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Article ; Online: HSPG-binding peptide corresponding to the exon 6a-encoded domain of VEGF inhibits tumor growth by blocking angiogenesis in murine model.

Lee, Tong-Young / Folkman, Judah / Javaherian, Kashi

PloS one

2010 Volume 5, Issue 4, Page(s) e9945

Abstract: Vascular endothelial growth factor VEGF(165) is a critical element for development of the vascular system in physiological and pathological angiogenesis. VEGF isoforms have different affinities for heparan sulphate proteoglycan (HSPG) as well as for VEGF ...

Abstract	Vascular endothelial growth factor VEGF(165) is a critical element for development of the vascular system in physiological and pathological angiogenesis. VEGF isoforms have different affinities for heparan sulphate proteoglycan (HSPG) as well as for VEGF receptors; HSPGs are important regulators in vascular development. Therefore, inhibition of interactions between VEGF and HSPGs may prevent angiogenesis. Here, we demonstrate that an HSPG-binding synthetic peptide, corresponding to exon 6a-encoded domain of VEGF gene, has anti-angiogenic property. This 20 amino acids synthetic peptide prevents VEGF(165) binding to several different cell types, mouse embryonic sections and inhibits endothelial cell migration, despite its absence in VEGF(165) sequence. Our in vivo anti-tumor studies show that the peptide inhibits tumor growth in both mouse Lewis-Lung Carcinoma and human Liposarcoma tumor-bearing animal models. This is the first evidence that a synthetic VEGF fragment corresponding to exon 6a has functional antagonism both in vitro and in vivo. We conclude that the above HPSG binding peptide (6a-P) is a potent inhibitor of angiogenesis-dependent diseases.
MeSH term(s)	Animals ; Antineoplastic Agents/chemical synthesis ; Antineoplastic Agents/pharmacology ; Binding Sites ; Carcinoma, Lewis Lung/drug therapy ; Cell Proliferation/drug effects ; Disease Models, Animal ; Heparan Sulfate Proteoglycans/metabolism ; Humans ; Liposarcoma/drug therapy ; Mice ; Molecular Mimicry ; Neoplasms/drug therapy ; Neoplasms/pathology ; Neovascularization, Pathologic/drug therapy ; Neovascularization, Pathologic/prevention & control ; Peptides/chemical synthesis ; Peptides/pharmacology ; Peptides/therapeutic use ; Vascular Endothelial Growth Factor A/chemistry ; Vascular Endothelial Growth Factor A/metabolism
Chemical Substances	Antineoplastic Agents ; Heparan Sulfate Proteoglycans ; Peptides ; Vascular Endothelial Growth Factor A
Language	English
Publishing date	2010-04-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0009945
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Article ; Online: HSPG-binding peptide corresponding to the exon 6a-encoded domain of VEGF inhibits tumor growth by blocking angiogenesis in murine model.

Tong-Young Lee / Judah Folkman / Kashi Javaherian

PLoS ONE, Vol 5, Iss 4, p e

2010 Volume 9945

Abstract	Vascular endothelial growth factor VEGF(165) is a critical element for development of the vascular system in physiological and pathological angiogenesis. VEGF isoforms have different affinities for heparan sulphate proteoglycan (HSPG) as well as for VEGF receptors; HSPGs are important regulators in vascular development. Therefore, inhibition of interactions between VEGF and HSPGs may prevent angiogenesis. Here, we demonstrate that an HSPG-binding synthetic peptide, corresponding to exon 6a-encoded domain of VEGF gene, has anti-angiogenic property. This 20 amino acids synthetic peptide prevents VEGF(165) binding to several different cell types, mouse embryonic sections and inhibits endothelial cell migration, despite its absence in VEGF(165) sequence. Our in vivo anti-tumor studies show that the peptide inhibits tumor growth in both mouse Lewis-Lung Carcinoma and human Liposarcoma tumor-bearing animal models. This is the first evidence that a synthetic VEGF fragment corresponding to exon 6a has functional antagonism both in vitro and in vivo. We conclude that the above HPSG binding peptide (6a-P) is a potent inhibitor of angiogenesis-dependent diseases.
Keywords	Medicine ; R ; Science ; Q
Language	English
Publishing date	2010-04-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
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Article ; Online: Two Endogenous Antiangiogenic Inhibitors, Endostatin and Angiostatin, Demonstrate Biphasic Curves in their Antitumor Profiles.

