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S100A1 deficiency impairs postischemic angiogenesis via compromised proangiogenic endothelial cell function and nitric oxide synthase regulation novelty and significance
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| Veröffentlicht in: | Circulation research 112(2013), 1, Seite 66-78 |
|---|---|
| Personen und Körperschaften: | , , , , , , , |
| Titel: | S100A1 deficiency impairs postischemic angiogenesis via compromised proangiogenic endothelial cell function and nitric oxide synthase regulation novelty and significance/ Patrick Most, Carolin Lerchenmüller, Giuseppe Rengo, Adrian Mahlmann, Julia Ritterhoff, David Rohde, Chelain Goodman, Cornelius J. Busch, Felix Laube, Julian Heissenberg, Sven T. Pleger, Norbert Weiss, Hugo A. Katus, Walter J. Koch, Karsten Peppel |
| Format: | E-Book-Kapitel |
| Sprache: | Englisch |
| veröffentlicht: |
January 3, 2013
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| Gesamtaufnahme: |
: Circulation research, 112(2013), 1, Seite 66-78
, volume:112 |
| Schlagwörter: | |
| Quelle: | Verbunddaten SWB Lizenzfreie Online-Ressourcen |
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| 245 | 1 | 0 | |a S100A1 deficiency impairs postischemic angiogenesis via compromised proangiogenic endothelial cell function and nitric oxide synthase regulation novelty and significance |c Patrick Most, Carolin Lerchenmüller, Giuseppe Rengo, Adrian Mahlmann, Julia Ritterhoff, David Rohde, Chelain Goodman, Cornelius J. Busch, Felix Laube, Julian Heissenberg, Sven T. Pleger, Norbert Weiss, Hugo A. Katus, Walter J. Koch, Karsten Peppel |
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| 520 | |a Rationale: Mice lacking the EF-hand Ca2+ sensor S100A1 display endothelial dysfunction because of distorted Ca2+-activated nitric oxide (NO) generation. Objective: To determine the pathophysiological role of S100A1 in endothelial cell (EC) function in experimental ischemic revascularization. Methods and Results: Patients with chronic critical limb ischemia showed almost complete loss of S100A1 expression in hypoxic tissue. Ensuing studies in S100A1 knockout (SKO) mice subjected to femoral artery resection unveiled insufficient perfusion recovery and high rates of autoamputation. Defective in vivo angiogenesis prompted cellular studies in SKO ECs and human ECs, with small interfering RNA-mediated S100A1 knockdown demonstrating impaired in vitro and in vivo proangiogenic properties (proliferation, migration, tube formation) and attenuated vascular endothelial growth factor (VEGF)-stimulated and hypoxia-stimulated endothelial NO synthase (eNOS) activity. Mechanistically, S100A1 deficiency compromised eNOS activity in ECs by interrupted stimulatory S100A1/eNOS interaction and protein kinase C hyperactivation that resulted in inhibitory eNOS phosphorylation and enhanced VEGF receptor-2 degradation with attenuated VEGF signaling. Ischemic SKO tissue recapitulated the same molecular abnormalities with insufficient in vivo NO generation. Unresolved ischemia entailed excessive VEGF accumulation in SKO mice with aggravated VEGF receptor-2 degradation and blunted in vivo signaling through the proangiogenic phosphoinositide-3-kinase/Akt/eNOS cascade. The NO supplementation strategies rescued defective angiogenesis and salvaged limbs in SKO mice after femoral artery resection. Conclusions: Our study shows for the first time downregulation of S100A1 expression in patients with critical limb ischemia and identifies S100A1 as critical for EC function in postnatal ischemic angiogenesis. These findings link its pathological plasticity in critical limb ischemia to impaired neovascularization, prompting further studies to probe the microvascular therapeutic potential of S100A1. | ||
| 650 | 4 | |a angiogenesis | |
