lectin domain alone was expressed. Chimeric molecules, in which regions of the lectin domain of the non-Mel 14-reactive human pln HR were replaced with homologous regions of the murine pln HR, demonstrated that the Mel 14 recognition site is within the NH2-terminal 53 amino acids of the lectin domain. These results suggest that the Mel 14 monoclonal antibody recognizes a determinant within the lectin domain of the pln HR whose conformation may be dependent upon the presence of the egf domain. Since Mel 14 efficiently blocks lymphocyte-endothelial interactions, these results support the hypothesis that the pln HR lectin domain may be directly involved with binding of lymphocytes to a carbohydrate ligand on the pln postcapillary venule endothelium.

scholarly journals A composite model of the human postcapillary venule for investigation of microvascular leukocyte recruitment

2013 ◽  
Vol 28 (3) ◽  
pp. 1166-1180 ◽  
Author(s):  
Holly M. Lauridsen ◽  
Jordan S. Pober ◽  
Anjelica L. Gonzalez
Keyword(s):  
Composite Model ◽  
Leukocyte Recruitment ◽  
Postcapillary Venule

scholarly journals Requirement for vasoactive amines for production of delayed-type hypersensitvity skin reactions.

1975 ◽  
Vol 142 (3) ◽  
pp. 732-747 ◽  
Author(s):  
R K Gershon ◽  
P W Askenase ◽  
M D Gershon
Keyword(s):  
T Cells ◽  
Mast Cells ◽  
Suppressive Effect ◽  
Delayed Type Hypersensitivity ◽  
Postcapillary Venule ◽  
Skin Reactions ◽  
Effector Cells ◽  
Homologous Antigen ◽  
T Cell Regulation ◽  
Pass Through

The skin sites of the mouse where delayed-type hypersensitivity (DTH) reactions are most easily elicited (foot pads and ears) are particularly rich in 5-hydroxytryptamine (5-HT)-containing mast cells. Since mice are deficient in circulating basophils, which play a role in at least some DTH reactions, we investigated the possibility that the mast cells were playing an important role in the evolution of the skin reactions of DTH in mice. We found that reserpine, a drug which depletes mast cells of 5-HT, abolished the ability of the mouse to make DTH reactions in the skin. The suppressive effect of reserpine could be partially blocked by monoamine oxidase inhibitors which prevent the degradation of 5-HT in the cytosol of the mast cell. Spleen cells of immune, reserpine-treated mice transferred DTH reactions to nonimmune mice normally, indicating that the reserpine treatment did not affect immune T cells. DTH reactions could not be transferred into reserpine-treated mice. We suggest that T cells are continually emigrating from the blood, through postcapillary venule endothelium, by a mechanism which does not depend on vasoactive amines. If they are appropriately immune and meet the homologous antigen in the tissue, they induce mast cells to release vasoactive amines which cause postcapillary venule endothelial cells to separate, allowing the egress from the blood of cells which ordinarily do not recirculate. The secondarily arriving vasoactive amine-dependent cells are responsible for the micro- and macroscopic lesions of DTH reactions. Chemotactic factors may also be involved in bringing cells to the DTH reaction sites but we propose that T-cell regulation of vasoactive amine-containing cells allows the effector cells to pass through the endothelial gates after they are called.

Behavior of postcapillary venule pericytes during postnatal angiogenesis

1992 ◽  
Vol 213 (1) ◽  
pp. 33-45 ◽  
Author(s):  
Lucio Diaz-Flores ◽  
Ricardo Gutierrez ◽  
Hilda Varela
Keyword(s):  
Postcapillary Venule

scholarly journals Identification of a novel exon and spliced form of Duffy mRNA that is the predominant transcript in both erythroid and postcapillary venule endothelium

