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
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/15844
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oai:ri.conicet.gov.ar:11336/15844 |
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3498 |
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CONICET Digital (CONICET) |
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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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1842269205042298880 |
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13.13397 |