0130 : Endoglin is a new partner involved in platelet – endothelium interactions: role in microvessel stability?
Hereditary Hemorragic Telangectasia (HHT) is characterized by a bleeding tendency that is postulated to be a consequence of microvessel fragility. HHT type 1 patients present heterozygous mutations in the endoglin gene resulting in a loss of expression of membrane endoglin in their endothelial cells...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Rossi, Elisa [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2016transfer abstract |
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| 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:8 ; year:2016 ; number:3 ; pages:219 |
| Links: |
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| DOI / URN: |
10.1016/S1878-6480(16)30405-0 |
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ELV019382405 |
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| 245 | 1 | 0 | |a 0130 : Endoglin is a new partner involved in platelet – endothelium interactions: role in microvessel stability? |
| 264 | 1 | |c 2016transfer abstract | |
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| 520 | |a Hereditary Hemorragic Telangectasia (HHT) is characterized by a bleeding tendency that is postulated to be a consequence of microvessel fragility. HHT type 1 patients present heterozygous mutations in the endoglin gene resulting in a loss of expression of membrane endoglin in their endothelial cells (EC), while platelets in these patients display normal functions in vitro. We have reported previously that endothelial endoglin is involved, via its RGD motif, in inflammation though integrin-mediated leukocyte adhesion and transmigration. We recently found that endoglin-haplodeficient mice (Eng+/–) have significantly higher bleeding time than Eng+/+ animals, therefore, we haypothesized that endoglin may also act as an adhesion molecule via integrin recognition in the interaction between EC and platelets during hemostasis. Coating plastic wells with the extracellular domain of endoglin enhanced platelets adhesion to the wells under static condition and this interaction persist under flow condition. Similarly, platelets could adhere on confluent EC in an endoglin-mediated process, while the silencing of endoglin expression in EC, and the addition of soluble endoglin or of anti-endoglin antibodies, inhibited stable platelet adhesion to EC. Remarkably, platelets from Glanzmann's thrombasthenia patients lacking the€αIIbβ3 integrin were defective for adhesion on EC, wheras CHO cells, ectopically expressing the human αIIbβ3 integrin acquired the capacity to adhere on rat myoblast transfectants expressing human endoglin (L6E9-E), thus confirming the interaction between endoglin and the αIIbβ3 integrin. These results establish a new critical role for endoglin in integrin-mediated adhesion of platelets to endothelium and provide a better understanding on the cellular mechanisms involved in bleeding events occurring in HHT. | ||
| 520 | |a Hereditary Hemorragic Telangectasia (HHT) is characterized by a bleeding tendency that is postulated to be a consequence of microvessel fragility. HHT type 1 patients present heterozygous mutations in the endoglin gene resulting in a loss of expression of membrane endoglin in their endothelial cells (EC), while platelets in these patients display normal functions in vitro. We have reported previously that endothelial endoglin is involved, via its RGD motif, in inflammation though integrin-mediated leukocyte adhesion and transmigration. We recently found that endoglin-haplodeficient mice (Eng+/–) have significantly higher bleeding time than Eng+/+ animals, therefore, we haypothesized that endoglin may also act as an adhesion molecule via integrin recognition in the interaction between EC and platelets during hemostasis. Coating plastic wells with the extracellular domain of endoglin enhanced platelets adhesion to the wells under static condition and this interaction persist under flow condition. Similarly, platelets could adhere on confluent EC in an endoglin-mediated process, while the silencing of endoglin expression in EC, and the addition of soluble endoglin or of anti-endoglin antibodies, inhibited stable platelet adhesion to EC. Remarkably, platelets from Glanzmann's thrombasthenia patients lacking the€αIIbβ3 integrin were defective for adhesion on EC, wheras CHO cells, ectopically expressing the human αIIbβ3 integrin acquired the capacity to adhere on rat myoblast transfectants expressing human endoglin (L6E9-E), thus confirming the interaction between endoglin and the αIIbβ3 integrin. These results establish a new critical role for endoglin in integrin-mediated adhesion of platelets to endothelium and provide a better understanding on the cellular mechanisms involved in bleeding events occurring in HHT. | ||
