0260 : Endoglin in adhesion between endothelial and mural cells
The interaction and interplay between endothelial cells (ECs) and mural cells (such as vascular smooth muscle cells -VSMCs- and pericytes) play a pivotal role in vascular biology. Endoglin is an RGD-containing ligand of β1 integrins highly expressed by ECs during angiogenesis. Our working hypothesis...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Rossi, Elisa [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2015transfer abstract |
|---|
| Übergeordnetes Werk: |
Enthalten in: A behaviorally-integrated individual-level state-transition model that can predict rapid changes in evacuation demand days earlier - Guan, Xiangyang ELSEVIER, 2021, Amsterdam [u.a.] |
|---|---|
| Übergeordnetes Werk: |
volume:7 ; year:2015 ; number:2 ; pages:147 |
| Links: |
|---|
| DOI / URN: |
10.1016/S1878-6480(15)30046-X |
|---|
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ELV023573023 |
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| 245 | 1 | 0 | |a 0260 : Endoglin in adhesion between endothelial and mural cells |
| 264 | 1 | |c 2015transfer abstract | |
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| 520 | |a The interaction and interplay between endothelial cells (ECs) and mural cells (such as vascular smooth muscle cells -VSMCs- and pericytes) play a pivotal role in vascular biology. Endoglin is an RGD-containing ligand of β1 integrins highly expressed by ECs during angiogenesis. Our working hypothesis is that endothelial endoglin acts as an adhesion molecule via integrin recognition motifs, allowing the interaction between ECs and mural cells. We find that suppression of endoglin expression or addition of soluble endoglin inhibits the adhesion between ECs and VSMCs as shown by tubulogenesis assays on matrigel. The EC-VSMC adhesion was also abolished by an antiintegrin α5β1 inhibitory antibody, whereas it was markabsedly enhanced by the integrin activators MnCl2 or CXCL12. The CXCL12-dependent cell adhesion was abolished in the presence of soluble endoglin or a derived pentapeptide containing the RGD motif. Adhesion of cells overexpressing different endoglin mutant constructs, allowed the specific mapping of the endoglin RGD motif as involved in adhesion to VSMCs. Binding of soluble endoglin to VSMCs was markedly enhanced by MnCl2 and CXCL12 and this increase was inhibited by the RGD peptide. Moreover, transgenic mice overexpressing soluble endoglin show podocyturia and lower number of glomerular podocytes, suggesting that soluble endoglin induced the detachment of podocytes from glomerular capillaries. These results suggest a critical role for endoglin in integrin- mediated adhesion of mural cells and provide a better understanding on the mechanisms of vessel development and maturation in normal physiology as well as in pathologies such as preeclampsia, cancer or hereditary hemorrhagic telangiectasia. | ||
| 520 | |a The interaction and interplay between endothelial cells (ECs) and mural cells (such as vascular smooth muscle cells -VSMCs- and pericytes) play a pivotal role in vascular biology. Endoglin is an RGD-containing ligand of β1 integrins highly expressed by ECs during angiogenesis. Our working hypothesis is that endothelial endoglin acts as an adhesion molecule via integrin recognition motifs, allowing the interaction between ECs and mural cells. We find that suppression of endoglin expression or addition of soluble endoglin inhibits the adhesion between ECs and VSMCs as shown by tubulogenesis assays on matrigel. The EC-VSMC adhesion was also abolished by an antiintegrin α5β1 inhibitory antibody, whereas it was markabsedly enhanced by the integrin activators MnCl2 or CXCL12. The CXCL12-dependent cell adhesion was abolished in the presence of soluble endoglin or a derived pentapeptide containing the RGD motif. Adhesion of cells overexpressing different endoglin mutant constructs, allowed the specific mapping of the endoglin RGD motif as involved in adhesion to VSMCs. Binding of soluble endoglin to VSMCs was markedly enhanced by MnCl2 and CXCL12 and this increase was inhibited by the RGD peptide. Moreover, transgenic mice overexpressing soluble endoglin show podocyturia and lower number of glomerular podocytes, suggesting that soluble endoglin induced the detachment of podocytes from glomerular capillaries. These results suggest a critical role for endoglin in integrin- mediated adhesion of mural cells and provide a better understanding on the mechanisms of vessel development and maturation in normal physiology as well as in pathologies such as preeclampsia, cancer or hereditary hemorrhagic telangiectasia. | ||
