Basic fibroblast growth factor mediates neointimal formation in porcine aortic explants. by Sandra J. Daley

Cover of: Basic fibroblast growth factor mediates neointimal formation in porcine aortic explants. | Sandra J. Daley

Published by National Library of Canada = Bibliothèque nationale du Canada in Ottawa .

Written in English

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SeriesCanadian theses = Thèses canadiennes
The Physical Object
Pagination142 leaves.
Number of Pages142
ID Numbers
Open LibraryOL18629975M
ISBN 100612279022

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Basic Fibroblast Growth Factor Mediates Neointimal Formation in Porcine Aortic Explants Sandra J. Daley A thesis submitted in codormity with the requirements for the degree of Doctor of Philosophy Graduate Department of Cellular and Molecular Pathology University of Toronto O Request PDF | Basic fibroblast growth factor decreases elastin gene transcription in aortic smooth muscle cells | The extracellular matrix (ECM) protein elastin plays an essential role in the   ECs produce a number of growth factors involved in neointimal formation in organ culture and SMC proliferation in monolayer cell culture, including platelet-derived growth factor (PDGF) A and B, novel PDGF family members PDGF-C and PDGF-D with calculated molecular masses and kDa, respectively, acidic fibroblast growth factor (aFGF We previously showed that conditioned media from intact cultures induce neointimal formation in denuded aortic explants, and we speculated that basic fibroblast growth factor was the endothelial Fibroblast growth factor-2 acts through betaglycan which is known to bind both transforming growth factor-β and fibroblast growth factor-2 at different locations on the :// Proliferation of coronary smooth muscle cells (cSMCs) with subsequent formation of intimal thickening is an important event in the development of arteriosclerosis and restenosis after PTCA 1 and stent implantation.

2 Basic fibroblast growth factor (bFGF) synthesized by vascular SMC 3 4 is a powerful mitogen for SMC replication during atherogenesis 5 and in response to vessel wall injury.

6 The proliferative response may be divided into four phases: (1) medial smooth muscle cell (SMC) proliferation, which begins 24 h post injury, is associated with SMC death as well as the release of basic fibroblast growth factor (FGF-2), angiotensin II (AngII) and α-adrenergic hormones, (2) migration of SMCs across the internal elastic lamina Basic fibroblast growth factor modulates the mitogenic potency of the platelet-derived growth factor (PDGF) isoforms by specific upregulation of the PDGF alpha receptor in vascular smooth muscle cells.

Growth of aortic explants and arteriosclerosis. Neointimal formation in the porcine aortic organ culture. Cellular dynamics Possible sites for cGMP-mediated inhibition of VSMC proliferation.

(A) Early signal transduction events. Peptide growth factors, for example, platelet-derived growth factor (PDGF) and basic fibroblast growth factor (bFGF, FGF-2) stimulate tyrosine phosphorylation of receptors (PY) and couple to effector mechanisms, which include phospholipase C (PLC) isoforms, which generate the second   Platelet-derived growth factor (PDGF) was identified more than three decades ago as a serum growth factor for fibroblasts, smooth muscle cells (SMCs), and glia cells (Kohler and Lipton ; Ross et al.

; Westermark and Wasteson ).Human PDGF was originally identified as a disulfide-linked dimer of two different polypeptide chains, A and B, separable using reversed phase (). Multiple components in an epidermal growth factor-stimulated protein kinase cascade: in vitro activation of myelin basic protein/microtuble-associated protein-2 kinase.

Neointimal formation in the porcine aortic organ culture: cellular dynamics over one month. TGF-β stimulates the formation of aortic aneurysm, apparent from elevated levels of nuclear Smad2 in vascular tissue from patients that experienced a thoracic aortic aneurysm (TAA) (Gomez et al.

Inherited forms of TAA can be autosomal-dominant or :// Methods and Results—Rapamycin (1 to 10 nmol/L) inhibited basic fibroblast growth factor–induced migration of wild-type (WT) but not p27 Kip1 (−/−) SMCs in a dose-dependent manner (Paortic SMC explant migration were also studied with WT, p27(+/−), and p27(−/−) :// Fibroblast growth factor (FGF)-2, a potent growth Basic fibroblast growth factor mediates neointimal formation in porcine aortic explants.

book released following vascular injury, was also reduced in arteries of TRAIL(-/-) mice, and VSMCs isolated from these animals did not respond M A Reidy's research works w citations and 1, reads, including: SphingosinePhosphate Receptor 3 Promotes Neointimal Hyperplasia in Mouse Iliac-Femoral Arteries   Vascular endothelial growth factor (VEGF) in cells is a homodimeric glycoprotein that is best known for its capacity to induce angiogenesis, to increase vascular permeability, and to stimulate production of the thrombogenic protein tissue factor.