Javaherian, Kashi / Lee, Tong-Young / Tjin Tham Sjin, Robert M / Parris, George E / Hlatky, Lynn

Dose-response : a publication of International Hormesis Society

2010 Volume 9, Issue 3, Page(s) 369–376

Abstract: Angiogenesis refers to growth of blood vessels from pre-existing ones. In 1971, Folkman proposed that by choking off the blood supply to tumors, they are starved, leading to their demise. A few years ago, the monoclonal antibody Avastin became the first ... ...

Abstract	Angiogenesis refers to growth of blood vessels from pre-existing ones. In 1971, Folkman proposed that by choking off the blood supply to tumors, they are starved, leading to their demise. A few years ago, the monoclonal antibody Avastin became the first antiangiogenic biological approved by FDA, for treatment of cancer patients. Two other antiangiogenic endogenous protein fragments were isolated in Folkman's laboratory more than a decade ago. Here, we present a short review of data demonstrating that angiostatin and endostatin display a biphasic antitumor dose-response. This behavior is common among a large number of antiangiogenic agents and the reduced effectiveness of antiangiogenic agents at high dose rates may be due to suppression of growth of new vessels carrying the agent into the critical region around the tumor.
Language	English
Publishing date	2010-10-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	2440820-7
ISSN	1559-3258 ; 1559-3258
ISSN (online)	1559-3258
ISSN	1559-3258
DOI	10.2203/dose-response.10-020.Javaherian
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Article ; Online: Improvement in the standard treatment for experimental glioma by fusing antibody Fc domain to endostatin.

Grossman, Rachel / Tyler, Betty / Hwang, Lee / Zadnik, Patti / Lal, Bachchu / Javaherian, Kashi / Brem, Henry

Journal of neurosurgery

2011 Volume 115, Issue 6, Page(s) 1139–1146

Abstract: Object: Brain tumors pose many unique challenges to treatment. The authors hypothesized that Fc-endostatin may be beneficial. It is a newly synthesized recombinant human endostatin conjugated to the Fc domain of IgG with a long half-life (weeks) and ... ...

