Action of anti-M3 muscarinic acetylcholine receptor IgG of primary Sjögren's syndrome on the enzymatic antioxidant system in rat submandibular gland

Autores
Reina, Silvia Lorena; RodrÍguez, Marcelo; Stranieri, Graciela; Borda, Enri Santiago
Año de publicación
2015
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
BACKGROUND: We demonstrate that serum immunoglobulin G (IgG) directed against glandular M3 muscarinic acetylcholine receptors (M₃mAChR) and pilocarpine triggers the increment of superoxide dismutase (SOD) and catalase (CAT) and the production of nitric oxide (NO) and prostaglandin E₂(PGE₂). METHODS: Enzyme-linked immunosorbent assay (ELISA) was performed in the presence of the human M₂mAChR synthetic peptide as antigen to detect in serum of pSS patients the autoantibodies. Further, SOD and CAT specific activity and NO were determined chemically in the presence of anti-M₃mAChR IgG and pilocarpine. The level of PGE₂generation in the presence of autoantibody and pilocarpine was determined by ELISA. RESULTS: An association between anti-M₂mAChR autoantibodies and pilocarpine given the increment of the specific activity of SOD and CAT in the serum of pSS patients and in the rat submandibular gland was observed. As a result of this action, M₃synthetic peptide and atropine abrogated the stimulatory action. The L-type calcium channel, calcium/calmodulin complex and COX-2 inhibitors selectively blocked the increment of the specific activity of SOD and CAT in the rat submandibular gland. An increased production of NO and PGE₂by the cholinergic autoantibody and pilocarpine was also detected. CONCLUSION: On the basis of these results, the increment of the specific activity of SOD and CAT in pSS patients as compared to control healthy individuals may be seen as a defensive reaction to the increment of the amount of ROS, which becoming uncontrollable, leads to irreversible cellular and tissue damage.
Fil: Reina, Silvia Lorena. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: RodrÍguez, Marcelo. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Stranieri, Graciela. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Borda, Enri Santiago. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Materia
Sjögren Syndrome
Anti-M3 Peptide Igg
Catalase
Nitrites
Prostaglandin E2
Superoxide Dismutase
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/15844

id CONICETDig_24249fda1383abeefad8e904f48882ec
oai_identifier_str oai:ri.conicet.gov.ar:11336/15844
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Action of anti-M3 muscarinic acetylcholine receptor IgG of primary Sjögren's syndrome on the enzymatic antioxidant system in rat submandibular glandReina, Silvia LorenaRodrÍguez, MarceloStranieri, GracielaBorda, Enri SantiagoSjögren SyndromeAnti-M3 Peptide IggCatalaseNitritesProstaglandin E2Superoxide Dismutasehttps://purl.org/becyt/ford/3.5https://purl.org/becyt/ford/3BACKGROUND: We demonstrate that serum immunoglobulin G (IgG) directed against glandular M3 muscarinic acetylcholine receptors (M₃mAChR) and pilocarpine triggers the increment of superoxide dismutase (SOD) and catalase (CAT) and the production of nitric oxide (NO) and prostaglandin E₂(PGE₂). METHODS: Enzyme-linked immunosorbent assay (ELISA) was performed in the presence of the human M₂mAChR synthetic peptide as antigen to detect in serum of pSS patients the autoantibodies. Further, SOD and CAT specific activity and NO were determined chemically in the presence of anti-M₃mAChR IgG and pilocarpine. The level of PGE₂generation in the presence of autoantibody and pilocarpine was determined by ELISA. RESULTS: An association between anti-M₂mAChR autoantibodies and pilocarpine given the increment of the specific activity of SOD and CAT in the serum of pSS patients and in the rat submandibular gland was observed. As a result of this action, M₃synthetic peptide and atropine abrogated the stimulatory action. The L-type calcium channel, calcium/calmodulin complex and COX-2 inhibitors selectively blocked the increment of the specific activity of SOD and CAT in the rat submandibular gland. An increased production of NO and PGE₂by the cholinergic autoantibody and pilocarpine was also detected. CONCLUSION: On the basis of these results, the increment of the specific activity of SOD and CAT in pSS patients as compared to control healthy individuals may be seen as a defensive reaction to the increment of the amount of ROS, which becoming uncontrollable, leads to irreversible cellular and tissue damage.Fil: Reina, Silvia Lorena. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: RodrÍguez, Marcelo. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Stranieri, Graciela. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Borda, Enri Santiago. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaWiley2015-11info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/15844Reina, Silvia Lorena; RodrÍguez, Marcelo; Stranieri, Graciela; Borda, Enri Santiago; Action of anti-M3 muscarinic acetylcholine receptor IgG of primary Sjögren's syndrome on the enzymatic antioxidant system in rat submandibular gland; Wiley; Journal Of Oral Pathology And Medicine; 44; 10; 11-2015; 876-8830904-25121600-0714enginfo:eu-repo/semantics/altIdentifier/doi/10.1111/jop.12313info:eu-repo/semantics/altIdentifier/url/http://onlinelibrary.wiley.com/doi/10.1111/jop.12313/abstractinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:53:09Zoai:ri.conicet.gov.ar:11336/15844instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 09:53:09.816CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Action of anti-M3 muscarinic acetylcholine receptor IgG of primary Sjögren's syndrome on the enzymatic antioxidant system in rat submandibular gland
title Action of anti-M3 muscarinic acetylcholine receptor IgG of primary Sjögren's syndrome on the enzymatic antioxidant system in rat submandibular gland
spellingShingle Action of anti-M3 muscarinic acetylcholine receptor IgG of primary Sjögren's syndrome on the enzymatic antioxidant system in rat submandibular gland
Reina, Silvia Lorena
Sjögren Syndrome
Anti-M3 Peptide Igg
Catalase
Nitrites
Prostaglandin E2
Superoxide Dismutase
title_short Action of anti-M3 muscarinic acetylcholine receptor IgG of primary Sjögren's syndrome on the enzymatic antioxidant system in rat submandibular gland
title_full Action of anti-M3 muscarinic acetylcholine receptor IgG of primary Sjögren's syndrome on the enzymatic antioxidant system in rat submandibular gland
title_fullStr Action of anti-M3 muscarinic acetylcholine receptor IgG of primary Sjögren's syndrome on the enzymatic antioxidant system in rat submandibular gland
title_full_unstemmed Action of anti-M3 muscarinic acetylcholine receptor IgG of primary Sjögren's syndrome on the enzymatic antioxidant system in rat submandibular gland
title_sort Action of anti-M3 muscarinic acetylcholine receptor IgG of primary Sjögren's syndrome on the enzymatic antioxidant system in rat submandibular gland
dc.creator.none.fl_str_mv Reina, Silvia Lorena
RodrÍguez, Marcelo
Stranieri, Graciela
Borda, Enri Santiago
author Reina, Silvia Lorena
author_facet Reina, Silvia Lorena
RodrÍguez, Marcelo
Stranieri, Graciela
Borda, Enri Santiago
author_role author
author2 RodrÍguez, Marcelo
Stranieri, Graciela
Borda, Enri Santiago
author2_role author
author
author
dc.subject.none.fl_str_mv Sjögren Syndrome
Anti-M3 Peptide Igg
Catalase
Nitrites
Prostaglandin E2
Superoxide Dismutase
topic Sjögren Syndrome
Anti-M3 Peptide Igg
Catalase
Nitrites
Prostaglandin E2
Superoxide Dismutase
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.5
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv BACKGROUND: We demonstrate that serum immunoglobulin G (IgG) directed against glandular M3 muscarinic acetylcholine receptors (M₃mAChR) and pilocarpine triggers the increment of superoxide dismutase (SOD) and catalase (CAT) and the production of nitric oxide (NO) and prostaglandin E₂(PGE₂). METHODS: Enzyme-linked immunosorbent assay (ELISA) was performed in the presence of the human M₂mAChR synthetic peptide as antigen to detect in serum of pSS patients the autoantibodies. Further, SOD and CAT specific activity and NO were determined chemically in the presence of anti-M₃mAChR IgG and pilocarpine. The level of PGE₂generation in the presence of autoantibody and pilocarpine was determined by ELISA. RESULTS: An association between anti-M₂mAChR autoantibodies and pilocarpine given the increment of the specific activity of SOD and CAT in the serum of pSS patients and in the rat submandibular gland was observed. As a result of this action, M₃synthetic peptide and atropine abrogated the stimulatory action. The L-type calcium channel, calcium/calmodulin complex and COX-2 inhibitors selectively blocked the increment of the specific activity of SOD and CAT in the rat submandibular gland. An increased production of NO and PGE₂by the cholinergic autoantibody and pilocarpine was also detected. CONCLUSION: On the basis of these results, the increment of the specific activity of SOD and CAT in pSS patients as compared to control healthy individuals may be seen as a defensive reaction to the increment of the amount of ROS, which becoming uncontrollable, leads to irreversible cellular and tissue damage.