| 700 | 1 | |a Bachelot-Loza, Christilla |4 oth | |
| 700 | 1 | |a Pidard, Dominique |4 oth | |
| 700 | 1 | |a Gaussem, Pascale |4 oth | |
| 700 | 1 | |a Smadja, David |4 oth | |
| 700 | 1 | |a Chassac, Sonia |4 oth | |
| 700 | 1 | |a Pericacho, Miguel |4 oth | |
| 700 | 1 | |a Lopez-Novoa, José M. |4 oth | |
| 700 | 1 | |a Langa, Carmen |4 oth | |
| 700 | 1 | |a Gonzalez-Manchon, Consuelo |4 oth | |
| 700 | 1 | |a Bernabeu, Carmelo |4 oth | |
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10.1016/S1878-6480(16)30405-0 doi GBVA2016011000015.pica (DE-627)ELV019382405 (ELSEVIER)S1878-6480(16)30405-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 380 VZ 55.82 bkl Rossi, Elisa verfasserin aut 0130 : Endoglin is a new partner involved in platelet – endothelium interactions: role in microvessel stability? 2016transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Hereditary Hemorragic Telangectasia (HHT) is characterized by a bleeding tendency that is postulated to be a consequence of microvessel fragility. HHT type 1 patients present heterozygous mutations in the endoglin gene resulting in a loss of expression of membrane endoglin in their endothelial cells (EC), while platelets in these patients display normal functions in vitro. We have reported previously that endothelial endoglin is involved, via its RGD motif, in inflammation though integrin-mediated leukocyte adhesion and transmigration. We recently found that endoglin-haplodeficient mice (Eng+/–) have significantly higher bleeding time than Eng+/+ animals, therefore, we haypothesized that endoglin may also act as an adhesion molecule via integrin recognition in the interaction between EC and platelets during hemostasis. Coating plastic wells with the extracellular domain of endoglin enhanced platelets adhesion to the wells under static condition and this interaction persist under flow condition. Similarly, platelets could adhere on confluent EC in an endoglin-mediated process, while the silencing of endoglin expression in EC, and the addition of soluble endoglin or of anti-endoglin antibodies, inhibited stable platelet adhesion to EC. Remarkably, platelets from Glanzmann's thrombasthenia patients lacking the€αIIbβ3 integrin were defective for adhesion on EC, wheras CHO cells, ectopically expressing the human αIIbβ3 integrin acquired the capacity to adhere on rat myoblast transfectants expressing human endoglin (L6E9-E), thus confirming the interaction between endoglin and the αIIbβ3 integrin. These results establish a new critical role for endoglin in integrin-mediated adhesion of platelets to endothelium and provide a better understanding on the cellular mechanisms involved in bleeding events occurring in HHT. Hereditary Hemorragic Telangectasia (HHT) is characterized by a bleeding tendency that is postulated to be a consequence of microvessel fragility. HHT type 1 patients present heterozygous mutations in the endoglin gene resulting in a loss of expression of membrane endoglin in their endothelial cells (EC), while platelets in these patients display normal functions in vitro. We have reported previously that endothelial endoglin is involved, via its RGD motif, in inflammation though integrin-mediated leukocyte adhesion and transmigration. We recently found that endoglin-haplodeficient mice (Eng+/–) have significantly higher bleeding time than Eng+/+ animals, therefore, we haypothesized that endoglin may also act as an adhesion molecule via integrin recognition in the interaction between EC and platelets during hemostasis. Coating plastic wells with the extracellular domain of endoglin enhanced platelets adhesion to the wells under static condition and this interaction persist under flow condition. Similarly, platelets could adhere on confluent EC in an endoglin-mediated process, while the silencing of endoglin expression in EC, and the addition of soluble endoglin or of anti-endoglin antibodies, inhibited stable platelet adhesion to EC. Remarkably, platelets from Glanzmann's thrombasthenia patients lacking the€αIIbβ3 integrin were defective for adhesion on EC, wheras CHO cells, ectopically expressing the human αIIbβ3 integrin acquired the capacity to adhere on rat myoblast transfectants expressing human endoglin (L6E9-E), thus confirming the interaction between endoglin and the αIIbβ3 integrin. These results establish a new critical role for endoglin in integrin-mediated adhesion of platelets to endothelium and provide a better understanding on the cellular mechanisms involved in bleeding events occurring in HHT. Bachelot-Loza, Christilla oth Pidard, Dominique oth Gaussem, Pascale oth Smadja, David oth Chassac, Sonia oth Pericacho, Miguel oth Lopez-Novoa, José M. oth Langa, Carmen oth Gonzalez-Manchon, Consuelo 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:8 year:2016 number:3 pages:219 https://doi.org/10.1016/S1878-6480(16)30405-0 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 55.82 Güterverkehr VZ AR 8 2016 3 219 045F 610 |
