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
Repositorio Institucional (UCA)
Institución
Pontificia Universidad Católica Argentina
OAI Identificador
oai:ucacris:123456789/8762

id RIUCA_cd17934ed9482b11ca122173d214475e
oai_identifier_str oai:ucacris:123456789/8762
network_acronym_str RIUCA
repository_id_str 2585
network_name_str Repositorio Institucional (UCA)
spelling 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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