Blood ◽  
1996 ◽  
Vol 87 (1) ◽  
pp. 378-385 ◽  
Author(s):  
S Iwamoto ◽  
J Li ◽  
T Omi ◽  
S Ikemoto ◽  
E Kajii
Keyword(s):  
Northern Blotting ◽  
Major Product ◽  
The Body ◽  
Postcapillary Venule ◽  
Start Position ◽  
Erythroleukemia Cells ◽  
Rapid Amplification ◽  
Erythroleukemic Cell ◽  
Ribonuclease Protection ◽  
Novel Exon

The Duffy gene has been shown not to be split by introns, even in its 5′ untranslated region, and to be expressed not only in erythroid but in postcapillary venule endothelium of almost every organ in the body. To further investigate the transcriptional start position in erythroid and postcapillary venule endothelium, we performed 5′-rapid amplification of cDNA ends (5′-RACE). While every positive clone of 5′- RACE encoded the identical sequence of previously identified cDNA downstream from nucleotide 203, the upstream sequences were different. The upstream sequences corresponded to the sequence from nucleotide - 279 to -308/-357 in erythroblasts and from -279 to -355/-383 in lung and were regarded as comprising a novel exon. This novel exon encoded seven residues initiated with a methionine, linked to nucleotide 203 in- frame and in agreement with the GT-AG splicing rule. The major erythroid transcriptional start position was identified in human erythroleukemia cells by primer extension and in bone marrow by ribonuclease protection analysis at 34 bases upstream from the first ATG codon. Distinctively, in lung and kidney, the transcription was started at 82 bases upstream from the ATG. Both Northern blotting and reverse transcription-polymerase chain reaction followed by Southern analysis indicated a predominance of the novel spliced form of mRNA of about 50- to 200-fold comparing with the unspliced form, in every studied organ and erythroid lineage cells. The spliced form of cDNA has been transfected into a human erythroleukemic cell line, K562, and the expressed protein reacted with Duffy-specific murine monoclonal antibody Fy6. These studies indicate that the product from the spliced form of mRNA is the major product of the Duffy gene in the erythroid lineage and postcapillary venule endothelium.

scholarly journals Local Secretion of Urocortin 1 Promotes Microvascular Permeability during Lipopolysaccharide-Induced Inflammation

Endocrinology ◽  
2009 ◽  
Vol 150 (12) ◽  
pp. 5428-5437 ◽  
Author(s):  
Elizabeth L. Cureton ◽  
Alexander Q. Ereso ◽  
Gregory P. Victorino ◽  
Brian Curran ◽  
Daniel P. Poole ◽  
...  
Keyword(s):  
Immune Cell ◽  
Signal Transduction Pathway ◽  
Fold Increase ◽  
Microvascular Permeability ◽  
Hydraulic Permeability ◽  
Receptor Subtypes ◽  
Receptor Blockade ◽  
Postcapillary Venule ◽  
Urocortin 1

Abstract Urocortin 1 (Ucn1) is a neuropeptide that regulates vascular tone and is implicated in both the vascular and immune cell-mediated responses to inflammation. The role of Ucn1 in regulating microvascular permeability has not been determined. We hypothesized that local Ucn1 release promotes microvascular permeability and that this effect augments the local gastrointestinal vascular response to lipopolysaccharide (LPS)-induced systemic inflammation. We measured hydraulic (Lp) and macromolecule permeability in mesenteric venules. We show that a continuous infusion of 10−7m Ucn1 in a postcapillary venule increased Lp 2-fold over baseline, as did LPS-induced inflammation. However, simultaneous infusion of Ucn1 and LPS markedly increased Lp by 7-fold. After local knockdown of Ucn1 using RNA interference, infusion of Ucn1 with LPS resulted in return to 2-fold increase, confirming that Ucn1 synergistically augments hydraulic permeability during inflammation. LPS and Ucn1 treatment also resulted in increased numbers of interstitial microspheres, which colocalized with CD31+ immune cells. Ucn1 activity is mediated through two receptor subtypes, CRH-R1 and CRH-R2. CRH-R1 receptor blockade exacerbated, whereas CRH-R2 receptor blockade decreased the LPS-induced increase in Lp. Finally, treatment with the c-JUN N-terminal kinase (JNK) antagonist SP600125 during infusion of LPS, but not Ucn1, decreased Lp. These findings suggest that Ucn1 increases microvascular permeability and acts synergistically with LPS to increase fluid and macromolecule losses during inflammation. Knockdown of endogenous Ucn1 during inflammation attenuates synergistic increases in Lp. Ucn1’s effect on Lp is partially mediated by the CRH-R2 receptor and acts independently of the c-JUN N-terminal kinase signal transduction pathway.