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10.1016/S1878-6480(16)30405-0 doi GBVA2016011000015.pica (DE-627)ELV019382405 (ELSEVIER)S1878-6480(16)30405-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 380 VZ 55.82 bkl Rossi, Elisa verfasserin aut 0130 : Endoglin is a new partner involved in platelet – endothelium interactions: role in microvessel stability? 2016transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Hereditary Hemorragic Telangectasia (HHT) is characterized by a bleeding tendency that is postulated to be a consequence of microvessel fragility. HHT type 1 patients present heterozygous mutations in the endoglin gene resulting in a loss of expression of membrane endoglin in their endothelial cells (EC), while platelets in these patients display normal functions in vitro. We have reported previously that endothelial endoglin is involved, via its RGD motif, in inflammation though integrin-mediated leukocyte adhesion and transmigration. We recently found that endoglin-haplodeficient mice (Eng+/–) have significantly higher bleeding time than Eng+/+ animals, therefore, we haypothesized that endoglin may also act as an adhesion molecule via integrin recognition in the interaction between EC and platelets during hemostasis. Coating plastic wells with the extracellular domain of endoglin enhanced platelets adhesion to the wells under static condition and this interaction persist under flow condition. Similarly, platelets could adhere on confluent EC in an endoglin-mediated process, while the silencing of endoglin expression in EC, and the addition of soluble endoglin or of anti-endoglin antibodies, inhibited stable platelet adhesion to EC. Remarkably, platelets from Glanzmann's thrombasthenia patients lacking the€αIIbβ3 integrin were defective for adhesion on EC, wheras CHO cells, ectopically expressing the human αIIbβ3 integrin acquired the capacity to adhere on rat myoblast transfectants expressing human endoglin (L6E9-E), thus confirming the interaction between endoglin and the αIIbβ3 integrin. These results establish a new critical role for endoglin in integrin-mediated adhesion of platelets to endothelium and provide a better understanding on the cellular mechanisms involved in bleeding events occurring in HHT. Hereditary Hemorragic Telangectasia (HHT) is characterized by a bleeding tendency that is postulated to be a consequence of microvessel fragility. HHT type 1 patients present heterozygous mutations in the endoglin gene resulting in a loss of expression of membrane endoglin in their endothelial cells (EC), while platelets in these patients display normal functions in vitro. We have reported previously that endothelial endoglin is involved, via its RGD motif, in inflammation though integrin-mediated leukocyte adhesion and transmigration. We recently found that endoglin-haplodeficient mice (Eng+/–) have significantly higher bleeding time than Eng+/+ animals, therefore, we haypothesized that endoglin may also act as an adhesion molecule via integrin recognition in the interaction between EC and platelets during hemostasis. Coating plastic wells with the extracellular domain of endoglin enhanced platelets adhesion to the wells under static condition and this interaction persist under flow condition. Similarly, platelets could adhere on confluent EC in an endoglin-mediated process, while the silencing of endoglin expression in EC, and the addition of soluble endoglin or of anti-endoglin antibodies, inhibited stable platelet adhesion to EC. Remarkably, platelets from Glanzmann's thrombasthenia patients lacking the€αIIbβ3 integrin were defective for adhesion on EC, wheras CHO cells, ectopically expressing the human αIIbβ3 integrin acquired the capacity to adhere on rat myoblast transfectants expressing human endoglin (L6E9-E), thus confirming the interaction between endoglin and the αIIbβ3 integrin. These results establish a new critical role for endoglin in integrin-mediated adhesion of platelets to endothelium and provide a better understanding on the cellular mechanisms involved in bleeding events occurring in HHT. Bachelot-Loza, Christilla oth Pidard, Dominique oth Gaussem, Pascale oth Smadja, David oth Chassac, Sonia oth Pericacho, Miguel oth Lopez-Novoa, José M. oth Langa, Carmen oth Gonzalez-Manchon, Consuelo 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:8 year:2016 number:3 pages:219 https://doi.org/10.1016/S1878-6480(16)30405-0 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 55.82 Güterverkehr VZ AR 8 2016 3 219 045F 610 |
