Lidocaine‐induced apoptosis of gingival fibroblasts: participation of cAMP and PKC activity

Autores
Quinteros Villarruel, Emmanuel; Borda, Enri Santiago; Sterin Borda, Leonor; Orman, Betina
Año de publicación
2010
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Local anaesthetics are drugs that prevent or relieve pain by interrupting nervous conduction, and are the most commonly used drugs in dentistry. Their main target of action are voltage-dependent Na+ channels. The Na+ channel is modulated by phosphorylation of two enzymes: protein kinase A (PKA) and protein kinase C (PKC). We studied the ability of lidocaine to modulate programmed cell death of human gingival fibroblasts, and the mechanisms involved in this process. Lidocaine (10-5 to 10-7 M) stimulated apoptosis in primary cultures and the caspase-3 activity in a concentration-dependent manner. The stimulatory effect of lidocaine on apoptosis was attenuated in the presence of HA 1004 (PKA inhibitor), and stimulated by staurosporine and Go 6976 (PKC inhibitors). Lidocaine-induced apoptotic nuclei correlated positively with cAMP accumulation and negatively with PKC activity. These results show that lidocaine promotes apoptosis in human gingival fibroblasts at concentrations used for local anaesthesia. The mechanism involves PKA stimulation and PKC inhibition, which in turn, stimulates caspase-3 and leads to programmed cell death.
Fil: Quinteros Villarruel, Emmanuel. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; Argentina
Fil: Borda, Enri Santiago. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; Argentina
Fil: Sterin Borda, Leonor. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; Argentina
Fil: Orman, Betina. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; Argentina
Materia
Local Anesthetic
Gingiva
Lidocaine
Apoptosis
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:11336/280484
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/280484
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Lidocaine‐induced apoptosis of gingival fibroblasts: participation of cAMP and PKC activityQuinteros Villarruel, EmmanuelBorda, Enri SantiagoSterin Borda, LeonorOrman, BetinaLocal AnestheticGingivaLidocaineApoptosishttps://purl.org/becyt/ford/3.3https://purl.org/becyt/ford/3Local anaesthetics are drugs that prevent or relieve pain by interrupting nervous conduction, and are the most commonly used drugs in dentistry. Their main target of action are voltage-dependent Na+ channels. The Na+ channel is modulated by phosphorylation of two enzymes: protein kinase A (PKA) and protein kinase C (PKC). We studied the ability of lidocaine to modulate programmed cell death of human gingival fibroblasts, and the mechanisms involved in this process. Lidocaine (10-5 to 10-7 M) stimulated apoptosis in primary cultures and the caspase-3 activity in a concentration-dependent manner. The stimulatory effect of lidocaine on apoptosis was attenuated in the presence of HA 1004 (PKA inhibitor), and stimulated by staurosporine and Go 6976 (PKC inhibitors). Lidocaine-induced apoptotic nuclei correlated positively with cAMP accumulation and negatively with PKC activity. These results show that lidocaine promotes apoptosis in human gingival fibroblasts at concentrations used for local anaesthesia. The mechanism involves PKA stimulation and PKC inhibition, which in turn, stimulates caspase-3 and leads to programmed cell death.Fil: Quinteros Villarruel, Emmanuel. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; ArgentinaFil: Borda, Enri Santiago. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; ArgentinaFil: Sterin Borda, Leonor. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; ArgentinaFil: Orman, Betina. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; ArgentinaAcademic Press Ltd - Elsevier Science Ltd2010-11info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/280484Quinteros Villarruel, Emmanuel; Borda, Enri Santiago; Sterin Borda, Leonor; Orman, Betina; Lidocaine‐induced apoptosis of gingival fibroblasts: participation of cAMP and PKC activity; Academic Press Ltd - Elsevier Science Ltd; Cell Biology International; 35; 8; 11-2010; 783-7881065-6995CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/10.1042/CBI20100200info:eu-repo/semantics/altIdentifier/doi/10.1042/CBI20100200info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2026-02-26T10:10:31Zoai:ri.conicet.gov.ar:11336/280484instacron: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:34982026-02-26 10:10:31.638CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Lidocaine‐induced apoptosis of gingival fibroblasts: participation of cAMP and PKC activity
title Lidocaine‐induced apoptosis of gingival fibroblasts: participation of cAMP and PKC activity
spellingShingle Lidocaine‐induced apoptosis of gingival fibroblasts: participation of cAMP and PKC activity
Quinteros Villarruel, Emmanuel
Local Anesthetic
Gingiva
Lidocaine
Apoptosis