| 700 | 1 | |a Smadja, David |4 oth | |
| 700 | 1 | |a Boscolo, Elisa |4 oth | |
| 700 | 1 | |a Langa, Carmen |4 oth | |
| 700 | 1 | |a Arevalo, Miguel A. |4 oth | |
| 700 | 1 | |a Pericacho, Miguel |4 oth | |
| 700 | 1 | |a Kauskot, Alexandre |4 oth | |
| 700 | 1 | |a Botella, Luisa M. |4 oth | |
| 700 | 1 | |a Gaussem, Pascale |4 oth | |
| 700 | 1 | |a Bischoff, Joyce |4 oth | |
| 700 | 1 | |a Lopez-Novoa, Josè-Miguel |4 oth | |
| 700 | 1 | |a Bernabeu, Carmelo |4 oth | |
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10.1016/S1878-6480(15)30046-X doi GBVA2015011000017.pica (DE-627)ELV023573023 (ELSEVIER)S1878-6480(15)30046-X DE-627 ger DE-627 rakwb eng 610 610 DE-600 380 VZ 55.82 bkl Rossi, Elisa verfasserin aut 0260 : Endoglin in adhesion between endothelial and mural cells 2015transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The interaction and interplay between endothelial cells (ECs) and mural cells (such as vascular smooth muscle cells -VSMCs- and pericytes) play a pivotal role in vascular biology. Endoglin is an RGD-containing ligand of β1 integrins highly expressed by ECs during angiogenesis. Our working hypothesis is that endothelial endoglin acts as an adhesion molecule via integrin recognition motifs, allowing the interaction between ECs and mural cells. We find that suppression of endoglin expression or addition of soluble endoglin inhibits the adhesion between ECs and VSMCs as shown by tubulogenesis assays on matrigel. The EC-VSMC adhesion was also abolished by an antiintegrin α5β1 inhibitory antibody, whereas it was markabsedly enhanced by the integrin activators MnCl2 or CXCL12. The CXCL12-dependent cell adhesion was abolished in the presence of soluble endoglin or a derived pentapeptide containing the RGD motif. Adhesion of cells overexpressing different endoglin mutant constructs, allowed the specific mapping of the endoglin RGD motif as involved in adhesion to VSMCs. Binding of soluble endoglin to VSMCs was markedly enhanced by MnCl2 and CXCL12 and this increase was inhibited by the RGD peptide. Moreover, transgenic mice overexpressing soluble endoglin show podocyturia and lower number of glomerular podocytes, suggesting that soluble endoglin induced the detachment of podocytes from glomerular capillaries. These results suggest a critical role for endoglin in integrin- mediated adhesion of mural cells and provide a better understanding on the mechanisms of vessel development and maturation in normal physiology as well as in pathologies such as preeclampsia, cancer or hereditary hemorrhagic telangiectasia. The interaction and interplay between endothelial cells (ECs) and mural cells (such as vascular smooth muscle cells -VSMCs- and pericytes) play a pivotal role in vascular biology. Endoglin is an RGD-containing ligand of β1 integrins highly expressed by ECs during angiogenesis. Our working hypothesis is that endothelial endoglin acts as an adhesion molecule via integrin recognition motifs, allowing the interaction between ECs and mural cells. We find that suppression of endoglin expression or addition of soluble endoglin inhibits the adhesion between ECs and VSMCs as shown by tubulogenesis assays on matrigel. The EC-VSMC adhesion was also abolished by an antiintegrin α5β1 inhibitory antibody, whereas it was markabsedly enhanced by the integrin activators MnCl2 or CXCL12. The CXCL12-dependent cell adhesion was abolished in the presence of soluble endoglin or a derived pentapeptide containing the RGD motif. Adhesion of cells overexpressing different endoglin mutant constructs, allowed the specific mapping of the endoglin RGD motif as involved in adhesion to VSMCs. Binding of soluble endoglin to VSMCs was markedly enhanced by MnCl2 and CXCL12 and this increase was