1 First isolated from a tumor-conditioned medium, it is now clear that nonmalignant cells including vascular smooth muscle cells (SMCs), monocytes This molecule turned out to be basic fibroblast growth factor (bFGF) which Denis Gospodarowicz had purified earlier from the bovine pituitary gland.

Thus, the birth of the aortic ring model occurred at a very propitious time when the angiogenesis field was entering the age of molecular biology and new discoveries were creating a need for Dimethylarginine Dimethylaminohydrolase Promotes Endothelial Repair After Vascular Injury Hakuoh Konishi, Karsten Sydow, John P.

Cooke Dimethylarginine dimethylaminohydrolase (DDAH) degrades asymmetric dimethylarginine (ADMA), the endogenous inhibitor of nitric oxide synthase (NOS).

Our DDAH transgenic mice manifest increased DDAH and NOS activity, reduced plasma and tissue Homophilic binding of N-cadherin between neuronal growth cones and astrocytes, oligodendrocytes, and Schwann cells mediates neurite outgrowth.

32 In this setting, N-cadherin interacts with and activates the fibroblast growth factor (FGF) receptor through dimerization.

FGF receptor activation through N-cadherin may also play a role in the   Different growth factors such as VEGF, endothelial cell growth factors (ECGFs), and basic fibroblast growth factor (bFGF) have been delivered through alginate carriers during tissue engineering. At low pH solutions, release of biomolecules from alginate decreases and this phenomenon can be used for drug :// Primate smooth muscle cell migration from aortic explants is mediated by endogenous platelet-derived growth factor and basic fibroblast growth factor acting through matrix metalloproteinases 2 and 9.

Circulation. ; – Crossref Medline Google Scholar; 8 Kenagy RD, Vergel S, Mattsson E, Bendeck M, Reidy MA, Clowes AW. The role of Soluble transforming growth factor-beta type II receptor inhibits negative remodeling, fibroblast transdifferentiation, and intimal lesion formation but not endothelial growth.

Specific effects of estrogen on growth factor and major histocompatibility complex class II antigen expression in rat aortic   1. Introduction. As an endothelial-specific growth factor, vascular endothelial growth factor (VEGF) has been typically considered to exert its biological function mainly through two tyrosine kinase receptors on the endothelial cell membrane, namely, Flt-1 (Fms-like tyrosine kinase, also called VEGFR1), and Flk-1(the kinase domain region KDR, also called VEGFR2, or its murine homologue Regulation of Neovascularization in the Lung.

Angiogenesis is a feature of chronic lung diseases such as asthma and pulmonary fibrosis. Studies in adenosine deaminase (ADA)-deficient mice, characterized by elevated lung tissue levels of adenosine, strongly suggest a causal association between adenosine and an inflammatory phenotype (Blackburn et al.

; Blackburn ). K. Hasegawa, S. Wakino, T. Tanaka, et ylarginine dimethylaminohydrolase 2 increases vascular endothelial growth factor expression through Sp1 transcription factor in endothelial cells Arterioscler Thromb Vasc Biol, 26 (), pp. Fibroblast growth factor 2 (FGF2 or basic FGF) plays a critical role in the induction of medial VSMC proliferation in balloon-injured arteries ().

In marked contrast, neutralizing antibodies to FGF2 failed to inhibit intimal VSMC proliferation after balloon angioplasty (53), and only a small increase in proliferation was seen when FGF2 was Biosc. 5 d ().doc  Web view. It has long been known that endothelial Ca2+ signals drive angiogenesis by recruiting multiple Ca2+-sensitive decoders in response to pro-angiogenic cues, such as vascular endothelial growth factor, basic fibroblast growth factor, stromal derived factor-1α and angiopoietins.