| 650 | 4 | |a endothelium | |
| 650 | 4 | |a nitric oxide | |
| 650 | 4 | |a S100A1 | |
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| contents | Rationale: Mice lacking the EF-hand Ca2+ sensor S100A1 display endothelial dysfunction because of distorted Ca2+-activated nitric oxide (NO) generation. Objective: To determine the pathophysiological role of S100A1 in endothelial cell (EC) function in experimental ischemic revascularization. Methods and Results: Patients with chronic critical limb ischemia showed almost complete loss of S100A1 expression in hypoxic tissue. Ensuing studies in S100A1 knockout (SKO) mice subjected to femoral artery resection unveiled insufficient perfusion recovery and high rates of autoamputation. Defective in vivo angiogenesis prompted cellular studies in SKO ECs and human ECs, with small interfering RNA-mediated S100A1 knockdown demonstrating impaired in vitro and in vivo proangiogenic properties (proliferation, migration, tube formation) and attenuated vascular endothelial growth factor (VEGF)-stimulated and hypoxia-stimulated endothelial NO synthase (eNOS) activity. Mechanistically, S100A1 deficiency compromised eNOS activity in ECs by interrupted stimulatory S100A1/eNOS interaction and protein kinase C hyperactivation that resulted in inhibitory eNOS phosphorylation and enhanced VEGF receptor-2 degradation with attenuated VEGF signaling. Ischemic SKO tissue recapitulated the same molecular abnormalities with insufficient in vivo NO generation. Unresolved ischemia entailed excessive VEGF accumulation in SKO mice with aggravated VEGF receptor-2 degradation and blunted in vivo signaling through the proangiogenic phosphoinositide-3-kinase/Akt/eNOS cascade. The NO supplementation strategies rescued defective angiogenesis and salvaged limbs in SKO mice after femoral artery resection. Conclusions: Our study shows for the first time downregulation of S100A1 expression in patients with critical limb ischemia and identifies S100A1 as critical for EC function in postnatal ischemic angiogenesis. These findings link its pathological plasticity in critical limb ischemia to impaired neovascularization, prompting further studies to probe the microvascular therapeutic potential of S100A1. |
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| spelling | Most, Patrick 1969- VerfasserIn (DE-588)124606431 (DE-627)363440267 (DE-576)29440919X aut, S100A1 deficiency impairs postischemic angiogenesis via compromised proangiogenic endothelial cell function and nitric oxide synthase regulation novelty and significance Patrick Most, Carolin Lerchenmüller, Giuseppe Rengo, Adrian Mahlmann, Julia Ritterhoff, David Rohde, Chelain Goodman, Cornelius J. Busch, Felix Laube, Julian Heissenberg, Sven T. Pleger, Norbert Weiss, Hugo A. Katus, Walter J. Koch, Karsten Peppel, January 3, 2013, 12, Text txt rdacontent, Computermedien c rdamedia, Online-Ressource cr rdacarrier, Gesehen am 23.05.2018, Rationale: Mice lacking the EF-hand Ca2+ sensor S100A1 display endothelial dysfunction because of distorted Ca2+-activated nitric oxide (NO) generation. Objective: To determine the pathophysiological role of S100A1 in endothelial cell (EC) function in experimental ischemic revascularization. Methods and Results: Patients with chronic critical limb ischemia showed almost complete loss of S100A1 expression in hypoxic tissue. Ensuing studies in S100A1 knockout (SKO) mice subjected to femoral artery resection unveiled insufficient perfusion recovery and high rates of autoamputation. Defective in vivo angiogenesis prompted cellular studies in SKO ECs and human ECs, with small interfering RNA-mediated S100A1 knockdown demonstrating impaired in vitro and in vivo proangiogenic properties (proliferation, migration, tube formation) and attenuated vascular endothelial