inhibited by the RGD peptide. Moreover, transgenic mice overexpressing soluble endoglin show podocyturia and lower number of glomerular podocytes, suggesting that soluble endoglin induced the detachment of podocytes from glomerular capillaries. These results suggest a critical role for endoglin in integrin- mediated adhesion of mural cells and provide a better understanding on the mechanisms of vessel development and maturation in normal physiology as well as in pathologies such as preeclampsia, cancer or hereditary hemorrhagic telangiectasia. Smadja, David oth Boscolo, Elisa oth Langa, Carmen oth Arevalo, Miguel A. oth Pericacho, Miguel oth Kauskot, Alexandre oth Botella, Luisa M. oth Gaussem, Pascale oth Bischoff, Joyce oth Lopez-Novoa, Josè-Miguel oth Bernabeu, Carmelo oth Enthalten in Elsevier Masson Guan, Xiangyang ELSEVIER A behaviorally-integrated individual-level state-transition model that can predict rapid changes in evacuation demand days earlier 2021 Amsterdam [u.a.] (DE-627)ELV006385559 volume:7 year:2015 number:2 pages:147 https://doi.org/10.1016/S1878-6480(15)30046-X Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 55.82 Güterverkehr VZ AR 7 2015 2 147 045F 610 |
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10.1016/S1878-6480(15)30046-X doi GBVA2015011000017.pica (DE-627)ELV023573023 (ELSEVIER)S1878-6480(15)30046-X DE-627 ger DE-627 rakwb eng 610 610 DE-600 380 VZ 55.82 bkl Rossi, Elisa verfasserin aut 0260 : Endoglin in adhesion between endothelial and mural cells 2015transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The interaction and interplay between endothelial cells (ECs) and mural cells (such as vascular smooth muscle cells -VSMCs- and pericytes) play a pivotal role in vascular biology. Endoglin is an RGD-containing ligand of β1 integrins highly expressed by ECs during angiogenesis. Our working hypothesis is that endothelial endoglin acts as an adhesion molecule via integrin recognition motifs, allowing the interaction between ECs and mural cells. We find that suppression of endoglin expression or addition of soluble endoglin inhibits the adhesion between ECs and VSMCs as shown by tubulogenesis assays on matrigel. The EC-VSMC adhesion was also abolished by an antiintegrin α5β1 inhibitory antibody, whereas it was markabsedly enhanced by the integrin activators MnCl2 or CXCL12. The CXCL12-dependent cell adhesion was abolished in the presence of soluble endoglin or a derived pentapeptide containing the RGD motif. Adhesion of cells overexpressing different endoglin mutant constructs, allowed the specific mapping of the endoglin RGD motif as involved in adhesion to VSMCs. Binding of soluble endoglin to VSMCs was markedly enhanced by MnCl2 and CXCL12 and this increase was inhibited by the RGD peptide. Moreover, transgenic mice overexpressing soluble endoglin show podocyturia and lower number of glomerular podocytes, suggesting that soluble endoglin induced the detachment of podocytes from glomerular capillaries. These results suggest a critical role for endoglin in integrin- mediated adhesion of mural cells and provide a better understanding on the mechanisms of vessel development and maturation in normal physiology as well as in pathologies such as preeclampsia, cancer or hereditary hemorrhagic telangiectasia. The interaction and interplay between endothelial cells (ECs) and mural cells (such as vascular smooth muscle cells -VSMCs- and pericytes) play a pivotal role in vascular biology. Endoglin is an RGD-containing ligand of β1 integrins highly expressed by ECs during angiogenesis. Our working hypothesis is that endothelial endoglin acts as an adhesion molecule via integrin recognition motifs, allowing the interaction between ECs and mural cells. We find that suppression of endoglin expression or addition of soluble endoglin inhibits the adhesion between ECs and VSMCs as shown by tubulogenesis assays on matrigel. The EC-VSMC adhesion was also abolished by an antiintegrin α5β1 inhibitory antibody, whereas it was markabsedly enhanced by the integrin activators MnCl2 or CXCL12. The CXCL12-dependent cell adhesion was abolished in the presence of soluble endoglin or a derived pentapeptide containing the RGD motif. Adhesion