The Experts below are selected from a list of 9201 Experts worldwide ranked by ideXlab platform
Lars Jakobsson - One of the best experts on this subject based on the ideXlab platform.
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endoglin prevents vascular malformation by regulating flow induced cell migration and specification through vegfr2 signalling
Nature Cell Biology, 2017Co-Authors: Lars Muhl, Christer Betsholtz, Mikhail Burmakin, Yixin Wang, Anneclaire Duchez, Helen M Arthur, Lars JakobssonAbstract:Two studies by Sugden et al. and Jin et al. show that endoglin regulates endothelial cell migration through VEGFR2 signalling and controls Blood Vessel Diameter in response to Blood flow.
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Endoglin prevents vascular malformation by regulating flow-induced cell migration and specification through VEGFR2 signalling
Nature Cell Biology, 2017Co-Authors: Lars Muhl, Christer Betsholtz, Mikhail Burmakin, Yixin Wang, Anneclaire Duchez, Helen m. Arthur, Lars JakobssonAbstract:Two studies by Sugden et al. and Jin et al. show that endoglin regulates endothelial cell migration through VEGFR2 signalling and controls Blood Vessel Diameter in response to Blood flow. Loss-of-function (LOF) mutations in the endothelial cell (EC)-enriched gene endoglin ( ENG) cause the human disease hereditary haemorrhagic telangiectasia-1, characterized by vascular malformations promoted by vascular endothelial growth factor A (VEGFA). How ENG deficiency alters EC behaviour to trigger these anomalies is not understood. Mosaic ENG deletion in the postnatal mouse rendered Eng LOF ECs insensitive to flow-mediated venous to arterial migration. Eng LOF ECs retained within arterioles acquired venous characteristics and secondary ENG-independent proliferation resulting in arteriovenous malformation (AVM). Analysis following simultaneous Eng LOF and overexpression (OE) revealed that ENG OE ECs dominate tip-cell positions and home preferentially to arteries. ENG knockdown altered VEGFA-mediated VEGFR2 kinetics and promoted AKT signalling. Blockage of PI(3)K/AKT partly normalized flow-directed migration of ENG LOF ECs in vitro and reduced the severity of AVM in vivo . This demonstrates the requirement of ENG in flow-mediated migration and modulation of VEGFR2 signalling in vascular patterning.
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Endoglin prevents vascular malformation by regulating flow-induced cell migration and specification through VEGFR2 signalling
Nature Cell Biology, 2017Co-Authors: Yi Jin, Christer Betsholtz, Lars Muhl, Mikhail Burmakin, Yixin Wang, Anneclaire Duchez, Helen M Arthur, Lars JakobssonAbstract:Two studies by Sugden et al. and Jin et al. show that endoglin regulates endothelial cell migration through VEGFR2 signalling and controls Blood Vessel Diameter in response to Blood flow.
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Laminin deposition is dispensable for vasculogenesis but regulates Blood Vessel Diameter independent of flow
The FASEB Journal, 2007Co-Authors: Lars Jakobsson, Anna Domogatskaya, Karl Tryggvason, David Edgar, Lena Claesson-welshAbstract:Basement membranes (BMs) consisting of laminins, collagens, and heparan sulfate proteoglycans (HSPGs) are vital for proper endothelial cell function, but many aspects of their role in vascular deve...
Steven W. Levison - One of the best experts on this subject based on the ideXlab platform.
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Vascular Endothelial Growth Factors A and C are Induced in the SVZ Following Neonatal Hypoxia–Ischemia and Exert Different Effects on Neonatal Glial Progenitors
Translational Stroke Research, 2013Co-Authors: Jennifer M. Bain, Lisamarie Moore, Zhihua Ren, Sophia Simonishvili, Steven W. LevisonAbstract:Episodes of neonatal hypoxia–ischemia (H-I) are strongly associated with cerebral palsy and a wide spectrum of other neurological deficits in children. Two key processes required to repair damaged organs are to amplify the number of precursors capable of regenerating damaged cells and to direct their differentiation towards the cell types that need to be replaced. Since hypoxia induces vascular endothelial growth factor (VEGF) production, it is logical to predict that VEGFs are key mediators of tissue repair after H-I injury. The goal of this study was to test the hypothesis that certain VEGF isoforms increase during recovery from neonatal H-I and that they would differentially affect the proliferation and differentiation of subventricular zone (SVZ) progenitors. During the acute recovery period from H-I, both VEGF-A and VEGF-C were transiently induced in the SVZ, which correlated with an increase in SVZ Blood Vessel Diameter. These growth factors were produced by glial progenitors, astrocytes, and to a lesser extent, microglia. VEGF-A promoted the production of astrocytes from SVZ glial progenitors, while VEGF-C stimulated the proliferation of both early and late oligodendrocyte progenitor cells (OPCs), which was abolished by blocking VEGFR-3. Altogether, these results provide new insights into the signals that coordinate the reactive responses of the progenitors in the SVZ to neonatal H-I. Our studies further suggest that therapeutics that can extend VEGF-C production and/or agonists that stimulate VEGFR-3 will promote OPC development to enhance myelination after perinatal brain injury.