growth factor (VEGF)-stimulated and hypoxia-stimulated endothelial NO synthase (eNOS) activity. Mechanistically, S100A1 deficiency compromised eNOS activity in ECs by interrupted stimulatory S100A1/eNOS interaction and protein kinase C hyperactivation that resulted in inhibitory eNOS phosphorylation and enhanced VEGF receptor-2 degradation with attenuated VEGF signaling. Ischemic SKO tissue recapitulated the same molecular abnormalities with insufficient in vivo NO generation. Unresolved ischemia entailed excessive VEGF accumulation in SKO mice with aggravated VEGF receptor-2 degradation and blunted in vivo signaling through the proangiogenic phosphoinositide-3-kinase/Akt/eNOS cascade. The NO supplementation strategies rescued defective angiogenesis and salvaged limbs in SKO mice after femoral artery resection. Conclusions: Our study shows for the first time downregulation of S100A1 expression in patients with critical limb ischemia and identifies S100A1 as critical for EC function in postnatal ischemic angiogenesis. These findings link its pathological plasticity in critical limb ischemia to impaired neovascularization, prompting further studies to probe the microvascular therapeutic potential of S100A1., angiogenesis, endothelium, nitric oxide, S100A1, Lerchenmüller, Carolin 1983- VerfasserIn (DE-588)1034967509 (DE-627)746579918 (DE-576)382589661 aut, Ritterhoff, Julia VerfasserIn (DE-588)1043976426 (DE-627)771174101 (DE-576)396460941 aut, Rohde, David 1981- VerfasserIn (DE-588)1025512685 (DE-627)722472846 (DE-576)370430999 aut, Busch, Cornelius 1973- VerfasserIn (DE-588)124466842 (DE-627)363367748 (DE-576)294185305 aut, Laube, Felix 1981- VerfasserIn (DE-588)1031901949 (DE-627)73751518X (DE-576)379602474 aut, Heißenberg, Julian VerfasserIn (DE-588)1151535400 (DE-627)1011890054 (DE-576)497858452 aut, Pleger, Sven Torsten 1973- VerfasserIn (DE-588)129962473 (DE-627)484985221 (DE-576)297924001 aut, Enthalten in Circulation research New York, NY : Assoc., 1953 112(2013), 1, Seite 66-78 Online-Ressource (DE-627)266880126 (DE-600)1467838-X (DE-576)075145766 1524-4571 nnns, volume:112 year:2013 number:1 pages:66-78 extent:12, http://dx.doi.org/10.1161/CIRCRESAHA.112.275156 Verlag Resolving-System kostenfrei Volltext, http://circres.ahajournals.org/content/112/1/66 Verlag kostenfrei Volltext, http://dx.doi.org/10.1161/CIRCRESAHA.112.275156 LFER, LFER 2018-05-24T00:00:00Z |
| spellingShingle | Most, Patrick, Lerchenmüller, Carolin, Ritterhoff, Julia, Rohde, David, Busch, Cornelius, Laube, Felix, Heißenberg, Julian, Pleger, Sven Torsten, S100A1 deficiency impairs postischemic angiogenesis via compromised proangiogenic endothelial cell function and nitric oxide synthase regulation novelty and significance, Rationale: Mice lacking the EF-hand Ca2+ sensor S100A1 display endothelial dysfunction because of distorted Ca2+-activated nitric oxide (NO) generation. Objective: To determine the pathophysiological role of S100A1 in endothelial cell (EC) function in experimental ischemic revascularization. Methods and Results: Patients with chronic critical limb ischemia showed almost complete loss of S100A1 expression in hypoxic tissue. Ensuing studies in S100A1 knockout (SKO) mice subjected to femoral artery resection unveiled insufficient perfusion recovery and high rates of autoamputation. Defective in vivo angiogenesis prompted cellular studies in SKO ECs and human ECs, with small interfering RNA-mediated S100A1 knockdown demonstrating impaired in vitro and in vivo proangiogenic properties (proliferation, migration, tube formation) and attenuated vascular endothelial growth factor (VEGF)-stimulated and hypoxia-stimulated endothelial NO synthase (eNOS) activity. Mechanistically, S100A1 deficiency compromised eNOS activity in ECs by interrupted stimulatory S100A1/eNOS interaction