of cells overexpressing different endoglin mutant constructs, allowed the specific mapping of the endoglin RGD motif as involved in adhesion to VSMCs. Binding of soluble endoglin to VSMCs was markedly enhanced by MnCl2 and CXCL12 and this increase was inhibited by the RGD peptide. Moreover, transgenic mice overexpressing soluble endoglin show podocyturia and lower number of glomerular podocytes, suggesting that soluble endoglin induced the detachment of podocytes from glomerular capillaries. These results suggest a critical role for endoglin in integrin- mediated adhesion of mural cells and provide a better understanding on the mechanisms of vessel development and maturation in normal physiology as well as in pathologies such as preeclampsia, cancer or hereditary hemorrhagic telangiectasia. Smadja, David oth Boscolo, Elisa oth Langa, Carmen oth Arevalo, Miguel A. oth Pericacho, Miguel oth Kauskot, Alexandre oth Botella, Luisa M. oth Gaussem, Pascale oth Bischoff, Joyce oth Lopez-Novoa, Josè-Miguel oth Bernabeu, Carmelo oth Enthalten in Elsevier Masson Guan, Xiangyang ELSEVIER A behaviorally-integrated individual-level state-transition model that can predict rapid changes in evacuation demand days earlier 2021 Amsterdam [u.a.] (DE-627)ELV006385559 volume:7 year:2015 number:2 pages:147 https://doi.org/10.1016/S1878-6480(15)30046-X Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 55.82 Güterverkehr VZ AR 7 2015 2 147 045F 610 |
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10.1016/S1878-6480(15)30046-X doi GBVA2015011000017.pica (DE-627)ELV023573023 (ELSEVIER)S1878-6480(15)30046-X DE-627 ger DE-627 rakwb eng 610 610 DE-600 380 VZ 55.82 bkl Rossi, Elisa verfasserin aut 0260 : Endoglin in adhesion between endothelial and mural cells 2015transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The interaction and interplay between endothelial cells (ECs) and mural cells (such as vascular smooth muscle cells -VSMCs- and pericytes) play a pivotal role in vascular biology. Endoglin is an RGD-containing ligand of β1 integrins highly expressed by ECs during angiogenesis. Our working hypothesis is that endothelial endoglin acts as an adhesion molecule via integrin recognition motifs, allowing the interaction between ECs and mural cells. We find that suppression of endoglin expression or addition of soluble endoglin inhibits the adhesion between ECs and VSMCs as shown by tubulogenesis assays on matrigel. The EC-VSMC adhesion was also abolished by an antiintegrin α5β1 inhibitory antibody, whereas it was markabsedly enhanced by the integrin activators MnCl2 or CXCL12. The CXCL12-dependent cell adhesion was abolished in the presence of soluble endoglin or a derived pentapeptide containing the RGD motif. Adhesion of cells overexpressing different endoglin mutant constructs, allowed the specific mapping of the endoglin RGD motif as involved in adhesion to VSMCs. Binding of soluble endoglin to VSMCs was markedly enhanced by MnCl2 and CXCL12 and this increase was inhibited by the RGD peptide. Moreover, transgenic mice overexpressing soluble endoglin show podocyturia and lower number of glomerular podocytes, suggesting that soluble endoglin induced the detachment of podocytes from glomerular capillaries. These results suggest a critical role for endoglin in integrin- mediated adhesion of mural cells and provide a better understanding on the mechanisms of vessel development and maturation in normal physiology as well as in pathologies such as preeclampsia, cancer or hereditary hemorrhagic telangiectasia. The interaction and interplay between endothelial cells (ECs) and mural cells (such as vascular smooth muscle cells -VSMCs- and pericytes) play a pivotal role in vascular biology. Endoglin is an RGD-containing ligand of β1 integrins highly expressed by ECs during angiogenesis. Our working hypothesis is that endothelial endoglin acts as an adhesion molecule via integrin recognition motifs, allowing the interaction between ECs and mural cells. We find that suppression of endoglin expression or addition of soluble endoglin inhibits the adhesion between ECs and VSMCs as shown by tubulogenesis assays on matrigel. The EC-VSMC adhesion was also abolished