<script type="text/javascript">
<!--
document.write('<div id="oa_widget"></div>');
document.write('<script type="text/javascript" src="https://www.openaire.eu/index.php?option=com_openaire&view=widget&format=raw&projectId=undefined&type=result"></script>');
-->
</script>

COPY SCRIPT

For further information contact us at helpdesk@openaire.eu

Claim

Blunted apoptosis of erythrocytes in mice deficient in the heterotrimeric G-protein subunit Gαi2

descriptionPublicationkeyboard_double_arrow_right Article , Other literature type 08 Aug 2016 Germany, Argentina Springer Science and Business Media LLCScientific Reports, volume 6 (eissn: 2045-2322,

Authors: Rosi Bissinger; Elisabeth Lang; Mehrdad Ghashghaeinia; Yogesh Singh; Christine Zelenak; Birgit Fehrenbacher; Sabina Honisch; +12 Authors

doi: 10.1038/srep30925 , 10.17169/refubium-19624

pmid: 27499046

pmc: PMC4976336

handle: 11336/40386

Blunted apoptosis of erythrocytes in mice deficient in the heterotrimeric G-protein subunit Gαi2

- Summary
- Subjects
- References
  (60)
- Related research
  (11)
- Metrics

Abstract

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.

Countries

Germany, Argentina

Related Organizations

National Scientific and Technical Research Council
Argentina
Charité - University Medicine Berlin
Germany
National Institutes of Health
United States
ENVIRONMENTAL HEALTH SCIENCES
Pontifical Catholic University of Argentina
Argentina

View all View all

Subjects by Vocabulary

Microsoft Academic Graph classification: Ceramide Programmed cell death G protein Biology chemistry.chemical_compound Phosphatidylserine Molecular biology Cell biology Cytosol Erythrocyte maturation chemistry Apoptosis Sphingomyelin

Medical Subject Headings: genetic structures

Keywords

G Protein, Erythrocyte Indices, 500 Naturwissenschaften und Mathematik::570 Biowissenschaften; Biologie, 570, CIENCIAS MÉDICAS Y DE LA SALUD, Erythrocytes, Cell Survival, Inmunología, Eryptosis, 610, BIOLOGIA CELULAR, Phosphatidylserines, 600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit, Article, Mice, Animals, Humans, Gi2alpha, PROTEINA, Erythocyte, Mice, Knockout, Multidisciplinary, //purl.org/becyt/ford/3.1 [https], APOPTOSIS, Medicina Básica, CELULAS DE LA SANGRE, //purl.org/becyt/ford/3 [https], GTP-Binding Protein alpha Subunit, Gi2

60 references, page 1 of 6

Carmichael C. Y. & Wainford R. D. Brain Galphai 2 -subunit proteins and the prevention of salt sensitive hypertension. Front Physiol 6, 233 (2015).26347659 [OpenAIRE] [PubMed]

Wettschureck N. & Offermanns S. Mammalian G proteins and their cell type specific functions. Physiol Rev 85, 1159–1204 (2005).16183910 [OpenAIRE] [PubMed]

Simon M. I., Strathmann M. P. & Gautam N. Diversity of G proteins in signal transduction. Science 252, 802–808 (1991).1902986 [OpenAIRE] [PubMed]

Devanathan V.et al.Platelet Gi protein Galphai2 is an essential mediator of thrombo-inflammatory organ damage in mice. Proc. Natl. Acad. Sci. USA 112, 6491–6496 (2015).25944935 [OpenAIRE] [PubMed]

Pero R. S.et al.Galphai2-mediated signaling events in the endothelium are involved in controlling leukocyte extravasation. Proc. Natl. Acad. Sci. USA 104, 4371–4376 (2007).17360531 [OpenAIRE] [PubMed]

Ngai J., Inngjerdingen M., Berge T. & Tasken K. Interplay between the heterotrimeric G-protein subunits Galphaq and Galphai2 sets the threshold for chemotaxis and TCR activation. BMC. Immunol 10, 27 (2009).19426503 [OpenAIRE] [PubMed]

Zarbock A., Deem T. L., Burcin T. L. & Ley K. Galphai2 is required for chemokine-induced neutrophil arrest. Blood 110, 3773–3779 (2007).17699741 [OpenAIRE] [PubMed]

Minetti G. C.et al.Galphai2 signaling is required for skeletal muscle growth, regeneration, and satellite cell proliferation and differentiation. Mol. Cell Biol 34, 619–630 (2014).24298018 [OpenAIRE] [PubMed]

Lopez-Aranda M. F.et al.Activation of caspase-3 pathway by expression of sGalphai2 protein in BHK cells. Neurosci. Lett 439, 37–41 (2008).18502580 [OpenAIRE] [PubMed]

Myeong J.et al.Close spatio-association of the transient receptor potential canonical 4 (TRPC4) channel with Galphai in TRPC4 activation process. Am. J. Physiol Cell Physiol 308, C879–C889 (2015).25788576 [OpenAIRE] [PubMed]

chevron_left
1
2
3
4
5
chevron_right

11 Research products, page 1 of 2

Long‐term treatment with anti‐α4 integrin antibodies aggravates colitis in Gαi2‐deficient mice
2005IsAmongTopNSimilarDocuments
A quantitative study of the mechanisms behind thymic atrophy in Gαi2-deficient mice during colitis development.
2012IsAmongTopNSimilarDocuments
Interplay between Pathogenic and Immune Regulatory Mechanisms in G-alpha-i2 deficient colitis
2011IsAmongTopNSimilarDocuments
Dietary Antigen‐Specific T‐Cell Responses: Switch from an Interleukin‐10‐Dominated Response in Normal Mice to a T‐Helper 1 Cytokine Profile in Gαi2‐Deficient Mice prior to Colitis
2005IsAmongTopNSimilarDocuments
Impaired B cell responses to orally administered antigens in lamina propria but not Peyer's patches of Gαi2-deficient mice prior to colitis
2005IsAmongTopNSimilarDocuments
Acellular Bordetella pertussis vaccine enhances mucosal interleukin- 10 production, induces apoptosis of activated Th1 cells and attenuates colitis in Gαi2-deficient mice
2005IsAmongTopNSimilarDocuments
Gαi2 + vomeronasal neurons govern the initial outcome of an acute social competition
2020IsAmongTopNSimilarDocuments
More damaging than we think: Systemic effects of intestinal inflammation
2009IsAmongTopNSimilarDocuments
CD4+FoxP3+ Regulatory T Cells from Gαi2−/− Mice Are Functionally Active In Vitro, but Do Not Prevent Colitis
2011IsAmongTopNSimilarDocuments
B cell developmental requirement for the G alpha i2 gene.
2003IsAmongTopNSimilarDocuments

chevron_left
1
2
chevron_right

Impact byBIP!

	citations This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).	26
	popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.	Average
	influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).	Average
	impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.	Top 10%

Usage byUsageCounts

visibility	views	4
download	downloads	1

	citations This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).	26
	popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.	Average
	influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).	Average
	impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.	Top 10%