Angiogenetic signaling through hypoxia
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Angiogenetic signaling through hypoxia : HMGB1: an angiogenetic switch molecule. / Schlueter, Claudia; Weber, Holger; Meyer, Britta; Rogalla, Piere; Röser, Kerstin; Hauke, Sven; Bullerdiek, Jörn.
in: AM J PATHOL, Jahrgang 166, Nr. 4, 04.2005, S. 1259-63.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Angiogenetic signaling through hypoxia
T2 - HMGB1: an angiogenetic switch molecule
AU - Schlueter, Claudia
AU - Weber, Holger
AU - Meyer, Britta
AU - Rogalla, Piere
AU - Röser, Kerstin
AU - Hauke, Sven
AU - Bullerdiek, Jörn
PY - 2005/4
Y1 - 2005/4
N2 - The initiation of angiogenesis, called the angiogenetic switch, is a crucial early step in tumor progression and propagation, ensuring an adequate oxygen supply. The rapid growth of tumors is accompanied by a reduced microvessel density, resulting in chronic hypoxia that often leads to necrotic areas within the tumor. These hypoxic and necrotic regions exhibit increased expression of angiogenetic growth factors, eg, vascular endothelial growth factor, and may also attract macrophages, which are known to produce a number of potent angiogenetic cytokines and growth factors. A group of molecules that may act as mediators of angiogenesis are the so-called high-mobility group proteins. Recent studies showed that HMGB1, known as an architectural chromatin-binding protein, can be extracellularly released by passive diffusion from necrotic cells and activated macrophages. To examine the angiogenetic effects of HMGB1 on endothelial cells an in vitro spheroid model was used. The results of the endothelial-sprouting assay clearly show that exogenous HMGB1 induced endothelial cell migration and sprouting in vitro in a dose-dependent manner. Thus, this is the first report showing strong evidence for HMGB1-induced sprouting of endothelial cells.
AB - The initiation of angiogenesis, called the angiogenetic switch, is a crucial early step in tumor progression and propagation, ensuring an adequate oxygen supply. The rapid growth of tumors is accompanied by a reduced microvessel density, resulting in chronic hypoxia that often leads to necrotic areas within the tumor. These hypoxic and necrotic regions exhibit increased expression of angiogenetic growth factors, eg, vascular endothelial growth factor, and may also attract macrophages, which are known to produce a number of potent angiogenetic cytokines and growth factors. A group of molecules that may act as mediators of angiogenesis are the so-called high-mobility group proteins. Recent studies showed that HMGB1, known as an architectural chromatin-binding protein, can be extracellularly released by passive diffusion from necrotic cells and activated macrophages. To examine the angiogenetic effects of HMGB1 on endothelial cells an in vitro spheroid model was used. The results of the endothelial-sprouting assay clearly show that exogenous HMGB1 induced endothelial cell migration and sprouting in vitro in a dose-dependent manner. Thus, this is the first report showing strong evidence for HMGB1-induced sprouting of endothelial cells.
KW - Cell Movement
KW - Dose-Response Relationship, Drug
KW - Endothelial Cells
KW - HMGB1 Protein
KW - Humans
KW - Hypoxia
KW - Immunohistochemistry
KW - Macrophages
KW - Models, Biological
KW - Neovascularization, Pathologic
KW - Spheroids, Cellular
KW - Tumor Cells, Cultured
KW - Journal Article
KW - Research Support, Non-U.S. Gov't
U2 - 10.1016/S0002-9440(10)62344-9
DO - 10.1016/S0002-9440(10)62344-9
M3 - SCORING: Journal article
C2 - 15793304
VL - 166
SP - 1259
EP - 1263
JO - AM J PATHOL
JF - AM J PATHOL
SN - 0002-9440
IS - 4
ER -