by an antiintegrin α5β1 inhibitory antibody, whereas it was markabsedly enhanced by the integrin activators MnCl2 or CXCL12. The CXCL12-dependent cell adhesion was abolished in the presence of soluble endoglin or a derived pentapeptide containing the RGD motif. Adhesion of cells overexpressing different endoglin mutant constructs, allowed the specific mapping of the endoglin RGD motif as involved in adhesion to VSMCs. Binding of soluble endoglin to VSMCs was markedly enhanced by MnCl2 and CXCL12 and this increase was inhibited by the RGD peptide. Moreover, transgenic mice overexpressing soluble endoglin show podocyturia and lower number of glomerular podocytes, suggesting that soluble endoglin induced the detachment of podocytes from glomerular capillaries. These results suggest a critical role for endoglin in integrin- mediated adhesion of mural cells and provide a better understanding on the mechanisms of vessel development and maturation in normal physiology as well as in pathologies such as preeclampsia, cancer or hereditary hemorrhagic telangiectasia. Smadja, David oth Boscolo, Elisa oth Langa, Carmen oth Arevalo, Miguel A. oth Pericacho, Miguel oth Kauskot, Alexandre oth Botella, Luisa M. oth Gaussem, Pascale oth Bischoff, Joyce oth Lopez-Novoa, Josè-Miguel oth Bernabeu, Carmelo oth Enthalten in Elsevier Masson Guan, Xiangyang ELSEVIER A behaviorally-integrated individual-level state-transition model that can predict rapid changes in evacuation demand days earlier 2021 Amsterdam [u.a.] (DE-627)ELV006385559 volume:7 year:2015 number:2 pages:147 https://doi.org/10.1016/S1878-6480(15)30046-X Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 55.82 Güterverkehr VZ AR 7 2015 2 147 045F 610 |
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10.1016/S1878-6480(15)30046-X doi GBVA2015011000017.pica (DE-627)ELV023573023 (ELSEVIER)S1878-6480(15)30046-X DE-627 ger DE-627 rakwb eng 610 610 DE-600 380 VZ 55.82 bkl Rossi, Elisa verfasserin aut 0260 : Endoglin in adhesion between endothelial and mural cells 2015transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The interaction and interplay between endothelial cells (ECs) and mural cells (such as vascular smooth muscle cells -VSMCs- and pericytes) play a pivotal role in vascular biology. Endoglin is an RGD-containing ligand of β1 integrins highly expressed by ECs during angiogenesis. Our working hypothesis is that endothelial endoglin acts as an adhesion molecule via integrin recognition motifs, allowing the interaction between ECs and mural cells. We find that suppression of endoglin expression or addition of soluble endoglin inhibits the adhesion between ECs and VSMCs as shown by tubulogenesis assays on matrigel. The EC-VSMC adhesion was also abolished by an antiintegrin α5β1 inhibitory antibody, whereas it was markabsedly enhanced by the integrin activators MnCl2 or CXCL12. The CXCL12-dependent cell adhesion was abolished in the presence of soluble endoglin or a derived pentapeptide containing the RGD motif. Adhesion of cells overexpressing different endoglin mutant constructs, allowed the specific mapping of the endoglin RGD motif as involved in adhesion to VSMCs. Binding of soluble endoglin to VSMCs was markedly enhanced by MnCl2 and CXCL12 and this increase was inhibited by the RGD peptide. Moreover, transgenic mice overexpressing soluble endoglin show podocyturia and lower number of glomerular podocytes, suggesting that soluble endoglin induced the detachment of podocytes from glomerular capillaries. These results suggest a critical role for endoglin in integrin- mediated adhesion of mural cells and provide a better understanding on the mechanisms of vessel development and maturation in normal physiology as well as in pathologies such as preeclampsia, cancer or hereditary hemorrhagic telangiectasia. The interaction and interplay between endothelial cells (ECs) and mural cells (such as vascular smooth muscle cells -VSMCs- and pericytes) play a pivotal role in vascular biology. Endoglin is an RGD-containing ligand of β1 integrins highly expressed by ECs during angiogenesis. Our working hypothesis is that endothelial endoglin acts as an adhesion molecule via integrin recognition motifs, allowing