Recently, it was shown that intracellular Ca2+ signaling also drives vasculogenesis by stimulation proliferation, tube   The fibroblast growth factor (FGF) family consists of at least 15 structurally related polypeptide growth factors. Their expression is controlled at the levels of transcription, mRNA stability, and translation.

The bioavailability of FGFs is further modulated by posttranslational processing and regulated protein :// Pickering JG, Uniyal S, Ford CM et last growth factor-2 potentiates vascular smooth muscle cell migration to platelet-derived growth factor: upregulation of α II β I integrin and disassembly of actin filaments.

Circ Res ;– Ward MR, Agrotis A, Kanellakis P, Hall J, Jennings G, Bobik A. Tranilast prevents activation of transforming growth factor-beta system, leukocyte accumulation, and neointimal growth in porcine coronary arteries after stenting.

Arterioscler Thromb Vasc Biol. Primate smooth muscle cell migration from aortic explants is mediated by endogenous platelet-derived growth factor and basic fibroblast growth factor acting through matrix metalloproteinases 2 and 9. Circulation ;   Connective tissue growth factor (CTGF) is a cysteine-rich peptide that exhibits platelet-derived growth factor (PDGF)-like biological and immunological activities.

CTGF is 1. Introduction. Proteoglycans (PGs) are ubiquitous macromolecules that consist of a core protein, to which one or more glycosaminoglycans (chondroitin sulfate, dermatan sulfate, heparan sulfate or keratin sulfate) are covalently complex molecules influence many arterial properties, such as viscoelasticity, permeability, lipid metabolism, hemostasis, thrombosis and extracellular Canalis E, Centrella M, McCarthy T (a) Effects of basic fibroblast growth factor on bone formation in vitro.

J Clin Invest PubMed Google Scholar Canalis E, McCarthy T, Centrella M (b) Isolation and characterization of insulin-like growth factor I Oho, S., et al., Increased elastin-degrading activity and neointimal formation in porcine aortic organ culture. Reduction of both features with a serine proteinase inhibitor.

Arterioscler Thromb Vasc Biol, 15(12): p. PubMed Google Scholar Baffour R, Berman J, Garb J, Rhee S, Kaufman J, Friedmann P. Enhanced angiogenesis and growth of collaterals by in vivo administration of recombinant basic fibroblast growth factor in a rabbit model of acute lower limb ischemia: dose-response effect of basic fibroblast growth factor.

J Vasc Surg. ;– PubMed CrossRef Google Scholar Other growth factors, including insulin‐like growth factor‐1 93, 94, throm 95, 96, endothelin‐1 97, and angiotensin‐II 98, 99, are probably all involved.

It is an interesting question to what extent injury mechanisms contribute to atherosclerotic plaque ://(SICI)() For patients with end-stage renal disease requiring hemodialysis, their vascular access is both their lifeline and their Achilles heel. Despite being recommended as primary vascular access, the arteriovenous fistula (AVF) shows sub-optimal results, with about 50% of patients needing a revision during the year following creation.

After the AVF is created, the venous wall must adapt to new   Grafting aortic segments from tenascin-C null mice into null recipients significantly reduced neointimal hyperplasia and SMC proliferation compared to wild-type grafting.

Similarly, in a distal anastomotic stricture model of free artery graft stenosis, tenascin-C expression was induced over time in the media and neointima of the graft body in TGF-β1 large latent complex.

LLC is composed of (I) a mature TGF-β1; (II) a latency associated peptide, which is a 75 kD homodimer with three side chains, two of which have the amino acid asparagine linked to mannosephosphate oligosaccharides; and (III) a latent TGF-β binding protein of – kD, that contains 17 epidermal growth factor-like domains (14 of which are associated with.

Heparin-binding epidermal growth-factor-like growth factor (HB-EGF) from macrophages also plays a role in smooth muscle cell (SMC) migration. However, the expected outcome would be a mosaic of macrophages and smooth muscle cells, as seen in Fig.

3. Additional mechanisms must explain the formation of a distinct fibrous ://[email protected] Search form. Search3. Extracellular response after PCI.

It is now recognized that ECM is an active component of the vessel wall responsible for cellular interactions that play a critical role in the pathophysiology of vascular diseases.

17 The ECM is composed of a variety of molecules, including collagen, elastin, glycoproteins, and proteoglycans. In a muscular coronary artery, type III collagen is the most

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