| allfields_unstemmed |
10.1016/S1878-6480(16)30405-0 doi GBVA2016011000015.pica (DE-627)ELV019382405 (ELSEVIER)S1878-6480(16)30405-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 380 VZ 55.82 bkl Rossi, Elisa verfasserin aut 0130 : Endoglin is a new partner involved in platelet – endothelium interactions: role in microvessel stability? 2016transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Hereditary Hemorragic Telangectasia (HHT) is characterized by a bleeding tendency that is postulated to be a consequence of microvessel fragility. HHT type 1 patients present heterozygous mutations in the endoglin gene resulting in a loss of expression of membrane endoglin in their endothelial cells (EC), while platelets in these patients display normal functions in vitro. We have reported previously that endothelial endoglin is involved, via its RGD motif, in inflammation though integrin-mediated leukocyte adhesion and transmigration. We recently found that endoglin-haplodeficient mice (Eng+/–) have significantly higher bleeding time than Eng+/+ animals, therefore, we haypothesized that endoglin may also act as an adhesion molecule via integrin recognition in the interaction between EC and platelets during hemostasis. Coating plastic wells with the extracellular domain of endoglin enhanced platelets adhesion to the wells under static condition and this interaction persist under flow condition. Similarly, platelets could adhere on confluent EC in an endoglin-mediated process, while the silencing of endoglin expression in EC, and the addition of soluble endoglin or of anti-endoglin antibodies, inhibited stable platelet adhesion to EC. Remarkably, platelets from Glanzmann's thrombasthenia patients lacking the€αIIbβ3 integrin were defective for adhesion on EC, wheras CHO cells, ectopically expressing the human αIIbβ3 integrin acquired the capacity to adhere on rat myoblast transfectants expressing human endoglin (L6E9-E), thus confirming the interaction between endoglin and the αIIbβ3 integrin. These results establish a new critical role for endoglin in integrin-mediated adhesion of platelets to endothelium and provide a better understanding on the cellular mechanisms involved in bleeding events occurring in HHT. Hereditary Hemorragic Telangectasia (HHT) is characterized by a bleeding tendency that is postulated to be a consequence of microvessel fragility. HHT type 1 patients present heterozygous mutations in the endoglin gene resulting in a loss of expression of membrane endoglin in their endothelial cells (EC), while platelets in these patients display normal functions in vitro. We have reported previously that endothelial endoglin is involved, via its RGD motif, in inflammation though integrin-mediated leukocyte adhesion and transmigration. We recently found that endoglin-haplodeficient mice (Eng+/–) have significantly higher bleeding time than Eng+/+ animals, therefore, we haypothesized that endoglin may also act as an adhesion molecule via integrin recognition in the interaction between EC and platelets during hemostasis. Coating plastic wells with the extracellular domain of endoglin enhanced platelets adhesion to the wells under static condition and this interaction persist under flow condition. Similarly, platelets could adhere on confluent EC in an endoglin-mediated process, while the silencing of endoglin expression in EC, and the addition of soluble endoglin or of anti-endoglin antibodies, inhibited stable platelet adhesion to EC. Remarkably, platelets from Glanzmann's thrombasthenia patients lacking the€αIIbβ3 integrin were defective for adhesion on EC, wheras CHO cells, ectopically expressing the human αIIbβ3 integrin acquired the capacity to adhere on rat myoblast transfectants expressing human endoglin (L6E9-E), thus confirming the interaction between endoglin and the αIIbβ3 integrin. These results establish a new critical role for endoglin in integrin-mediated adhesion of platelets to endothelium and provide a better understanding on the cellular mechanisms involved in bleeding events occurring in HHT. Bachelot-Loza, Christilla oth Pidard, Dominique oth Gaussem, Pascale oth Smadja, David oth Chassac, Sonia oth Pericacho, Miguel oth Lopez-Novoa, José M. oth Langa, Carmen oth Gonzalez-Manchon, Consuelo 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:8 year:2016 number:3 pages:219 https://doi.org/10.1016/S1878-6480(16)30405-0 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 55.82 Güterverkehr VZ AR 8 2016 3 219 045F 610 |
