Epidermal growth factor receptor activity upregulates lactate dehydrogenase a expression, lactate dehydrogenase activity, and lactate secretion in cultured ib3-1 cystic fibrosis lu...

Autores: Massip Copiz, María Macarena; Valdivieso, Ángel Gabriel; Clauzure, Mariángeles; Mori, Consuelo; Asensio, Cristian J. A.; Aguilar, María de los Angeles; Santa Coloma, Tomás Antonio
Año de publicación: 2021
Idioma: inglés
Tipo de recurso: artículo
Estado: versión publicada
Descripción: Fil: Massip Copiz, María Macarena. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina
Fil: Valdivieso, Ángel Gabriel. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina
Fil: Clauzure, Mariángeles. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina
Fil: Mori, Consuelo. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina
Fil: Asensio, Cristian. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina
Fil: Aguilar, María Á. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina
Fil: Santa Coloma, Tomás Antonio. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina
Abstract: Cystic fibrosis (CF) is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. It has been postulated that reduced HCO3− transport through CFTR may lead to a decreased airway surface liquid pH. In contrast, others have reported no changes in the extracellular pH (pHe). We have recently reported that in carcinoma Caco-2/pRS26 cells (transfected with short hairpin RNA for CFTR) or CF lung epithelial IB3-1 cells, the mutation in CFTR decreased mitochondrial complex I activity and increased lactic acid production, owing to an autocrine IL-1β loop. The secreted lactate accounted for the reduced pHe, because oxamate fully restored the pHe. These effects were attributed to the IL-1β autocrine loop and the downstream signaling kinases c-Src and JNK. Here we show that the pHe of IB3-1 cells can be restored to normal values (∼7.4) by incubation with the epidermal growth factor receptor (EGFR, HER1, ErbB1) inhibitors AG1478 and PD168393. PD168393 fully restored the pHe values of IB3-1 cells, suggesting that the reduced pHe is mainly due to increased EGFR activity and lactate. Also, in IB3-1 cells, lactate dehydrogenase A mRNA, protein expression, and activity are downregulated when EGFR is inhibited. Thus, a constitutive EGFR activation seems to be responsible for the reduced pHe in IB3-1 cells.
Fuente: Postprint de artículo publicado en Biochemistry and Cell Biology. 2021, 99 (4)
Materia: FIBROSIS QUISTICA
GENES
SISTEMA RESPIRATORIO
CELULAS
LACTATO DESHIDROGENASA
Nivel de accesibilidad: acceso abierto
Condiciones de uso: https://creativecommons.org/licenses/by-nc-sa/4.0/
Repositorio
Institución: Pontificia Universidad Católica Argentina
OAI Identificador: oai:ucacris:123456789/14036

Acceder

id	RIUCA_7fd550377175321741a7c5579f1a80a2
oai_identifier_str	oai:ucacris:123456789/14036
network_acronym_str	RIUCA
repository_id_str	2585
network_name_str	Repositorio Institucional (UCA)
spelling	Epidermal growth factor receptor activity upregulates lactate dehydrogenase a expression, lactate dehydrogenase activity, and lactate secretion in cultured ib3-1 cystic fibrosis lung epithelial cellsMassip Copiz, María MacarenaValdivieso, Ángel GabrielClauzure, MariángelesMori, ConsueloAsensio, Cristian J. A.Aguilar, María de los AngelesSanta Coloma, Tomás AntonioFIBROSIS QUISTICAGENESSISTEMA RESPIRATORIOCELULASLACTATO DESHIDROGENASAFil: Massip Copiz, María Macarena. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; ArgentinaFil: Valdivieso, Ángel Gabriel. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; ArgentinaFil: Clauzure, Mariángeles. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; ArgentinaFil: Mori, Consuelo. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; ArgentinaFil: Asensio, Cristian. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; ArgentinaFil: Aguilar, María Á. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; ArgentinaFil: Santa Coloma, Tomás Antonio. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; ArgentinaAbstract: Cystic fibrosis (CF) is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. It has been postulated that reduced HCO3− transport through CFTR may lead to a decreased airway surface liquid pH. In contrast, others have reported no changes in the extracellular pH (pHe). We have recently reported that in carcinoma Caco-2/pRS26 cells (transfected with short hairpin RNA for CFTR) or CF lung epithelial IB3-1 cells, the mutation in CFTR decreased mitochondrial complex I activity and increased lactic acid production, owing to an autocrine IL-1β loop. The secreted lactate accounted for the reduced pHe, because oxamate fully restored the pHe. These effects were attributed to the IL-1β autocrine loop and the downstream signaling kinases c-Src and JNK. Here we show that the pHe of IB3-1 cells can be restored to normal values (∼7.4) by incubation with the epidermal growth factor receptor (EGFR, HER1, ErbB1) inhibitors AG1478 and PD168393. PD168393 fully restored the pHe values of IB3-1 cells, suggesting that the reduced pHe is mainly due to increased EGFR activity and lactate. Also, in IB3-1 cells, lactate dehydrogenase A mRNA, protein expression, and activity are downregulated when EGFR is inhibited. Thus, a constitutive EGFR activation seems to be responsible for the reduced pHe in IB3-1 cells.2021info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttps://repositorio.uca.edu.ar/handle/123456789/140360829-8211 (impreso)1208-6002 (on line)10.1139/bcb-2020-052233481676Massip Copiz, M. M. et al. Epidermal growth factor receptor activity upregulates lactate dehydrogenase a expression, lactate dehydrogenase activity, and lactate secretion in cultured ib3-1 cystic fibrosis lung epithelial cells [en línea]. Postprint de artículo publicado en Biochemistry and Cell Biology. 2021, 99 (4). doi: 10.1139/bcb-2020-0522. Disponible en: https://repositorio.uca.edu.ar/handle/123456789/14036Postprint de artículo publicado en Biochemistry and Cell Biology. 2021, 99 (4)reponame:Repositorio Institucional (UCA)instname:Pontificia Universidad Católica Argentinaenginfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/4.0/2025-07-03T10:58:35Zoai:ucacris:123456789/14036instacron:UCAInstitucionalhttps://repositorio.uca.edu.ar/Universidad privadaNo correspondehttps://repositorio.uca.edu.ar/oaiclaudia_fernandez@uca.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:25852025-07-03 10:58:35.368Repositorio Institucional (UCA) - Pontificia Universidad Católica Argentinafalse
dc.title.none.fl_str_mv	Epidermal growth factor receptor activity upregulates lactate dehydrogenase a expression, lactate dehydrogenase activity, and lactate secretion in cultured ib3-1 cystic fibrosis lung epithelial cells
title	Epidermal growth factor receptor activity upregulates lactate dehydrogenase a expression, lactate dehydrogenase activity, and lactate secretion in cultured ib3-1 cystic fibrosis lung epithelial cells
spellingShingle	Epidermal growth factor receptor activity upregulates lactate dehydrogenase a expression, lactate dehydrogenase activity, and lactate secretion in cultured ib3-1 cystic fibrosis lung epithelial cells Massip Copiz, María Macarena FIBROSIS QUISTICA GENES SISTEMA RESPIRATORIO CELULAS LACTATO DESHIDROGENASA
title_short	Epidermal growth factor receptor activity upregulates lactate dehydrogenase a expression, lactate dehydrogenase activity, and lactate secretion in cultured ib3-1 cystic fibrosis lung epithelial cells
title_full	Epidermal growth factor receptor activity upregulates lactate dehydrogenase a expression, lactate dehydrogenase activity, and lactate secretion in cultured ib3-1 cystic fibrosis lung epithelial cells
title_fullStr	Epidermal growth factor receptor activity upregulates lactate dehydrogenase a expression, lactate dehydrogenase activity, and lactate secretion in cultured ib3-1 cystic fibrosis lung epithelial cells
title_full_unstemmed	Epidermal growth factor receptor activity upregulates lactate dehydrogenase a expression, lactate dehydrogenase activity, and lactate secretion in cultured ib3-1 cystic fibrosis lung epithelial cells
title_sort	Epidermal growth factor receptor activity upregulates lactate dehydrogenase a expression, lactate dehydrogenase activity, and lactate secretion in cultured ib3-1 cystic fibrosis lung epithelial cells