Christer Betsholtz - One of the best experts on this subject based on the ideXlab platform.
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endoglin prevents vascular malformation by regulating flow induced cell migration and specification through vegfr2 signalling
Nature Cell Biology, 2017Co-Authors: Lars Muhl, Christer Betsholtz, Mikhail Burmakin, Yixin Wang, Anneclaire Duchez, Helen M Arthur, Lars JakobssonAbstract:Two studies by Sugden et al. and Jin et al. show that endoglin regulates endothelial cell migration through VEGFR2 signalling and controls Blood Vessel Diameter in response to Blood flow.
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Endoglin prevents vascular malformation by regulating flow-induced cell migration and specification through VEGFR2 signalling
Nature Cell Biology, 2017Co-Authors: Lars Muhl, Christer Betsholtz, Mikhail Burmakin, Yixin Wang, Anneclaire Duchez, Helen m. Arthur, Lars JakobssonAbstract:Two studies by Sugden et al. and Jin et al. show that endoglin regulates endothelial cell migration through VEGFR2 signalling and controls Blood Vessel Diameter in response to Blood flow. Loss-of-function (LOF) mutations in the endothelial cell (EC)-enriched gene endoglin ( ENG) cause the human disease hereditary haemorrhagic telangiectasia-1, characterized by vascular malformations promoted by vascular endothelial growth factor A (VEGFA). How ENG deficiency alters EC behaviour to trigger these anomalies is not understood. Mosaic ENG deletion in the postnatal mouse rendered Eng LOF ECs insensitive to flow-mediated venous to arterial migration. Eng LOF ECs retained within arterioles acquired venous characteristics and secondary ENG-independent proliferation resulting in arteriovenous malformation (AVM). Analysis following simultaneous Eng LOF and overexpression (OE) revealed that ENG OE ECs dominate tip-cell positions and home preferentially to arteries. ENG knockdown altered VEGFA-mediated VEGFR2 kinetics and promoted AKT signalling. Blockage of PI(3)K/AKT partly normalized flow-directed migration of ENG LOF ECs in vitro and reduced the severity of AVM in vivo . This demonstrates the requirement of ENG in flow-mediated migration and modulation of VEGFR2 signalling in vascular patterning.
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Endoglin prevents vascular malformation by regulating flow-induced cell migration and specification through VEGFR2 signalling
Nature Cell Biology, 2017Co-Authors: Yi Jin, Christer Betsholtz, Lars Muhl, Mikhail Burmakin, Yixin Wang, Anneclaire Duchez, Helen M Arthur, Lars JakobssonAbstract:Two studies by Sugden et al. and Jin et al. show that endoglin regulates endothelial cell migration through VEGFR2 signalling and controls Blood Vessel Diameter in response to Blood flow.
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Notch3 Is Necessary for Blood Vessel Integrity in the Central Nervous System
Arteriosclerosis Thrombosis and Vascular Biology, 2015Co-Authors: Tanya L. Henshall, Annika Keller, Bengt R. Johansson, Elisabet Wallgard, Elisabeth Raschperger, Maarja Andaloussi Mäe, Shaobo Jin, Christer Betsholtz, Urban LendahlAbstract:OBJECTIVE: Vascular smooth muscle cells (VSMC) are important for contraction, Blood flow distribution, and regulation of Blood Vessel Diameter, but to what extent they contribute to the integrity o ...
Jennifer M. Bain - One of the best experts on this subject based on the ideXlab platform.