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10.1016/S1878-6480(16)30405-0 doi GBVA2016011000015.pica (DE-627)ELV019382405 (ELSEVIER)S1878-6480(16)30405-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 380 VZ 55.82 bkl Rossi, Elisa verfasserin aut 0130 : Endoglin is a new partner involved in platelet – endothelium interactions: role in microvessel stability? 2016transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Hereditary Hemorragic Telangectasia (HHT) is characterized by a bleeding tendency that is postulated to be a consequence of microvessel fragility. HHT type 1 patients present heterozygous mutations in the endoglin gene resulting in a loss of expression of membrane endoglin in their endothelial cells (EC), while platelets in these patients display normal functions in vitro. We have reported previously that endothelial endoglin is involved, via its RGD motif, in inflammation though integrin-mediated leukocyte adhesion and transmigration. We recently found that endoglin-haplodeficient mice (Eng+/–) have significantly higher bleeding time than Eng+/+ animals, therefore, we haypothesized that endoglin may also act as an adhesion molecule via integrin recognition in the interaction between EC and platelets during hemostasis. Coating plastic wells with the extracellular domain of endoglin enhanced platelets adhesion to the wells under static condition and this interaction persist under flow condition. Similarly, platelets could adhere on confluent EC in an endoglin-mediated process, while the silencing of endoglin expression in EC, and the addition of soluble endoglin or of anti-endoglin antibodies, inhibited stable platelet adhesion to EC. Remarkably, platelets from Glanzmann's thrombasthenia patients lacking the€αIIbβ3 integrin were defective for adhesion on EC, wheras CHO cells, ectopically expressing the human αIIbβ3 integrin acquired the capacity to adhere on rat myoblast transfectants expressing human endoglin (L6E9-E), thus confirming the interaction between endoglin and the αIIbβ3 integrin. These results establish a new critical role for endoglin in integrin-mediated adhesion of platelets to endothelium and provide a better understanding on the cellular mechanisms involved in bleeding events occurring in HHT. Hereditary Hemorragic Telangectasia (HHT) is characterized by a bleeding tendency that is postulated to be a consequence of microvessel fragility. HHT type 1 patients present heterozygous mutations in the endoglin gene resulting in a loss of expression of membrane endoglin in their endothelial cells (EC), while platelets in these patients display normal functions in vitro. We have reported previously that endothelial endoglin is involved, via its RGD motif, in inflammation though integrin-mediated leukocyte adhesion and transmigration. We recently found that endoglin-haplodeficient mice (Eng+/–) have significantly higher bleeding time than Eng+/+ animals, therefore, we haypothesized that endoglin may also act as an adhesion molecule via integrin recognition in the interaction between EC and platelets during hemostasis. Coating plastic wells with the extracellular domain of endoglin enhanced platelets adhesion to the wells under static condition and this interaction persist under flow condition. Similarly, platelets could adhere on confluent EC in an endoglin-mediated process, while the silencing of endoglin expression in EC, and the addition of soluble endoglin or of anti-endoglin antibodies, inhibited stable platelet adhesion to EC. Remarkably, platelets from Glanzmann's thrombasthenia patients lacking the€αIIbβ3 integrin were defective for adhesion on EC, wheras CHO cells, ectopically expressing the human αIIbβ3 integrin acquired the capacity to adhere on rat myoblast transfectants expressing human endoglin (L6E9-E), thus confirming the interaction between endoglin and the αIIbβ3 integrin. These results establish a new critical role for endoglin in integrin-mediated adhesion of platelets to endothelium and provide a better understanding on the cellular mechanisms involved in bleeding events occurring in HHT. Bachelot-Loza, Christilla oth Pidard, Dominique oth Gaussem, Pascale oth Smadja, David oth Chassac, Sonia oth Pericacho, Miguel oth Lopez-Novoa, José M. oth Langa, Carmen oth Gonzalez-Manchon, Consuelo 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:8 year:2016 number:3 pages:219 https://doi.org/10.1016/S1878-6480(16)30405-0 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 55.82 Güterverkehr VZ AR 8 2016 3 219 045F 610 |