and protein kinase C hyperactivation that resulted in inhibitory eNOS phosphorylation and enhanced VEGF receptor-2 degradation with attenuated VEGF signaling. Ischemic SKO tissue recapitulated the same molecular abnormalities with insufficient in vivo NO generation. Unresolved ischemia entailed excessive VEGF accumulation in SKO mice with aggravated VEGF receptor-2 degradation and blunted in vivo signaling through the proangiogenic phosphoinositide-3-kinase/Akt/eNOS cascade. The NO supplementation strategies rescued defective angiogenesis and salvaged limbs in SKO mice after femoral artery resection. Conclusions: Our study shows for the first time downregulation of S100A1 expression in patients with critical limb ischemia and identifies S100A1 as critical for EC function in postnatal ischemic angiogenesis. These findings link its pathological plasticity in critical limb ischemia to impaired neovascularization, prompting further studies to probe the microvascular therapeutic potential of S100A1., angiogenesis, endothelium, nitric oxide, S100A1 |
| swb_id_str | 505423138 |
| title | S100A1 deficiency impairs postischemic angiogenesis via compromised proangiogenic endothelial cell function and nitric oxide synthase regulation novelty and significance |
| title_auth | S100A1 deficiency impairs postischemic angiogenesis via compromised proangiogenic endothelial cell function and nitric oxide synthase regulation novelty and significance |
| title_full | S100A1 deficiency impairs postischemic angiogenesis via compromised proangiogenic endothelial cell function and nitric oxide synthase regulation novelty and significance Patrick Most, Carolin Lerchenmüller, Giuseppe Rengo, Adrian Mahlmann, Julia Ritterhoff, David Rohde, Chelain Goodman, Cornelius J. Busch, Felix Laube, Julian Heissenberg, Sven T. Pleger, Norbert Weiss, Hugo A. Katus, Walter J. Koch, Karsten Peppel |
| title_fullStr | S100A1 deficiency impairs postischemic angiogenesis via compromised proangiogenic endothelial cell function and nitric oxide synthase regulation novelty and significance Patrick Most, Carolin Lerchenmüller, Giuseppe Rengo, Adrian Mahlmann, Julia Ritterhoff, David Rohde, Chelain Goodman, Cornelius J. Busch, Felix Laube, Julian Heissenberg, Sven T. Pleger, Norbert Weiss, Hugo A. Katus, Walter J. Koch, Karsten Peppel |
| title_full_unstemmed | S100A1 deficiency impairs postischemic angiogenesis via compromised proangiogenic endothelial cell function and nitric oxide synthase regulation novelty and significance Patrick Most, Carolin Lerchenmüller, Giuseppe Rengo, Adrian Mahlmann, Julia Ritterhoff, David Rohde, Chelain Goodman, Cornelius J. Busch, Felix Laube, Julian Heissenberg, Sven T. Pleger, Norbert Weiss, Hugo A. Katus, Walter J. Koch, Karsten Peppel |
| title_in_hierarchy | S100A1 deficiency impairs postischemic angiogenesis via compromised proangiogenic endothelial cell function and nitric oxide synthase regulation novelty and significance / Patrick Most, Carolin Lerchenmüller, Giuseppe Rengo, Adrian Mahlmann, Julia Ritterhoff, David Rohde, Chelain Goodman, Cornelius J. Busch, Felix Laube, Julian Heissenberg, Sven T. Pleger, Norbert Weiss, Hugo A. Katus, Walter J. Koch, Karsten Peppel, |
| title_short | S100A1 deficiency impairs postischemic angiogenesis via compromised proangiogenic endothelial cell function and nitric oxide synthase regulation novelty and significance |
| title_sort | s100a1 deficiency impairs postischemic angiogenesis via compromised proangiogenic endothelial cell function and nitric oxide synthase regulation novelty and significance |
| topic | angiogenesis, endothelium, nitric oxide, S100A1 |
| topic_facet | angiogenesis, endothelium, nitric oxide, S100A1 |
| url | http://dx.doi.org/10.1161/CIRCRESAHA.112.275156, http://circres.ahajournals.org/content/112/1/66 |