the interaction between ECs and mural cells. We find that suppression of endoglin expression or addition of soluble endoglin inhibits the adhesion between ECs and VSMCs as shown by tubulogenesis assays on matrigel. The EC-VSMC adhesion was also abolished by an antiintegrin α5β1 inhibitory antibody, whereas it was markabsedly enhanced by the integrin activators MnCl2 or CXCL12. The CXCL12-dependent cell adhesion was abolished in the presence of soluble endoglin or a derived pentapeptide containing the RGD motif. Adhesion of cells overexpressing different endoglin mutant constructs, allowed the specific mapping of the endoglin RGD motif as involved in adhesion to VSMCs. Binding of soluble endoglin to VSMCs was markedly enhanced by MnCl2 and CXCL12 and this increase was inhibited by the RGD peptide. Moreover, transgenic mice overexpressing soluble endoglin show podocyturia and lower number of glomerular podocytes, suggesting that soluble endoglin induced the detachment of podocytes from glomerular capillaries. These results suggest a critical role for endoglin in integrin- mediated adhesion of mural cells and provide a better understanding on the mechanisms of vessel development and maturation in normal physiology as well as in pathologies such as preeclampsia, cancer or hereditary hemorrhagic telangiectasia. Smadja, David oth Boscolo, Elisa oth Langa, Carmen oth Arevalo, Miguel A. oth Pericacho, Miguel oth Kauskot, Alexandre oth Botella, Luisa M. oth Gaussem, Pascale oth Bischoff, Joyce oth Lopez-Novoa, Josè-Miguel oth Bernabeu, Carmelo oth Enthalten in Elsevier Masson Guan, Xiangyang ELSEVIER A behaviorally-integrated individual-level state-transition model that can predict rapid changes in evacuation demand days earlier 2021 Amsterdam [u.a.] (DE-627)ELV006385559 volume:7 year:2015 number:2 pages:147 https://doi.org/10.1016/S1878-6480(15)30046-X Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 55.82 Güterverkehr VZ AR 7 2015 2 147 045F 610 |
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10.1016/S1878-6480(15)30046-X doi GBVA2015011000017.pica (DE-627)ELV023573023 (ELSEVIER)S1878-6480(15)30046-X DE-627 ger DE-627 rakwb eng 610 610 DE-600 380 VZ 55.82 bkl Rossi, Elisa verfasserin aut 0260 : Endoglin in adhesion between endothelial and mural cells 2015transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The interaction and interplay between endothelial cells (ECs) and mural cells (such as vascular smooth muscle cells -VSMCs- and pericytes) play a pivotal role in vascular biology. Endoglin is an RGD-containing ligand of β1 integrins highly expressed by ECs during angiogenesis. Our working hypothesis is that endothelial endoglin acts as an adhesion molecule via integrin recognition motifs, allowing the interaction between ECs and mural cells. We find that suppression of endoglin expression or addition of soluble endoglin inhibits the adhesion between ECs and VSMCs as shown by tubulogenesis assays on matrigel. The EC-VSMC adhesion was also abolished by an antiintegrin α5β1 inhibitory antibody, whereas it was markabsedly enhanced by the integrin activators MnCl2 or CXCL12. The CXCL12-dependent cell adhesion was abolished in the presence of soluble endoglin or a derived pentapeptide containing the RGD motif. Adhesion of cells overexpressing different endoglin mutant constructs, allowed the specific mapping of the endoglin RGD motif as involved in adhesion to VSMCs. Binding of soluble endoglin to VSMCs was markedly enhanced by MnCl2 and CXCL12 and this increase was inhibited by the RGD peptide. Moreover, transgenic mice overexpressing soluble endoglin show podocyturia and lower number of glomerular podocytes, suggesting that soluble endoglin induced the detachment of podocytes from glomerular capillaries. These results suggest a critical role for endoglin in integrin- mediated adhesion of mural cells and provide a better understanding on the mechanisms of vessel development and maturation in normal physiology as well as in pathologies such as preeclampsia, cancer or hereditary hemorrhagic telangiectasia. The interaction and interplay between endothelial cells (ECs) and mural cells (such as vascular smooth muscle cells -VSMCs- and