Abstract	Object: Brain tumors pose many unique challenges to treatment. The authors hypothesized that Fc-endostatin may be beneficial. It is a newly synthesized recombinant human endostatin conjugated to the Fc domain of IgG with a long half-life (weeks) and unknown toxicity. The authors examined the efficacy of Fc-endostatin using various delivery methods. Methods: Efficacy was assessed using the intracranial 9L gliosarcoma rat model treated with Fc-endostatin for use in rodents (mFc-endostatin), which was administered either systemically or locally via different delivery methods. Oral temozolomide (TMZ) was administered in combination with mFc-endostatin to determine if there was a beneficial synergistic effect. Results: Intracranial delivery of mFc-endostatin via a polymer or convection-enhanced delivery 5 days after tumor implantation increased median survival, compared with the control group (p = 0.0048 and 0.003, respectively). Animals treated weekly with subcutaneous mFc-endostatin (started 5 days post-tumor implantation) also had statistically improved survival as compared with controls (p = 0.0008). However, there was no statistical difference in survival between the local and systemic delivery groups. Control animals had a median survival of 13 days. Animals treated either with subcutaneous mFc-endostatin weekly or with polymer had a median survival of 18 and 15 days, respectively, and those treated with oral TMZ for 5 days (Days 5-9) had a median survival of 21 days. Survival was further increased with a combination of oral TMZ and mFc-endostatin polymer, with a median survival of 28 days (p = 0.029, compared with TMZ alone). Subcutaneous mFc-endostatin administered every week starting 18 days before tumor implantation significantly increased median survival when compared with controls (p = 0.0007), with 12.5% of the animals ultimately becoming long-term survivors (that is, survival longer than 120 days). The addition of TMZ to either weekly or daily subcutaneous mFc-endostatin and its administration 18 days before tumor implantation significantly increased survival (p = 0.017 and 0.0001, respectively, compared with TMZ alone). Note that 12.5% of the animals treated with weekly subcutaneous mFc-endostatin and TMZ were long-term survivors. Conclusions: Systemically or directly (local) delivered mFc-endostatin prolonged the survival of rats implanted with intracranial 9L gliosarcoma. This benefit was further enhanced when mFc-endostatin was combined with the oral chemotherapeutic agent TMZ.
MeSH term(s)	Administration, Oral ; Angiogenesis Inhibitors/pharmacology ; Angiogenesis Inhibitors/toxicity ; Animals ; Antineoplastic Agents, Alkylating/pharmacology ; Antineoplastic Combined Chemotherapy Protocols/pharmacology ; Brain Neoplasms/drug therapy ; Brain Neoplasms/mortality ; Dacarbazine/analogs & derivatives ; Dacarbazine/pharmacology ; Disease Models, Animal ; Drug Delivery Systems/methods ; Endostatins/pharmacology ; Endostatins/toxicity ; Gliosarcoma/drug therapy ; Gliosarcoma/mortality ; Immunoglobulin Fc Fragments/pharmacology ; Immunoglobulin Fc Fragments/toxicity ; Male ; Rats ; Rats, Inbred F344 ; Survival Analysis
Chemical Substances	Angiogenesis Inhibitors ; Antineoplastic Agents, Alkylating ; Endostatins ; Immunoglobulin Fc Fragments ; Dacarbazine (7GR28W0FJI) ; temozolomide (YF1K15M17Y)
Language	English
Publishing date	2011-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3089-2
ISSN	1933-0693 ; 0022-3085
ISSN (online)	1933-0693
ISSN	0022-3085
DOI	10.3171/2011.8.JNS11125
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Article ; Online: Inhibition of Corneal Neovascularization by Subconjunctival Injection of Fc-Endostatin, a Novel Inhibitor of Angiogenesis

Junko Yoshida / Robert T. Wicks / Andrea I. Zambrano / Betty M. Tyler / Kashi Javaherian / Rachel Grossman / Yassine J. Daoud / Peter Gehlbach / Henry Brem / Walter J. Stark

Journal of Ophthalmology, Vol

2015 Volume 2015

Keywords	Ophthalmology ; RE1-994 ; Medicine ; R
Language	English
Publishing date	2015-01-01T00:00:00Z
Publisher	Hindawi Publishing Corporation
Document type	Article ; Online
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Article: Inhibition of Corneal Neovascularization by Subconjunctival Injection of Fc-Endostatin, a Novel Inhibitor of Angiogenesis.

Yoshida, Junko / Wicks, Robert T / Zambrano, Andrea I / Tyler, Betty M / Javaherian, Kashi / Grossman, Rachel / Daoud, Yassine J / Gehlbach, Peter / Brem, Henry / Stark, Walter J

Journal of ophthalmology

2015 Volume 2015, Page(s) 137136

Abstract: We assessed the antiangiogenic effects of subconjunctival injection of Fc-endostatin (FcE) using a human vascular endothelial growth factor-induced rabbit corneal neovascularization model. Angiogenesis was induced in rabbit corneas through intrastromal ... ...