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10.1016/S1878-6480(16)30405-0 doi GBVA2016011000015.pica (DE-627)ELV019382405 (ELSEVIER)S1878-6480(16)30405-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 380 VZ 55.82 bkl Rossi, Elisa verfasserin aut 0130 : Endoglin is a new partner involved in platelet – endothelium interactions: role in microvessel stability? 2016transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Hereditary Hemorragic Telangectasia (HHT) is characterized by a bleeding tendency that is postulated to be a consequence of microvessel fragility. HHT type 1 patients present heterozygous mutations in the endoglin gene resulting in a loss of expression of membrane endoglin in their endothelial cells (EC), while platelets in these patients display normal functions in vitro. We have reported previously that endothelial endoglin is involved, via its RGD motif, in inflammation though integrin-mediated leukocyte adhesion and transmigration. We recently found that endoglin-haplodeficient mice (Eng+/–) have significantly higher bleeding time than Eng+/+ animals, therefore, we haypothesized that endoglin may also act as an adhesion molecule via integrin recognition in the interaction between EC and platelets during hemostasis. Coating plastic wells with the extracellular domain of endoglin enhanced platelets adhesion to the wells under static condition and this interaction persist under flow condition. Similarly, platelets could adhere on confluent EC in an endoglin-mediated process, while the silencing of endoglin expression in EC, and the addition of soluble endoglin or of anti-endoglin antibodies, inhibited stable platelet adhesion to EC. Remarkably, platelets from Glanzmann's thrombasthenia patients lacking the€αIIbβ3 integrin were defective for adhesion on EC, wheras CHO cells, ectopically expressing the human αIIbβ3 integrin acquired the capacity to adhere on rat myoblast transfectants expressing human endoglin (L6E9-E), thus confirming the interaction between endoglin and the αIIbβ3 integrin. These results establish a new critical role for endoglin in integrin-mediated adhesion of platelets to endothelium and provide a better understanding on the cellular mechanisms involved in bleeding events occurring in HHT. Hereditary Hemorragic Telangectasia (HHT) is characterized by a bleeding tendency that is postulated to be a consequence of microvessel fragility. HHT type 1 patients present heterozygous mutations in the endoglin gene resulting in a loss of expression of membrane endoglin in their endothelial cells (EC), while platelets in these patients display normal functions in vitro. We have reported previously that endothelial endoglin is involved, via its RGD motif, in inflammation though integrin-mediated leukocyte adhesion and transmigration. We recently found that endoglin-haplodeficient mice (Eng+/–) have significantly higher bleeding time than Eng+/+ animals, therefore, we haypothesized that endoglin may also act as an adhesion molecule via integrin recognition in the interaction between EC and platelets during hemostasis. Coating plastic wells with the extracellular domain of endoglin enhanced platelets adhesion to the wells under static condition and this interaction persist under flow condition. Similarly, platelets could adhere on confluent EC in an endoglin-mediated process, while the silencing of endoglin expression in EC, and the addition of soluble endoglin or of anti-endoglin antibodies, inhibited stable platelet adhesion to EC. Remarkably, platelets from Glanzmann's thrombasthenia patients lacking the€αIIbβ3 integrin were defective for adhesion on EC, wheras CHO cells, ectopically expressing the human αIIbβ3 integrin acquired the capacity to adhere on rat myoblast transfectants expressing human endoglin (L6E9-E), thus confirming the interaction between endoglin and the αIIbβ3 integrin. These results establish a new critical role for endoglin in integrin-mediated adhesion of platelets to endothelium and provide a better understanding on the cellular mechanisms involved in bleeding events occurring in HHT. Bachelot-Loza, Christilla oth Pidard, Dominique oth Gaussem, Pascale oth Smadja, David oth Chassac, Sonia oth Pericacho, Miguel oth Lopez-Novoa, José M. oth Langa, Carmen oth Gonzalez-Manchon, Consuelo 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:8 year:2016 number:3 pages:219 https://doi.org/10.1016/S1878-6480(16)30405-0 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 55.82 Güterverkehr VZ AR 8 2016 3 219 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:8 year:2016 number:3 pages:219 |
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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@@ Bachelot-Loza, Christilla @@oth@@ Pidard, Dominique @@oth@@ Gaussem, Pascale @@oth@@ Smadja, David @@oth@@ Chassac, Sonia @@oth@@ Pericacho, Miguel @@oth@@ Lopez-Novoa, José M. @@oth@@ Langa, Carmen @@oth@@ Gonzalez-Manchon, Consuelo @@oth@@ Bernabeu, Carmelo @@oth@@ |
