Blunted apoptosis of erythrocytes in mice deficient in the heterotrimeric G-protein subunit Gαi2
- Autores
- Bissinger, Rosi; Lang, Elisabeth; Ghashghaeinia, Mehrdad; Singh, Yogesh; Zelenak, Christine; Fehrenbacher, Birgit; Honisch, Sabina; Chen, Hong; Fakhri, Hajar; Umbach, Anja T.; Liu, Guilai; Rexhepaj, Rexhep; Liu, Guoxing; Schaller, Martin; Mack, Andreas F.; Lupescu, Adrian; Birnbaumer, Lutz; Lang, Florian; Qadri, Syed M.
- Año de publicación
- 2016
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Fil: Bissinger, Rosi. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; Alemania
Fil: Lang, Elisabeth. University of Duesseldorf. Hepatology and Infectious Diseases. Department of Gastroenterology; Alemania
Fil: Ghashghaeinia, Mehrdad. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; Alemania
Fil: Zelenak, Christine. Charité Medical University. Department of Internal Medicine; Alemania
Fil: Fehrenbacher, Birgit. University of Tuebingen. Department of Dermatology; Alemania
Fil: Honisch, Sabina. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; Alemania
Fil: Chen, Hong. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; Alemania
Fil: Fakhri, Hajar. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; Alemania
Fil: Umbach, Anja T. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; Alemania
Fil: Liu, Guilai. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; Alemania
Fil: Rexhepaj, Rexhep. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; Alemania
Fil: Rexhepaj, Rexhep. University of Bonn. Institute of Biochemistry and Molecular Biology; Alemania
Fil: Liu, Guoxing. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; Alemania
Fil: Schaller, Martin. University of Tuebingen. Department of Dermatology; Alemania
Fil: Mack, Andreas F. University of Tuebingen. Institute of Anatomy; Alemania
Fil: Lupescu, Adrian. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; Alemania
Fil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas; Argentina
Fil: Birnbaumer, Lutz. National Institute of Health. Neurobiology Laboratory; Estados Unidos
Fil: Lang, Florian. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; Alemania
Fil: Qadri, Syed M. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; Alemania
Fil: Qadri, Syed M. McMaster University. Department of Pathology and Molecular Medicine; Canadá
Abstract: Putative functions of the heterotrimeric G-protein subunit Gαi2-dependent signaling include ion channel regulation, cell differentiation, proliferation and apoptosis. Erythrocytes may, similar to apoptosis of nucleated cells, undergo eryptosis, characterized by cell shrinkage and cell membrane scrambling with phosphatidylserine (PS) exposure. Eryptosis may be triggered by increased cytosolic Ca(2+) activity and ceramide. In the present study, we show that Gαi2 is expressed in both murine and human erythrocytes and further examined the survival of erythrocytes drawn from Gαi2-deficient mice (Gαi2(-/-)) and corresponding wild-type mice (Gαi2(+/+)). Our data show that plasma erythropoietin levels, erythrocyte maturation markers, erythrocyte counts, hematocrit and hemoglobin concentration were similar in Gαi2(-/-) and Gαi2(+/+) mice but the mean corpuscular volume was significantly larger in Gαi2(-/-) mice. Spontaneous PS exposure of circulating Gαi2(-/-) erythrocytes was significantly lower than that of circulating Gαi2(+/+) erythrocytes. PS exposure was significantly lower in Gαi2(-/-) than in Gαi2(+/+) erythrocytes following ex vivo exposure to hyperosmotic shock, bacterial sphingomyelinase or C6 ceramide. Erythrocyte Gαi2 deficiency further attenuated hyperosmotic shock-induced increase of cytosolic Ca(2+) activity and cell shrinkage. Moreover, Gαi2(-/-) erythrocytes were more resistant to osmosensitive hemolysis as compared to Gαi2(+/+) erythrocytes. In conclusion, Gαi2 deficiency in erythrocytes confers partial protection against suicidal cell death. - Fuente
- Scientific Reports. 2016;6(1):1-10
- Materia
-
APOPTOSIS
PROTEINA
BIOLOGIA CELULAR
CELULAS DE LA SANGRE - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/4.0/
- Repositorio
- Institución
- Pontificia Universidad Católica Argentina
- OAI Identificador