Abstract	We assessed the antiangiogenic effects of subconjunctival injection of Fc-endostatin (FcE) using a human vascular endothelial growth factor-induced rabbit corneal neovascularization model. Angiogenesis was induced in rabbit corneas through intrastromal implantations of VEGF polymer implanted 2 mm from the limbus. NZW rabbits were separated into groups receiving twice weekly subconjunctival injections of either saline; 25 mg/mL bevacizumab; 2 mg/mL FcE; or 20 mg/mL FcE. Corneas were digitally imaged at 5 time points. An angiogenesis index (AI) was calculated (vessel length (mm) × vessel number score) for each observation. All treatment groups showed a significant decrease in the vessel length and AI compared to saline on all observation days (P < 0.001). By day 15, FcE 2 inhibited angiogenesis significantly better than FcE 20 (P < 0.01). There was no significant difference between FcE 2 and BV, although the values trended towards significantly increased inhibition by BV. BV was a significantly better inhibitor than FcE 20 by day 8 (P < 0.01). FcE was safe and significantly inhibited new vessel growth in a rabbit corneal neovascularization model. Lower concentration FcE 2 exhibited better inhibition than FcE 20, consistent with previous FcE studies referencing a biphasic dose-response curve. Additional studies are necessary to further elucidate the efficacy and clinical potential of this novel angiogenesis inhibitor.
Language	English
Publishing date	2015-09-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	2546525-9
ISSN	2090-0058 ; 2090-004X
ISSN (online)	2090-0058
ISSN	2090-004X
DOI	10.1155/2015/137136
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Article ; Online: Angiostatin regulates the expression of antiangiogenic and proapoptotic pathways via targeted inhibition of mitochondrial proteins.

Lee, Tong-Young / Muschal, Stefan / Pravda, Elke A / Folkman, Judah / Abdollahi, Amir / Javaherian, Kashi

Blood

2009 Volume 114, Issue 9, Page(s) 1987–1998

Abstract: Angiostatin, a proteolytic fragment of plasminogen, is a potent endogenous antiangiogenic agent. The molecular mechanisms governing angiostatin's antiangiogenic and antitumor effects are not well understood. Here, we report the identification of ... ...

Abstract	Angiostatin, a proteolytic fragment of plasminogen, is a potent endogenous antiangiogenic agent. The molecular mechanisms governing angiostatin's antiangiogenic and antitumor effects are not well understood. Here, we report the identification of mitochondrial compartment as the ultimate target of angiostatin. After internalization of angiostatin into the cell, at least 2 proteins within the mitochondria bind this molecule: malate dehydrogenase, a member of Krebs cycle, and adenosine triphosphate synthase. In vitro and in vivo studies revealed differential regulation of key prosurvival and angiogenesis-related proteins in angiostatin-treated tumors and tumor-endothelium. Angiostatin induced apoptosis via down-regulation of mitochondrial BCL-2. Angiostatin treatment led to down-regulation of c-Myc and elevated levels of another key antiangiogenic protein, thrombospondin-1, reinforcing its antitumor and antiangiogenic effects. Further evidence is provided for reduced recruitment and infiltration of bone marrow-derived macrophages in angiostatin-treated tumors. The observed effects of angiostatin were restricted to the tumor site and were not observed in other major organs of the mice, indicating unique tumor specific bioavailability. Together, our data suggest mitochondria as a novel target for antiangiogenic therapy and provide mechanistic insights to the antiangiogenic and antitumor effects of angiostatin.
MeSH term(s)	Angiogenesis Inhibitors/pharmacology ; Angiostatins/physiology ; Animals ; Apoptosis ; Cell Line, Tumor ; Enzyme-Linked Immunosorbent Assay ; Gene Expression Regulation ; Humans ; Male ; Mice ; Mice, SCID ; Mitochondria/metabolism ; Models, Biological ; Neoplasms/therapy ; Proto-Oncogene Proteins c-bcl-2/metabolism
Chemical Substances	Angiogenesis Inhibitors ; Proto-Oncogene Proteins c-bcl-2 ; Angiostatins (86090-08-6)
Language	English
Publishing date	2009-05-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2008-12-197236
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Article: Endostatin binds biglycan and LDL and interferes with LDL retention to the subendothelial matrix during atherosclerosis.