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0130 : Endoglin is a new partner involved in platelet – endothelium interactions: role in microvessel stability? |
| abstract |
Hereditary Hemorragic Telangectasia (HHT) is characterized by a bleeding tendency that is postulated to be a consequence of microvessel fragility. HHT type 1 patients present heterozygous mutations in the endoglin gene resulting in a loss of expression of membrane endoglin in their endothelial cells (EC), while platelets in these patients display normal functions in vitro. We have reported previously that endothelial endoglin is involved, via its RGD motif, in inflammation though integrin-mediated leukocyte adhesion and transmigration. We recently found that endoglin-haplodeficient mice (Eng+/–) have significantly higher bleeding time than Eng+/+ animals, therefore, we haypothesized that endoglin may also act as an adhesion molecule via integrin recognition in the interaction between EC and platelets during hemostasis. Coating plastic wells with the extracellular domain of endoglin enhanced platelets adhesion to the wells under static condition and this interaction persist under flow condition. Similarly, platelets could adhere on confluent EC in an endoglin-mediated process, while the silencing of endoglin expression in EC, and the addition of soluble endoglin or of anti-endoglin antibodies, inhibited stable platelet adhesion to EC. Remarkably, platelets from Glanzmann's thrombasthenia patients lacking the€αIIbβ3 integrin were defective for adhesion on EC, wheras CHO cells, ectopically expressing the human αIIbβ3 integrin acquired the capacity to adhere on rat myoblast transfectants expressing human endoglin (L6E9-E), thus confirming the interaction between endoglin and the αIIbβ3 integrin. These results establish a new critical role for endoglin in integrin-mediated adhesion of platelets to endothelium and provide a better understanding on the cellular mechanisms involved in bleeding events occurring in HHT. |
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Hereditary Hemorragic Telangectasia (HHT) is characterized by a bleeding tendency that is postulated to be a consequence of microvessel fragility. HHT type 1 patients present heterozygous mutations in the endoglin gene resulting in a loss of expression of membrane endoglin in their endothelial cells (EC), while platelets in these patients display normal functions in vitro. We have reported previously that endothelial endoglin is involved, via its RGD motif, in inflammation though integrin-mediated leukocyte adhesion and transmigration. We recently found that endoglin-haplodeficient mice (Eng+/–) have significantly higher bleeding time than Eng+/+ animals, therefore, we haypothesized that endoglin may also act as an adhesion molecule via integrin recognition in the interaction between EC and platelets during hemostasis. Coating plastic wells with the extracellular domain of endoglin enhanced platelets adhesion to the wells under static condition and this interaction persist under flow condition. Similarly, platelets could adhere on confluent EC in an endoglin-mediated process, while the silencing of endoglin expression in EC, and the addition of soluble endoglin or of anti-endoglin antibodies, inhibited stable platelet adhesion to EC. Remarkably, platelets from Glanzmann's thrombasthenia patients lacking the€αIIbβ3 integrin were defective for adhesion on EC, wheras CHO cells, ectopically expressing the human αIIbβ3 integrin acquired the capacity to adhere on rat myoblast transfectants expressing human endoglin (L6E9-E), thus confirming the interaction between endoglin and the αIIbβ3 integrin. These results establish a new critical role for endoglin in integrin-mediated adhesion of platelets to endothelium and provide a better understanding on the cellular mechanisms involved in bleeding events occurring in HHT. |
| abstract_unstemmed |
Hereditary Hemorragic Telangectasia (HHT) is characterized by a bleeding tendency that is postulated to be a consequence of microvessel fragility. HHT type 1 patients present heterozygous mutations in the endoglin gene resulting in a loss of expression of membrane endoglin in their endothelial cells (EC), while platelets in these patients display normal functions in vitro. We have reported previously that endothelial endoglin is involved, via its RGD motif, in inflammation though integrin-mediated leukocyte adhesion and transmigration. We recently found that endoglin-haplodeficient mice (Eng+/–) have significantly higher bleeding time than Eng+/+ animals, therefore, we haypothesized that endoglin may also act as an adhesion molecule via integrin recognition in the interaction between EC and platelets during