- oai:ucacris:123456789/8762
Ver los metadatos del registro completo
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Blunted apoptosis of erythrocytes in mice deficient in the heterotrimeric G-protein subunit Gαi2Bissinger, RosiLang, ElisabethGhashghaeinia, MehrdadSingh, YogeshZelenak, ChristineFehrenbacher, BirgitHonisch, SabinaChen, HongFakhri, HajarUmbach, Anja T.Liu, GuilaiRexhepaj, RexhepLiu, GuoxingSchaller, MartinMack, Andreas F.Lupescu, AdrianBirnbaumer, LutzLang, FlorianQadri, Syed M.APOPTOSISPROTEINABIOLOGIA CELULARCELULAS DE LA SANGREFil: Bissinger, Rosi. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; AlemaniaFil: Lang, Elisabeth. University of Duesseldorf. Hepatology and Infectious Diseases. Department of Gastroenterology; AlemaniaFil: Ghashghaeinia, Mehrdad. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; AlemaniaFil: Zelenak, Christine. Charité Medical University. Department of Internal Medicine; AlemaniaFil: Fehrenbacher, Birgit. University of Tuebingen. Department of Dermatology; AlemaniaFil: Honisch, Sabina. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; AlemaniaFil: Chen, Hong. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; AlemaniaFil: Fakhri, Hajar. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; AlemaniaFil: Umbach, Anja T. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; AlemaniaFil: Liu, Guilai. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; AlemaniaFil: Rexhepaj, Rexhep. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; AlemaniaFil: Rexhepaj, Rexhep. University of Bonn. Institute of Biochemistry and Molecular Biology; AlemaniaFil: Liu, Guoxing. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; AlemaniaFil: Schaller, Martin. University of Tuebingen. Department of Dermatology; AlemaniaFil: Mack, Andreas F. University of Tuebingen. Institute of Anatomy; AlemaniaFil: Lupescu, Adrian. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; AlemaniaFil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas; ArgentinaFil: Birnbaumer, Lutz. National Institute of Health. Neurobiology Laboratory; Estados UnidosFil: Lang, Florian. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; AlemaniaFil: Qadri, Syed M. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; AlemaniaFil: Qadri, Syed M. McMaster University. Department of Pathology and Molecular Medicine; CanadáAbstract: Putative functions of the heterotrimeric G-protein subunit Gαi2-dependent signaling include ion channel regulation, cell differentiation, proliferation and apoptosis. Erythrocytes may, similar to apoptosis of nucleated cells, undergo eryptosis, characterized by cell shrinkage and cell membrane scrambling with phosphatidylserine (PS) exposure. Eryptosis may be triggered by increased cytosolic Ca(2+) activity and ceramide. In the present study, we show that Gαi2 is expressed in both murine and human erythrocytes and further examined the survival of erythrocytes drawn from Gαi2-deficient mice (Gαi2(-/-)) and corresponding wild-type mice (Gαi2(+/+)). Our data show that plasma erythropoietin levels, erythrocyte maturation markers, erythrocyte counts, hematocrit and hemoglobin concentration were similar in Gαi2(-/-) and Gαi2(+/+) mice but the mean corpuscular volume was significantly larger in Gαi2(-/-) mice. Spontaneous PS exposure of circulating Gαi2(-/-) erythrocytes was significantly lower than that of circulating Gαi2(+/+) erythrocytes. PS exposure was significantly lower in Gαi2(-/-) than in Gαi2(+/+) erythrocytes following ex vivo exposure to hyperosmotic shock, bacterial sphingomyelinase or C6 ceramide. Erythrocyte Gαi2 deficiency further attenuated hyperosmotic shock-induced increase of cytosolic Ca(2+) activity and cell shrinkage. Moreover, Gαi2(-/-) erythrocytes were more resistant to osmosensitive hemolysis as compared to Gαi2(+/+) erythrocytes. In conclusion, Gαi2 deficiency in erythrocytes confers partial protection against suicidal cell death.Nature Research2016info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttps://repositorio.uca.edu.ar/handle/123456789/87622045-232210.1038/srep3092527499046Bissinger R, Lang E, Ghashghaeinia M, et al. Blunted apoptosis of erythrocytes in mice deficient in the heterotrimeric G-protein subunit Gαi2 [en línea]. Scientific Reports. 