Zeng, Xiaokun / Chen, Joshua / Miller, Yury I / Javaherian, Kashi / Moulton, Karen S

Journal of lipid research

2005 Volume 46, Issue 9, Page(s) 1849–1859

Abstract: Retention of lipoproteins to proteoglycans in the subendothelial matrix (SEM) is an early event in atherosclerosis. We recently reported that collagen XVIII and its proteolytically released fragment endostatin (ES) are differentially depleted in blood ... ...

Abstract	Retention of lipoproteins to proteoglycans in the subendothelial matrix (SEM) is an early event in atherosclerosis. We recently reported that collagen XVIII and its proteolytically released fragment endostatin (ES) are differentially depleted in blood vessels affected by atherosclerosis. Loss of collagen XVIII/ES in atherosclerosis-prone mice enhanced plaque neovascularization and increased the vascular permeability to lipids by distinct mechanisms. Impaired endothelial barrier function increased the influx of lipoproteins across the endothelium; however, we hypothesized that enhanced retention might be a second mechanism leading to the increased lipid content in atheromas lacking collagen XVIII. We now demonstrate a novel property of ES that binds both the matrix proteoglycan biglycan and LDL and interferes with LDL retention to biglycan and to SEM. A peptide encompassing the alpha coil in the ES crystal structure mediates the major blocking effect of ES on LDL retention. ES inhibits the macrophage uptake of biglycan-associated LDL indirectly by interfering with LDL retention to biglycan, but it has no direct effect on the macrophage uptake of native or modified lipoproteins. Thus, loss of ES in advanced atheromas enhances lipoprotein retention in SEM. Our data reveal a third protective role of this vascular basement membrane component during atherosclerosis.
MeSH term(s)	Animals ; Aorta/chemistry ; Arteriosclerosis/metabolism ; Basement Membrane/metabolism ; Biglycan ; Binding Sites ; Binding, Competitive ; Collagen Type XVIII/metabolism ; Endostatins/analysis ; Endostatins/metabolism ; Endostatins/pharmacology ; Endothelium/metabolism ; Extracellular Matrix Proteins ; Glycosaminoglycans/metabolism ; Humans ; Lipoproteins/metabolism ; Lipoproteins, LDL/metabolism ; Macrophages/metabolism ; Macrophages, Peritoneal ; Mice ; Mice, Inbred C57BL ; Proteoglycans/metabolism ; Recombinant Proteins ; Umbilical Veins
Chemical Substances	BGN protein, human ; Bgn protein, mouse ; Biglycan ; Collagen Type XVIII ; Endostatins ; Extracellular Matrix Proteins ; Glycosaminoglycans ; Lipoproteins ; Lipoproteins, LDL ; Proteoglycans ; Recombinant Proteins
Language	English
Publishing date	2005-07-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	80154-9
ISSN	1539-7262 ; 0022-2275
ISSN (online)	1539-7262
ISSN	0022-2275
DOI	10.1194/jlr.M500241-JLR200
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Article ; Online: Endostatin lowers blood pressure via nitric oxide and prevents hypertension associated with VEGF inhibition.

Sunshine, Sarah B / Dallabrida, Susan M / Durand, Ellen / Ismail, Nesreen S / Bazinet, Lauren / Birsner, Amy E / Sohn, Regina / Ikeda, Sadakatsu / Pu, William T / Kulke, Matthew H / Javaherian, Kashi / Zurakowski, David / Folkman, Judah M / Rupnick, Maria

Proceedings of the National Academy of Sciences of the United States of America

2012 Volume 109, Issue 28, Page(s) 11306–11311

Abstract: Antiangiogenesis therapy has become a vital part of the armamentarium against cancer. Hypertension is a dose-limiting toxicity for VEGF inhibitors. Thus, there is a pressing need to address the associated adverse events so these agents can be better used. ...