title_short Lidocaine‐induced apoptosis of gingival fibroblasts: participation of cAMP and PKC activity
title_full Lidocaine‐induced apoptosis of gingival fibroblasts: participation of cAMP and PKC activity
title_fullStr Lidocaine‐induced apoptosis of gingival fibroblasts: participation of cAMP and PKC activity
title_full_unstemmed Lidocaine‐induced apoptosis of gingival fibroblasts: participation of cAMP and PKC activity
title_sort Lidocaine‐induced apoptosis of gingival fibroblasts: participation of cAMP and PKC activity
dc.creator.none.fl_str_mv Quinteros Villarruel, Emmanuel
Borda, Enri Santiago
Sterin Borda, Leonor
Orman, Betina
author Quinteros Villarruel, Emmanuel
author_facet Quinteros Villarruel, Emmanuel
Borda, Enri Santiago
Sterin Borda, Leonor
Orman, Betina
author_role author
author2 Borda, Enri Santiago
Sterin Borda, Leonor
Orman, Betina
author2_role author
author
author
dc.subject.none.fl_str_mv Local Anesthetic
Gingiva
Lidocaine
Apoptosis
topic Local Anesthetic
Gingiva
Lidocaine
Apoptosis
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.3
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Local anaesthetics are drugs that prevent or relieve pain by interrupting nervous conduction, and are the most commonly used drugs in dentistry. Their main target of action are voltage-dependent Na+ channels. The Na+ channel is modulated by phosphorylation of two enzymes: protein kinase A (PKA) and protein kinase C (PKC). We studied the ability of lidocaine to modulate programmed cell death of human gingival fibroblasts, and the mechanisms involved in this process. Lidocaine (10-5 to 10-7 M) stimulated apoptosis in primary cultures and the caspase-3 activity in a concentration-dependent manner. The stimulatory effect of lidocaine on apoptosis was attenuated in the presence of HA 1004 (PKA inhibitor), and stimulated by staurosporine and Go 6976 (PKC inhibitors). Lidocaine-induced apoptotic nuclei correlated positively with cAMP accumulation and negatively with PKC activity. These results show that lidocaine promotes apoptosis in human gingival fibroblasts at concentrations used for local anaesthesia. The mechanism involves PKA stimulation and PKC inhibition, which in turn, stimulates caspase-3 and leads to programmed cell death.
Fil: Quinteros Villarruel, Emmanuel. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; Argentina
Fil: Borda, Enri Santiago. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; Argentina
Fil: Sterin Borda, Leonor. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; Argentina
Fil: Orman, Betina. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; Argentina
description Local anaesthetics are drugs that prevent or relieve pain by interrupting nervous conduction, and are the most commonly used drugs in dentistry. Their main target of action are voltage-dependent Na+ channels. The Na+ channel is modulated by phosphorylation of two enzymes: protein kinase A (PKA) and protein kinase C (PKC). We studied the ability of lidocaine to modulate programmed cell death of human gingival fibroblasts, and the mechanisms involved in this process. Lidocaine (10-5 to 10-7 M) stimulated apoptosis in primary cultures and the caspase-3 activity in a concentration-dependent manner. The stimulatory effect of lidocaine on apoptosis was attenuated in the presence of HA 1004 (PKA inhibitor), and stimulated by staurosporine and Go 6976 (PKC inhibitors). Lidocaine-induced apoptotic nuclei correlated positively with cAMP accumulation and negatively with PKC activity. These results show that lidocaine promotes apoptosis in human gingival fibroblasts at concentrations used for local anaesthesia. The mechanism involves PKA stimulation and PKC inhibition, which in turn, stimulates caspase-3 and leads to programmed cell death.
publishDate 2010
dc.date.none.fl_str_mv 2010-11
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/11336/280484
Quinteros Villarruel, Emmanuel; Borda, Enri Santiago; Sterin Borda, Leonor; Orman, Betina; Lidocaine‐induced apoptosis of gingival fibroblasts: participation of cAMP and PKC activity; Academic Press Ltd - Elsevier Science Ltd; Cell Biology International; 35; 8; 11-2010; 783-788
1065-6995
CONICET Digital
CONICET
url http://hdl.handle.net/11336/280484
identifier_str_mv Quinteros Villarruel, Emmanuel; Borda, Enri Santiago; Sterin Borda, Leonor; Orman, Betina; Lidocaine‐induced apoptosis of gingival fibroblasts: participation of cAMP and PKC activity; Academic Press Ltd - Elsevier Science Ltd; Cell Biology International; 35; 8; 11-2010; 783-788
1065-6995
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/10.1042/CBI20100200
info:eu-repo/semantics/altIdentifier/doi/10.1042/CBI20100200
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 Academic Press Ltd - Elsevier Science Ltd
publisher.none.fl_str_mv Academic Press Ltd - Elsevier Science Ltd
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
_version_ 1858305427518783489
score 13.176822

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