Fil: Reina, Silvia Lorena. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: RodrÍguez, Marcelo. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Stranieri, Graciela. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Borda, Enri Santiago. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
description BACKGROUND: We demonstrate that serum immunoglobulin G (IgG) directed against glandular M3 muscarinic acetylcholine receptors (M₃mAChR) and pilocarpine triggers the increment of superoxide dismutase (SOD) and catalase (CAT) and the production of nitric oxide (NO) and prostaglandin E₂(PGE₂). METHODS: Enzyme-linked immunosorbent assay (ELISA) was performed in the presence of the human M₂mAChR synthetic peptide as antigen to detect in serum of pSS patients the autoantibodies. Further, SOD and CAT specific activity and NO were determined chemically in the presence of anti-M₃mAChR IgG and pilocarpine. The level of PGE₂generation in the presence of autoantibody and pilocarpine was determined by ELISA. RESULTS: An association between anti-M₂mAChR autoantibodies and pilocarpine given the increment of the specific activity of SOD and CAT in the serum of pSS patients and in the rat submandibular gland was observed. As a result of this action, M₃synthetic peptide and atropine abrogated the stimulatory action. The L-type calcium channel, calcium/calmodulin complex and COX-2 inhibitors selectively blocked the increment of the specific activity of SOD and CAT in the rat submandibular gland. An increased production of NO and PGE₂by the cholinergic autoantibody and pilocarpine was also detected. CONCLUSION: On the basis of these results, the increment of the specific activity of SOD and CAT in pSS patients as compared to control healthy individuals may be seen as a defensive reaction to the increment of the amount of ROS, which becoming uncontrollable, leads to irreversible cellular and tissue damage.
publishDate 2015
dc.date.none.fl_str_mv 2015-11
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 http://hdl.handle.net/11336/15844
Reina, Silvia Lorena; RodrÍguez, Marcelo; Stranieri, Graciela; Borda, Enri Santiago; Action of anti-M3 muscarinic acetylcholine receptor IgG of primary Sjögren's syndrome on the enzymatic antioxidant system in rat submandibular gland; Wiley; Journal Of Oral Pathology And Medicine; 44; 10; 11-2015; 876-883
0904-2512
1600-0714
url http://hdl.handle.net/11336/15844
identifier_str_mv Reina, Silvia Lorena; RodrÍguez, Marcelo; Stranieri, Graciela; Borda, Enri Santiago; Action of anti-M3 muscarinic acetylcholine receptor IgG of primary Sjögren's syndrome on the enzymatic antioxidant system in rat submandibular gland; Wiley; Journal Of Oral Pathology And Medicine; 44; 10; 11-2015; 876-883
0904-2512
1600-0714
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1111/jop.12313
info:eu-repo/semantics/altIdentifier/url/http://onlinelibrary.wiley.com/doi/10.1111/jop.12313/abstract
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Wiley
publisher.none.fl_str_mv Wiley
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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