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dc.contributor.author
Solanki, Sumeet
dc.contributor.author
Dube, Prabhatchandra R.
dc.contributor.author
Tano, Jean Yves
dc.contributor.author
Birnbaumer, Lutz
dc.contributor.author
Vazquez, Guillermo
dc.date.available
2020-02-07T20:15:46Z
dc.date.issued
2014-09
dc.identifier.citation
Solanki, Sumeet; Dube, Prabhatchandra R.; Tano, Jean Yves; Birnbaumer, Lutz; Vazquez, Guillermo; Reduced endoplasmic reticulum stress-induced apoptosis and impaired unfolded protein response in TRPC3-deficient M1 macrophages; American Physiological Society; American Journal of Physiology-cell Physiology; 307; 6; 9-2014; C521-C531
dc.identifier.issn
0363-6143
dc.identifier.uri
http://hdl.handle.net/11336/96930
dc.description.abstract
Endoplasmic reticulum (ER) stress is a prominent mechanism of macrophage apoptosis in advanced atherosclerotic lesions. Recent studies from our laboratory showed that advanced atherosclerotic plaques in Apoe-/- mice with bone marrow deficiency of the calcium-permeable channel Transient Receptor Potential Canonical 3 (TRPC3) are characterized by reduced areas of necrosis and fewer apoptotic macrophages than animals transplanted with Trpc3+/+ bone marrow. In vitro, proinflammatory M1 but not anti-inflammatory M2 macrophages derived from Trpc3-/- Apoe-/- animals exhibited reduced ER stress-induced apoptosis. However, whether this was due to a specific effect of TRPC3 deficiency on macrophage ER stress signaling remained to be determined. In the present work we used polarized macrophages derived from mice with macrophage-specific deficiency of TRPC3 to examine the expression level of ER stress markers and the activation status of some typical mediators of macrophage apoptosis. We found that the reduced susceptibility of TRPC3-deficient M1 macrophages to ER stress-induced apoptosis correlates with an impaired unfolded protein response (UPR), reduced mitochondrion-dependent apoptosis, and reduced activation of the proapoptotic molecules calmodulin-dependent protein kinase II and signal transducer and activator of transcription 1. Notably, none of these pathways was altered in TRPC3- deficient M2 macrophages. These findings show for the first time an obligatory requirement for a member of the TRPC family of cation channels in ER stress-induced apoptosis in macrophages, underscoring a rather selective role of the TRPC3 channel on mechanisms related to the UPR signaling in M1 macrophages.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
American Physiological Society
dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
ENDOPLASMIC RETICULUM STRESS
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MACROPHAGE APOPTOSIS
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TRPC CHANNELS
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Bioquímica y Biología Molecular
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Ciencias Biológicas
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CIENCIAS NATURALES Y EXACTAS
dc.title
Reduced endoplasmic reticulum stress-induced apoptosis and impaired unfolded protein response in TRPC3-deficient M1 macrophages
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2019-10-28T18:26:37Z
dc.journal.volume
307
dc.journal.number
6
dc.journal.pagination
C521-C531
dc.journal.pais
Estados Unidos
dc.journal.ciudad
Bethesda
dc.description.fil
Fil: Solanki, Sumeet. University of Toledo; Estados Unidos
dc.description.fil
Fil: Dube, Prabhatchandra R.. University of Toledo; Estados Unidos
dc.description.fil
Fil: Tano, Jean Yves. University of Toledo; Estados Unidos
dc.description.fil
Fil: Birnbaumer, Lutz. National Institute of Environmental Health Sciences; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto de Investigaciones Biotecnológicas. Instituto de Investigaciones Biotecnológicas "Dr. Raúl Alfonsín" (sede Chascomús). Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas. Instituto de Investigaciones Biotecnológicas "Dr. Raúl Alfonsín" (sede Chascomús); Argentina
dc.description.fil
Fil: Vazquez, Guillermo. University of Toledo; Estados Unidos
dc.journal.title
American Journal of Physiology-cell Physiology
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4166736/
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://journals.physiology.org/doi/full/10.1152/ajpcell.00369.2013
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1152/ajpcell.00369.2013
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