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Thursday, August 6, 2020 | History

3 edition of Endothelial-derived CAP37 found in the catalog.

Endothelial-derived CAP37

Taunia Denise Lee

Endothelial-derived CAP37

Characterization and determination of its role in monocyte/endothelial interactions

by Taunia Denise Lee

  • 222 Want to read
  • 15 Currently reading

Published by [s.n.] .
Written in

  • Antibody Specificity,
  • Atherosclerosis,
  • Cell Adhesion,
  • Endotelium, Vascular,
  • Inflammation Mediators,
  • Leukocytes,
  • Monocytes,
  • cytology,
  • immunology

  • The Physical Object
    FormatUnknown Binding
    ID Numbers
    Open LibraryOL10344977M
    ISBN 100493472916
    ISBN 109780493472911

    - Free download as PDF File .pdf), Text File .txt) or read online for free. T lymphocyte recruitment by interleukin-8 (IL-8). ILinduced degranulation of neutrophils releases potent chemoattractants for human T lymphocytes both in vitro and in vivo. Pub.

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Endothelial-derived CAP37 by Taunia Denise Lee Download PDF EPUB FB2

Endothelial-derived CAP Characterization and determination of its role in monocyte/endothelial interactions [Taunia Denise Lee] on *FREE* shipping on qualifying offers. Cationic antimicrobial protein of 37 kd (CAP37), originally isolated from human neutrophils, is an important multifunctional inflammatory mediator.

Here we describe its localization within the vascular endothelium associated with atherosclerotic plaques. Evidence from in vitroimmunocytochemical, Northern blot, and reverse transcriptase-polymerase chain reaction analysis indicates that CAP37 is induced in endothelial Cited by: CAP37, a Novel Inflammatory Mediator: Its Expression in Endothelial Cells and Localization to Atherosclerotic Lesions.

Endothelial-derived CAP37 shows sequence identity with an extensive region of neutrophil-derived CAP This is the first demonstration of endogenous endothelial CAP37, confirmed by. In this example of atherosclerosis we speculate that CAP37 (either platelet, PMN, or endothelial derived) is responsible for endothelial cell contraction and permeability7, 28 as well as monocyte migration into the intima.

Our immunohistochemical data on atherosclerotic lesions demonstrate that the expression of CAP37 protein is not confined solely to the endothelium but is also detected Cited by: Since CAP37 is a potent activator of endothelial cells and monocytes, two of the key cellular components of the atherosclerotic plaque, this study was undertaken to determine whether CAP37 had.

Endothelial-derived gene EG-1 was discovered in Although first cloned from a human endothelial cell cDNA library (Angiogenesis), EG-1’s transcript has been shown to be present in other cell types as well, particularly in epithelial cells (Epithelial Tumors).

The calculated mass of EG-1 is 19, Da based on amino acid sequence alone, whereas the native complete protein is ~22 kDa.

Endothelial-derived gene EG-1 was discovered in Although first cloned from a human endothelial cell cDNA library (Angiogenesis), EG-1’s transcript has been shown to be present in other cell types as well, particularly in epithelial calculated mass of EG-1 is 19, Da based on amino acid sequence alone, whereas the native complete protein is ~22 kDa.

An endothelial dysfunction linked to an imbalance in the synthesis and/or the release of these various endothelial factors may explain the initiation of cardiovascular pathologies (from hypertension to atherosclerosis) or their development and perpetuation.

The endothelium, a monolayer of endothelial cells, constitutes the inner cellular lining of the blood vessels (arteries, veins and capillaries) and the.

n/a Ensembl ENSG ENSG n/a UniProt P n/a RefSeq (mRNA) NM_ n/a RefSeq (protein) NP_ n/a Location (UCSC) Chr – Mb n/a PubMed search n/a Wikidata View/Edit Human Azurocidin also known as cationic antimicrobial protein CAP37 or heparin-binding protein (HBP) is a protein that in humans is encoded by the AZU1 gene.

Contents 1 Aliases: AZU1, AZAMP, AZU, CAP37, HBP, HUMAZUR. Endothelium is a single layer of squamous endothelial cells that line the interior surface of blood vessels, and lymphatic vessels. The endothelium forms an interface between circulating blood or lymph in the lumen and the rest of the vessel wall.

Endothelial cells form the barrier between vessels and tissue and control the flow of substances and fluid into and out of a on: Lining of the inner surface of blood. Endothelial cells release phenotypically and quantitatively distinct MPs in activation and apoptosis.

As a result, MPs are sufficiently distinguished each other on their ability to contain some antigen presentation [26] and inner components, i.e.

matrix metalloproteinases (MMP)-2, MMP-9, MT1-MMP, chromatin, active molecules (heat shock proteins), some hormones (angiotensin II), growth factors Cited by: 1.

/ Role of endothelial cell-derived angptl2 in vascular inflammation leading to endothelial dysfunction and atherosclerosis progression. In: Arteriosclerosis, Thrombosis, and Vascular Biology.

; Vol. 34, No. These cells have been reported to stabilize and enhance human endothelial-derived vessels. 19,28 For example, Melero Martin et al 29 showed that co-implantation of ECFCs with either bone marrow-derived or cord blood-derived MSCs into immunodeficient mice resulted in the formation of vascular networks after one week, compared to no microvessel.

Nitric oxide, prostacyclin, endothelin (ET) and endothelial‐derived hyperpolarizing factor are powerful vasoactive substances released from the endothelium in response to both humoral and mechanical stimuli, and can profoundly affect both the function and structure of the underlying vascular smooth muscle.

Nitric oxide is a profound by: The endothelium is capable of remarkable plasticity. In the embryo, primitive endothelial cells differentiate to acquire arterial, venous or Cited by: Although diabetes is the most common cause of end-stage renal disease (ESRD) worldwide, most people with diabetic nephropathy will never develop ESRD but will instead die of cardiovascular (CV) disease (CVD).

The first evidence of kidney injury in diabetes is often microalbuminuria, itself also an independent risk marker for CVD. Although the two processes are Cited by: P1: FRK Febru Annual Reviews ARFM Annual Review of Immunology Vol Annu. Rev. Immunol. Downloaded from by HINARI on 09/01/ Preface This monograph contains the contributions of invited speakers and participants at the NATO Advanced Study Institute on Disease Markers in Exhaled Breath: Basic Mechanisms and Clinical Applications, held at the Knossos Royal Village in Crete, Greece, June July 1, Endothelial cells are the source of some potent molecules that influence the contractile state of vascular smooth muscle cells, including the vasodilators nitric oxide (NO), prostaglandin (PG)PGI2, endothelial-derived hyperpolariz-ing factor (EDHF), adrenomedullin, and the potent vasoconstrictor, endothelin PGE2, made predominantly in.

EDRF endothelial-derived relaxing factor eNOS endothelial nitric oxide synthase hs-CRP high-sensitivity C-reactive protein IL interleukin KLF2 Kruppel-like factor-2 LDL low-density lipoprotein MEKK3 mitogen-activated protein kinase/extracellular-regulated ki-nase kinase kinase-3 miRNA micro-RNA Nrf2 nuclear factor erythroid 2-related factor1 Updated: 2/5/ Alfred Ayala Aldrich Division of Surgical Research/Shock-Trauma Research Laboratories Rhode Island Hospital / the Alpert School of Medicine at Brown Univer.Cafestol Inhibits Cyclic-Strain-Induced Interleukin-8, Intercellular Adhesion Molecule-1, and Monocyte Chemoattractant Protein-1 Production in Vascular Endothelial Cells.

PubMed C.