pericytes) play a pivotal role in vascular biology. Endoglin is an RGD-containing ligand of β1 integrins highly expressed by ECs during angiogenesis. Our working hypothesis is that endothelial endoglin acts as an adhesion molecule via integrin recognition motifs, allowing the interaction between ECs and mural cells. We find that suppression of endoglin expression or addition of soluble endoglin inhibits the adhesion between ECs and VSMCs as shown by tubulogenesis assays on matrigel. The EC-VSMC adhesion was also abolished by an antiintegrin α5β1 inhibitory antibody, whereas it was markabsedly enhanced by the integrin activators MnCl2 or CXCL12. The CXCL12-dependent cell adhesion was abolished in the presence of soluble endoglin or a derived pentapeptide containing the RGD motif. Adhesion of cells overexpressing different endoglin mutant constructs, allowed the specific mapping of the endoglin RGD motif as involved in adhesion to VSMCs. Binding of soluble endoglin to VSMCs was markedly enhanced by MnCl2 and CXCL12 and this increase was inhibited by the RGD peptide. Moreover, transgenic mice overexpressing soluble endoglin show podocyturia and lower number of glomerular podocytes, suggesting that soluble endoglin induced the detachment of podocytes from glomerular capillaries. These results suggest a critical role for endoglin in integrin- mediated adhesion of mural cells and provide a better understanding on the mechanisms of vessel development and maturation in normal physiology as well as in pathologies such as preeclampsia, cancer or hereditary hemorrhagic telangiectasia. Smadja, David oth Boscolo, Elisa oth Langa, Carmen oth Arevalo, Miguel A. oth Pericacho, Miguel oth Kauskot, Alexandre oth Botella, Luisa M. oth Gaussem, Pascale oth Bischoff, Joyce oth Lopez-Novoa, Josè-Miguel oth Bernabeu, Carmelo oth Enthalten in Elsevier Masson Guan, Xiangyang ELSEVIER A behaviorally-integrated individual-level state-transition model that can predict rapid changes in evacuation demand days earlier 2021 Amsterdam [u.a.] (DE-627)ELV006385559 volume:7 year:2015 number:2 pages:147 https://doi.org/10.1016/S1878-6480(15)30046-X Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 55.82 Güterverkehr VZ AR 7 2015 2 147 045F 610 |
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Enthalten in A behaviorally-integrated individual-level state-transition model that can predict rapid changes in evacuation demand days earlier Amsterdam [u.a.] volume:7 year:2015 number:2 pages:147 |
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A behaviorally-integrated individual-level state-transition model that can predict rapid changes in evacuation demand days earlier |
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Rossi, Elisa @@aut@@ Smadja, David @@oth@@ Boscolo, Elisa @@oth@@ Langa, Carmen @@oth@@ Arevalo, Miguel A. @@oth@@ Pericacho, Miguel @@oth@@ Kauskot, Alexandre @@oth@@ Botella, Luisa M. @@oth@@ Gaussem, Pascale @@oth@@ Bischoff, Joyce @@oth@@ Lopez-Novoa, Josè-Miguel @@oth@@ Bernabeu, Carmelo @@oth@@ |
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The interaction and interplay between endothelial cells (ECs) and mural cells (such as vascular smooth muscle cells -VSMCs- and pericytes) play a pivotal role in vascular biology. Endoglin is an RGD-containing ligand of β1 integrins highly expressed by ECs during angiogenesis. Our working hypothesis is that endothelial endoglin acts as an adhesion molecule via integrin recognition motifs, allowing the interaction between ECs and mural cells. We find that suppression of endoglin expression or addition of soluble endoglin inhibits the adhesion between ECs and VSMCs as shown by tubulogenesis assays on matrigel. The EC-VSMC adhesion was also abolished by an antiintegrin α5β1 inhibitory antibody, whereas it was markabsedly enhanced by the integrin activators MnCl2 or CXCL12. The CXCL12-dependent cell adhesion was abolished in the presence of soluble endoglin or a derived pentapeptide containing the RGD motif. Adhesion of cells overexpressing different endoglin mutant constructs, allowed the specific mapping of the endoglin RGD motif as involved in adhesion to VSMCs. Binding of soluble endoglin to VSMCs was markedly enhanced by MnCl2 and CXCL12 and this increase was inhibited by the RGD peptide. Moreover, transgenic mice overexpressing soluble endoglin show podocyturia and lower number of glomerular podocytes, suggesting that soluble endoglin induced the detachment of podocytes from glomerular capillaries. These results suggest a critical role for endoglin in integrin- mediated adhesion of mural cells and provide a better understanding on the mechanisms of vessel development and maturation in normal physiology as well as in pathologies such as preeclampsia, cancer or hereditary hemorrhagic telangiectasia. |