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Vascular Endothelial Growth Factors A and C are Induced in the SVZ Following Neonatal Hypoxia–Ischemia and Exert Different Effects on Neonatal Glial Progenitors
Translational Stroke Research, 2013Co-Authors: Jennifer M. Bain, Lisamarie Moore, Zhihua Ren, Sophia Simonishvili, Steven W. LevisonAbstract:Episodes of neonatal hypoxia–ischemia (H-I) are strongly associated with cerebral palsy and a wide spectrum of other neurological deficits in children. Two key processes required to repair damaged organs are to amplify the number of precursors capable of regenerating damaged cells and to direct their differentiation towards the cell types that need to be replaced. Since hypoxia induces vascular endothelial growth factor (VEGF) production, it is logical to predict that VEGFs are key mediators of tissue repair after H-I injury. The goal of this study was to test the hypothesis that certain VEGF isoforms increase during recovery from neonatal H-I and that they would differentially affect the proliferation and differentiation of subventricular zone (SVZ) progenitors. During the acute recovery period from H-I, both VEGF-A and VEGF-C were transiently induced in the SVZ, which correlated with an increase in SVZ Blood Vessel Diameter. These growth factors were produced by glial progenitors, astrocytes, and to a lesser extent, microglia. VEGF-A promoted the production of astrocytes from SVZ glial progenitors, while VEGF-C stimulated the proliferation of both early and late oligodendrocyte progenitor cells (OPCs), which was abolished by blocking VEGFR-3. Altogether, these results provide new insights into the signals that coordinate the reactive responses of the progenitors in the SVZ to neonatal H-I. Our studies further suggest that therapeutics that can extend VEGF-C production and/or agonists that stimulate VEGFR-3 will promote OPC development to enhance myelination after perinatal brain injury.
Lars Muhl - One of the best experts on this subject based on the ideXlab platform.
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endoglin prevents vascular malformation by regulating flow induced cell migration and specification through vegfr2 signalling
Nature Cell Biology, 2017Co-Authors: Lars Muhl, Christer Betsholtz, Mikhail Burmakin, Yixin Wang, Anneclaire Duchez, Helen M Arthur, Lars JakobssonAbstract:Two studies by Sugden et al. and Jin et al. show that endoglin regulates endothelial cell migration through VEGFR2 signalling and controls Blood Vessel Diameter in response to Blood flow.
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Endoglin prevents vascular malformation by regulating flow-induced cell migration and specification through VEGFR2 signalling
Nature Cell Biology, 2017Co-Authors: Lars Muhl, Christer Betsholtz, Mikhail Burmakin, Yixin Wang, Anneclaire Duchez, Helen m. Arthur, Lars JakobssonAbstract:Two studies by Sugden et al. and Jin et al. show that endoglin regulates endothelial cell migration through VEGFR2 signalling and controls Blood Vessel Diameter in response to Blood flow. Loss-of-function (LOF) mutations in the endothelial cell (EC)-enriched gene endoglin ( ENG) cause the human disease hereditary haemorrhagic telangiectasia-1, characterized by vascular malformations promoted by vascular endothelial growth factor A (VEGFA). How ENG deficiency alters EC behaviour to trigger these anomalies is not understood. Mosaic ENG deletion in the postnatal mouse rendered Eng LOF ECs insensitive to flow-mediated venous to arterial migration. Eng LOF ECs retained within arterioles acquired venous characteristics and secondary ENG-independent proliferation resulting in arteriovenous malformation (AVM). Analysis following simultaneous Eng LOF and overexpression (OE) revealed that ENG OE ECs dominate tip-cell positions and home preferentially to arteries. ENG knockdown altered VEGFA-mediated VEGFR2 kinetics and promoted AKT signalling. Blockage of PI(3)K/AKT partly normalized flow-directed migration of ENG LOF ECs in vitro and reduced the severity of AVM in vivo . This demonstrates the requirement of ENG in flow-mediated migration and modulation of VEGFR2 signalling in vascular patterning.
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Endoglin prevents vascular malformation by regulating flow-induced cell migration and specification through VEGFR2 signalling
Nature Cell Biology, 2017Co-Authors: Yi Jin, Christer Betsholtz, Lars Muhl, Mikhail Burmakin, Yixin Wang, Anneclaire Duchez, Helen M Arthur, Lars JakobssonAbstract:Two studies by Sugden et al. and Jin et al. show that endoglin regulates endothelial cell migration through VEGFR2 signalling and controls Blood Vessel Diameter in response to Blood flow.