Abstract	Antiangiogenesis therapy has become a vital part of the armamentarium against cancer. Hypertension is a dose-limiting toxicity for VEGF inhibitors. Thus, there is a pressing need to address the associated adverse events so these agents can be better used. The hypertension may be mediated by reduced NO bioavailability resulting from VEGF inhibition. We proposed that the hypertension may be prevented by coadministration with endostatin (ES), an endogenous angiogenesis inhibitor with antitumor effects shown to increase endothelial NO production in vitro. We determined that Fc-conjugated ES promoted NO production in endothelial and smooth muscle cells. ES also lowered blood pressure in normotensive mice and prevented hypertension induced by anti-VEGF antibodies. This effect was associated with higher circulating nitrate levels and was absent in eNOS-knockout mice, implicating a NO-mediated mechanism. Retrospective study of patients treated with ES in a clinical trial revealed a small but significant reduction in blood pressure, suggesting that the findings may translate to the clinic. Coadministration of ES with VEGF inhibitors may offer a unique strategy to prevent drug-related hypertension and enhance antiangiogenic tumor suppression.
MeSH term(s)	Angiogenesis Inhibitors/pharmacology ; Animals ; Antibodies/chemistry ; Blood Pressure/physiology ; Clinical Trials, Phase II as Topic ; Endostatins/metabolism ; Female ; Heart/drug effects ; Humans ; Hypertension/metabolism ; Hypertension/prevention & control ; Male ; Mice ; Mice, Inbred C57BL ; Neovascularization, Pathologic/prevention & control ; Nitric Oxide/metabolism ; Vascular Endothelial Growth Factor A/antagonists & inhibitors
Chemical Substances	Angiogenesis Inhibitors ; Antibodies ; Endostatins ; Vascular Endothelial Growth Factor A ; Nitric Oxide (31C4KY9ESH)
Language	English
Publishing date	2012-06-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1203275109
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Article: Endostatin binds biglycan and LDL and interferes with LDL retention to the subendothelial matrix during atherosclerosis

Zeng, Xiaokun / Chen, Joshua / Miller, Yury I / Javaherian, Kashi / Moulton, Karen S

Journal of lipid research. 2005 Sep., v. 46, no. 9

2005

Abstract	Retention of lipoproteins to proteoglycans in the subendothelial matrix (SEM) is an early event in atherosclerosis. We recently reported that collagen XVIII and its proteolytically released fragment endostatin (ES) are differentially depleted in blood vessels affected by atherosclerosis. Loss of collagen XVIII/ES in atherosclerosis-prone mice enhanced plaque neovascularization and increased the vascular permeability to lipids by distinct mechanisms. Impaired endothelial barrier function increased the influx of lipoproteins across the endothelium; however, we hypothesized that enhanced retention might be a second mechanism leading to the increased lipid content in atheromas lacking collagen XVIII. We now demonstrate a novel property of ES that binds both the matrix proteoglycan biglycan and LDL and interferes with LDL retention to biglycan and to SEM. A peptide encompassing the [alpha] coil in the ES crystal structure mediates the major blocking effect of ES on LDL retention. ES inhibits the macrophage uptake of biglycan-associated LDL indirectly by interfering with LDL retention to biglycan, but it has no direct effect on the macrophage uptake of native or modified lipoproteins. Thus, loss of ES in advanced atheromas enhances lipoprotein retention in SEM. Our data reveal a third protective role of this vascular basement membrane component during atherosclerosis.
Language	English
Dates of publication	2005-09
Size	p. 1849-1859.
Document type	Article
ZDB-ID	80154-9
ISSN	1539-7262 ; 0022-2275
ISSN (online)	1539-7262
ISSN	0022-2275
Database	NAL-Catalogue (AGRICOLA)

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