hemostasis. Coating plastic wells with the extracellular domain of endoglin enhanced platelets adhesion to the wells under static condition and this interaction persist under flow condition. Similarly, platelets could adhere on confluent EC in an endoglin-mediated process, while the silencing of endoglin expression in EC, and the addition of soluble endoglin or of anti-endoglin antibodies, inhibited stable platelet adhesion to EC. Remarkably, platelets from Glanzmann's thrombasthenia patients lacking the€αIIbβ3 integrin were defective for adhesion on EC, wheras CHO cells, ectopically expressing the human αIIbβ3 integrin acquired the capacity to adhere on rat myoblast transfectants expressing human endoglin (L6E9-E), thus confirming the interaction between endoglin and the αIIbβ3 integrin. These results establish a new critical role for endoglin in integrin-mediated adhesion of platelets to endothelium and provide a better understanding on the cellular mechanisms involved in bleeding events occurring in HHT. |
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Similarly, platelets could adhere on confluent EC in an endoglin-mediated process, while the silencing of endoglin expression in EC, and the addition of soluble endoglin or of anti-endoglin antibodies, inhibited stable platelet adhesion to EC. Remarkably, platelets from Glanzmann's thrombasthenia patients lacking the€αIIbβ3 integrin were defective for adhesion on EC, wheras CHO cells, ectopically expressing the human αIIbβ3 integrin acquired the capacity to adhere on rat myoblast transfectants expressing human endoglin (L6E9-E), thus confirming the interaction between endoglin and the αIIbβ3 integrin. 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We recently found that endoglin-haplodeficient mice (Eng+/–) have significantly higher bleeding time than Eng+/+ animals, therefore, we haypothesized that endoglin may also act as an adhesion molecule via integrin recognition in the interaction between EC and platelets during hemostasis. Coating plastic wells with the extracellular domain of endoglin enhanced platelets adhesion to the wells under static condition and this interaction persist under flow condition. Similarly, platelets could adhere on confluent EC in an endoglin-mediated process, while the silencing of endoglin expression in EC, and the addition of soluble endoglin or of anti-endoglin antibodies, inhibited stable platelet adhesion to EC. Remarkably, platelets from Glanzmann's thrombasthenia patients lacking the€αIIbβ3 integrin were defective for adhesion on EC, wheras CHO cells, ectopically expressing the human αIIbβ3 integrin acquired the capacity to adhere on rat myoblast transfectants expressing human endoglin (L6E9-E), thus confirming the interaction between endoglin and the αIIbβ3 integrin. These results establish a new critical role for endoglin in integrin-mediated adhesion of platelets to endothelium and provide a better understanding on the cellular mechanisms involved in bleeding events occurring in HHT.</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Bachelot-Loza, Christilla</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Pidard, Dominique</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Gaussem, Pascale</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Smadja, David</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Chassac, Sonia</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Pericacho, Miguel</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Lopez-Novoa, José M.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Langa, Carmen</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Gonzalez-Manchon, Consuelo</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Bernabeu, Carmelo</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier Masson</subfield><subfield code="a">Guan, Xiangyang ELSEVIER</subfield><subfield code="t">A behaviorally-integrated individual-level state-transition model that can predict rapid changes in evacuation demand days earlier</subfield><subfield code="d">2021</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV006385559</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:8</subfield><subfield code="g">year:2016</subfield><subfield code="g">number:3</subfield><subfield code="g">pages:219</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/S1878-6480(16)30405-0</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">55.82</subfield><subfield code="j">Güterverkehr</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">8</subfield><subfield code="j">2016</subfield><subfield code="e">3</subfield><subfield code="h">219</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
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