Reperfusion-induced changes in capillary perfusion and filtration: effects of hypercholesterolemia

1999 ◽  
Vol 277 (2) ◽  
pp. H669-H675 ◽  
Author(s):  
Norman R. Harris
Keyword(s):  
Potential Role ◽  
Microvascular Dysfunction ◽  
Capillary Perfusion ◽  
Postcapillary Venule ◽  
Fluid Filtration ◽  
Median Increase ◽  
Cell Velocity ◽  
Before And After ◽  
Red Blood Cell Velocity ◽  
Induced Changes

Fluid filtration rate ( J v/ S) and red blood cell velocity ( V RBC) in individual mesenteric capillaries of normocholesterolemic (NC) and hypercholesterolemic (HC) rats were measured before and after ischemia and reperfusion (I/R). In NC rats, a correlation was found between baseline J v/ Sand the percent of the feeding arteriole length that was paired (<15 μm) with a postcapillary venule (A-V pairing), but not in the HC group. Additionally, in NC rats only, a correlation was found between baseline V RBC and A-V pairing. In capillaries in which A-V pairing was substantial (>20%), V RBCdropped after reperfusion in the HC group (54% of baseline; P < 0.05), but not in the NC group (79%). The decrease in V RBC in HC rats could be attenuated by a P-selectin antibody (PB1.3). PB1.3 was also able to attenuate the increase in I/R-induced capillary J v/ Sin HC rats (median increase = 1.26-fold vs. 1.53-fold without PB1.3). These data suggest a role for A-V pairing in capillary perfusion in NC rats and a potential role for P-selectin in I/R-induced microvascular dysfunction in HC rats.

scholarly journals Contractile proteins in pericytes. I. Immunoperoxidase localization of tropomyosin.

1985 ◽  
Vol 100 (5) ◽  
pp. 1379-1386 ◽  
Author(s):  
N C Joyce ◽  
M F Haire ◽  
G E Palade
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
High Concentration ◽  
Postcapillary Venule ◽  
Nonmuscle Cells ◽  
Dependent Protein ◽  
Contraction Regulation

In these studies we have compared the relative amounts and isoforms of tropomyosin in capillary and postcapillary venule pericytes, endothelial cells, and vascular smooth muscle cells in four rat microvascular beds: heart, diaphragm, pancreas, and the intestinal mucosa. The results, obtained by in situ immunoperoxidase localization, indicate that (a) tropomyosin is present in capillary and postcapillary venule pericytes in relatively high concentration; (b) the tropomyosin content of pericytes appears to be somewhat lower than in vascular smooth muscle cells but higher than in endothelia and other vessel-associated cells; and (c) pericytes, unlike endothelia and other nonmuscle cells, contain detectable levels of tropomyosin immunologically related to the smooth muscle isoform. These results and our previous findings concerning the presence of a cyclic GMP-dependent protein kinase (Joyce, N., P. DeCamilli, and J. Boyles, 1984, Microvasc. Res. 28:206-219) in pericytes demonstrate that these cells contain significant amounts of at least two proteins important for contraction regulation. Taken together, the evidence suggests that pericytes are contractile elements related to vascular smooth muscle cells, possibly involved, as are the latter, in the regulation of blood flow through the microvasculature.

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