2016;6(1):1-10. doi:10.1038/srep30925 Disponible en: https://repositorio.uca.edu.ar/handle/123456789/8762Scientific Reports. 2016;6(1):1-10reponame:Repositorio Institucional (UCA)instname:Pontificia Universidad Católica Argentinaenginfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/4.0/2025-07-03T10:56:54Zoai:ucacris:123456789/8762instacron:UCAInstitucionalhttps://repositorio.uca.edu.ar/Universidad privadaNo correspondehttps://repositorio.uca.edu.ar/oaiclaudia_fernandez@uca.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:25852025-07-03 10:56:55.223Repositorio Institucional (UCA) - Pontificia Universidad Católica Argentinafalse |
dc.title.none.fl_str_mv |
Blunted apoptosis of erythrocytes in mice deficient in the heterotrimeric G-protein subunit Gαi2 |
title |
Blunted apoptosis of erythrocytes in mice deficient in the heterotrimeric G-protein subunit Gαi2 |
spellingShingle |
Blunted apoptosis of erythrocytes in mice deficient in the heterotrimeric G-protein subunit Gαi2 Bissinger, Rosi APOPTOSIS PROTEINA BIOLOGIA CELULAR CELULAS DE LA SANGRE |
title_short |
Blunted apoptosis of erythrocytes in mice deficient in the heterotrimeric G-protein subunit Gαi2 |
title_full |
Blunted apoptosis of erythrocytes in mice deficient in the heterotrimeric G-protein subunit Gαi2 |
title_fullStr |
Blunted apoptosis of erythrocytes in mice deficient in the heterotrimeric G-protein subunit Gαi2 |
title_full_unstemmed |
Blunted apoptosis of erythrocytes in mice deficient in the heterotrimeric G-protein subunit Gαi2 |
title_sort |
Blunted apoptosis of erythrocytes in mice deficient in the heterotrimeric G-protein subunit Gαi2 |
dc.creator.none.fl_str_mv |
Bissinger, Rosi Lang, Elisabeth Ghashghaeinia, Mehrdad Singh, Yogesh Zelenak, Christine Fehrenbacher, Birgit Honisch, Sabina Chen, Hong Fakhri, Hajar Umbach, Anja T. Liu, Guilai Rexhepaj, Rexhep Liu, Guoxing Schaller, Martin Mack, Andreas F. Lupescu, Adrian Birnbaumer, Lutz Lang, Florian Qadri, Syed M. |
author |
Bissinger, Rosi |
author_facet |
Bissinger, Rosi Lang, Elisabeth Ghashghaeinia, Mehrdad Singh, Yogesh Zelenak, Christine Fehrenbacher, Birgit Honisch, Sabina Chen, Hong Fakhri, Hajar Umbach, Anja T. Liu, Guilai Rexhepaj, Rexhep Liu, Guoxing Schaller, Martin Mack, Andreas F. Lupescu, Adrian Birnbaumer, Lutz Lang, Florian Qadri, Syed M. |
author_role |
author |
author2 |
Lang, Elisabeth Ghashghaeinia, Mehrdad Singh, Yogesh Zelenak, Christine Fehrenbacher, Birgit Honisch, Sabina Chen, Hong Fakhri, Hajar Umbach, Anja T. Liu, Guilai Rexhepaj, Rexhep Liu, Guoxing Schaller, Martin Mack, Andreas F. Lupescu, Adrian Birnbaumer, Lutz Lang, Florian Qadri, Syed M. |
author2_role |
author author author author author author author author author author author author author author author author author author |
dc.subject.none.fl_str_mv |
APOPTOSIS PROTEINA BIOLOGIA CELULAR CELULAS DE LA SANGRE |
topic |
APOPTOSIS PROTEINA BIOLOGIA CELULAR CELULAS DE LA SANGRE |
dc.description.none.fl_txt_mv |
Fil: Bissinger, Rosi. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; Alemania Fil: Lang, Elisabeth. University of Duesseldorf. Hepatology and Infectious Diseases. Department of Gastroenterology; Alemania Fil: Ghashghaeinia, Mehrdad. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; Alemania Fil: Zelenak, Christine. Charité Medical University. Department of Internal Medicine; Alemania Fil: Fehrenbacher, Birgit. University of Tuebingen. Department of Dermatology; Alemania Fil: Honisch, Sabina. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; Alemania Fil: Chen, Hong. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; Alemania Fil: Fakhri, Hajar. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; Alemania Fil: Umbach, Anja T. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; Alemania Fil: Liu, Guilai. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; Alemania Fil: Rexhepaj, Rexhep. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; Alemania Fil: Rexhepaj, Rexhep. University of Bonn. Institute of Biochemistry and Molecular Biology; Alemania Fil: Liu, Guoxing. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; Alemania Fil: Schaller, Martin. University of Tuebingen. Department of Dermatology; Alemania Fil: Mack, Andreas F. University of Tuebingen. Institute of Anatomy; Alemania Fil: Lupescu, Adrian. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; Alemania Fil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas; Argentina Fil: Birnbaumer, Lutz. National Institute of Health. Neurobiology Laboratory; Estados Unidos Fil: Lang, Florian. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; Alemania Fil: Qadri, Syed M. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; Alemania Fil: Qadri, Syed M. McMaster University. Department of Pathology and Molecular Medicine; Canadá Abstract: Putative functions of the heterotrimeric G-protein subunit Gαi2-dependent signaling include ion channel regulation, cell differentiation, proliferation and apoptosis. Erythrocytes may, similar to apoptosis of nucleated cells, undergo eryptosis, characterized by cell shrinkage and cell membrane scrambling with phosphatidylserine (PS) exposure. Eryptosis may be triggered by increased cytosolic Ca(2+) activity and ceramide. In the present study, we show that Gαi2 is expressed in both murine and human erythrocytes and further examined the survival of erythrocytes drawn from Gαi2-deficient mice (Gαi2(-/-)) and corresponding wild-type mice (Gαi2(+/+)). Our data show that plasma erythropoietin levels, erythrocyte maturation markers, erythrocyte counts, hematocrit and hemoglobin concentration were similar in Gαi2(-/-) and Gαi2(+/+) mice but the mean corpuscular volume was significantly larger in Gαi2(-/-) mice. Spontaneous PS exposure of circulating Gαi2(-/-) erythrocytes was significantly lower than that of circulating Gαi2(+/+) erythrocytes. PS exposure was significantly lower in Gαi2(-/-) than in Gαi2(+/+) erythrocytes following ex vivo exposure to hyperosmotic shock, bacterial sphingomyelinase or C6 ceramide. Erythrocyte Gαi2 deficiency further attenuated hyperosmotic shock-induced increase of cytosolic Ca(2+) activity and cell shrinkage. Moreover, Gαi2(-/-) erythrocytes were more resistant to osmosensitive hemolysis as compared to Gαi2(+/+) erythrocytes. In conclusion, Gαi2 deficiency in erythrocytes confers partial protection against suicidal cell death. |
description |
Fil: Bissinger, Rosi. University of Tuebingen. Vascular Medicine and Physiology. Institute of Cardiology; Alemania |
publishDate |
2016 |
dc.date.none.fl_str_mv |
2016 |
dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
format |
article |
status_str |
publishedVersion |
dc.identifier.none.fl_str_mv |
https://repositorio.uca.edu.ar/handle/123456789/8762 2045-2322 10.1038/srep30925 27499046 Bissinger R, Lang E, Ghashghaeinia M, et al. Blunted apoptosis of erythrocytes in mice deficient in the heterotrimeric G-protein subunit Gαi2 [en línea]. Scientific Reports. 2016;6(1):1-10. doi:10.1038/srep30925 Disponible en: https://repositorio.uca.edu.ar/handle/123456789/8762 |
url |
https://repositorio.uca.edu.ar/handle/123456789/8762 |
identifier_str_mv |
2045-2322 10.1038/srep30925 27499046 Bissinger R, Lang E, Ghashghaeinia M, et al. Blunted apoptosis of erythrocytes in mice deficient in the heterotrimeric G-protein subunit Gαi2 [en línea]. Scientific Reports. 2016;6(1):1-10. doi:10.1038/srep30925 Disponible en: https://repositorio.uca.edu.ar/handle/123456789/8762 |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by-nc-sa/4.0/ |
eu_rights_str_mv |
openAccess |
rights_invalid_str_mv |
https://creativecommons.org/licenses/by-nc-sa/4.0/ |
dc.format.none.fl_str_mv |
application/pdf |
dc.publisher.none.fl_str_mv |
Nature Research |
publisher.none.fl_str_mv |
Nature Research |
dc.source.none.fl_str_mv |
Scientific Reports. 2016;6(1):1-10 reponame:Repositorio Institucional (UCA) instname:Pontificia Universidad Católica Argentina |
reponame_str |
Repositorio Institucional (UCA) |
collection |
Repositorio Institucional (UCA) |
instname_str |
Pontificia Universidad Católica Argentina |
repository.name.fl_str_mv |
Repositorio Institucional (UCA) - Pontificia Universidad Católica Argentina |
repository.mail.fl_str_mv |
claudia_fernandez@uca.edu.ar |
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13.070432 |