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The interaction and interplay between endothelial cells (ECs) and mural cells (such as vascular smooth muscle cells -VSMCs- and pericytes) play a pivotal role in vascular biology. Endoglin is an RGD-containing ligand of β1 integrins highly expressed by ECs during angiogenesis. Our working hypothesis is that endothelial endoglin acts as an adhesion molecule via integrin recognition motifs, allowing the interaction between ECs and mural cells. We find that suppression of endoglin expression or addition of soluble endoglin inhibits the adhesion between ECs and VSMCs as shown by tubulogenesis assays on matrigel. The EC-VSMC adhesion was also abolished by an antiintegrin α5β1 inhibitory antibody, whereas it was markabsedly enhanced by the integrin activators MnCl2 or CXCL12. The CXCL12-dependent cell adhesion was abolished in the presence of soluble endoglin or a derived pentapeptide containing the RGD motif. Adhesion of cells overexpressing different endoglin mutant constructs, allowed the specific mapping of the endoglin RGD motif as involved in adhesion to VSMCs. Binding of soluble endoglin to VSMCs was markedly enhanced by MnCl2 and CXCL12 and this increase was inhibited by the RGD peptide. Moreover, transgenic mice overexpressing soluble endoglin show podocyturia and lower number of glomerular podocytes, suggesting that soluble endoglin induced the detachment of podocytes from glomerular capillaries. These results suggest a critical role for endoglin in integrin- mediated adhesion of mural cells and provide a better understanding on the mechanisms of vessel development and maturation in normal physiology as well as in pathologies such as preeclampsia, cancer or hereditary hemorrhagic telangiectasia. |
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The interaction and interplay between endothelial cells (ECs) and mural cells (such as vascular smooth muscle cells -VSMCs- and pericytes) play a pivotal role in vascular biology. Endoglin is an RGD-containing ligand of β1 integrins highly expressed by ECs during angiogenesis. Our working hypothesis is that endothelial endoglin acts as an adhesion molecule via integrin recognition motifs, allowing the interaction between ECs and mural cells. We find that suppression of endoglin expression or addition of soluble endoglin inhibits the adhesion between ECs and VSMCs as shown by tubulogenesis assays on matrigel. The EC-VSMC adhesion was also abolished by an antiintegrin α5β1 inhibitory antibody, whereas it was markabsedly enhanced by the integrin activators MnCl2 or CXCL12. The CXCL12-dependent cell adhesion was abolished in the presence of soluble endoglin or a derived pentapeptide containing the RGD motif. Adhesion of cells overexpressing different endoglin mutant constructs, allowed the specific mapping of the endoglin RGD motif as involved in adhesion to VSMCs. Binding of soluble endoglin to VSMCs was markedly enhanced by MnCl2 and CXCL12 and this increase was inhibited by the RGD peptide. Moreover, transgenic mice overexpressing soluble endoglin show podocyturia and lower number of glomerular podocytes, suggesting that soluble endoglin induced the detachment of podocytes from glomerular capillaries. These results suggest a critical role for endoglin in integrin- mediated adhesion of mural cells and provide a better understanding on the mechanisms of vessel development and maturation in normal physiology as well as in pathologies such as preeclampsia, cancer or hereditary hemorrhagic telangiectasia. |
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