dc.creator.none.fl_str_mv	Massip Copiz, María Macarena Valdivieso, Ángel Gabriel Clauzure, Mariángeles Mori, Consuelo Asensio, Cristian J. A. Aguilar, María de los Angeles Santa Coloma, Tomás Antonio
author	Massip Copiz, María Macarena
author_facet	Massip Copiz, María Macarena Valdivieso, Ángel Gabriel Clauzure, Mariángeles Mori, Consuelo Asensio, Cristian J. A. Aguilar, María de los Angeles Santa Coloma, Tomás Antonio
author_role	author
author2	Valdivieso, Ángel Gabriel Clauzure, Mariángeles Mori, Consuelo Asensio, Cristian J. A. Aguilar, María de los Angeles Santa Coloma, Tomás Antonio
author2_role	author author author author author author
dc.subject.none.fl_str_mv	FIBROSIS QUISTICA GENES SISTEMA RESPIRATORIO CELULAS LACTATO DESHIDROGENASA
topic	FIBROSIS QUISTICA GENES SISTEMA RESPIRATORIO CELULAS LACTATO DESHIDROGENASA
dc.description.none.fl_txt_mv	Fil: Massip Copiz, María Macarena. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina Fil: Valdivieso, Ángel Gabriel. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina Fil: Clauzure, Mariángeles. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina Fil: Mori, Consuelo. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina Fil: Asensio, Cristian. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina Fil: Aguilar, María Á. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina Fil: Santa Coloma, Tomás Antonio. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina Abstract: Cystic fibrosis (CF) is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. It has been postulated that reduced HCO3− transport through CFTR may lead to a decreased airway surface liquid pH. In contrast, others have reported no changes in the extracellular pH (pHe). We have recently reported that in carcinoma Caco-2/pRS26 cells (transfected with short hairpin RNA for CFTR) or CF lung epithelial IB3-1 cells, the mutation in CFTR decreased mitochondrial complex I activity and increased lactic acid production, owing to an autocrine IL-1β loop. The secreted lactate accounted for the reduced pHe, because oxamate fully restored the pHe. These effects were attributed to the IL-1β autocrine loop and the downstream signaling kinases c-Src and JNK. Here we show that the pHe of IB3-1 cells can be restored to normal values (∼7.4) by incubation with the epidermal growth factor receptor (EGFR, HER1, ErbB1) inhibitors AG1478 and PD168393. PD168393 fully restored the pHe values of IB3-1 cells, suggesting that the reduced pHe is mainly due to increased EGFR activity and lactate. Also, in IB3-1 cells, lactate dehydrogenase A mRNA, protein expression, and activity are downregulated when EGFR is inhibited. Thus, a constitutive EGFR activation seems to be responsible for the reduced pHe in IB3-1 cells.
description	Fil: Massip Copiz, María Macarena. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina
publishDate	2021
dc.date.none.fl_str_mv	2021
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	https://repositorio.uca.edu.ar/handle/123456789/14036 0829-8211 (impreso) 1208-6002 (on line) 10.1139/bcb-2020-0522 33481676 Massip Copiz, M. M. et al. Epidermal growth factor receptor activity upregulates lactate dehydrogenase a expression, lactate dehydrogenase activity, and lactate secretion in cultured ib3-1 cystic fibrosis lung epithelial cells [en línea]. Postprint de artículo publicado en Biochemistry and Cell Biology. 2021, 99 (4). doi: 10.1139/bcb-2020-0522. Disponible en: https://repositorio.uca.edu.ar/handle/123456789/14036
url	https://repositorio.uca.edu.ar/handle/123456789/14036
identifier_str_mv	0829-8211 (impreso) 1208-6002 (on line) 10.1139/bcb-2020-0522 33481676 Massip Copiz, M. M. et al. Epidermal growth factor receptor activity upregulates lactate dehydrogenase a expression, lactate dehydrogenase activity, and lactate secretion in cultured ib3-1 cystic fibrosis lung epithelial cells [en línea]. Postprint de artículo publicado en Biochemistry and Cell Biology. 2021, 99 (4). doi: 10.1139/bcb-2020-0522. Disponible en: https://repositorio.uca.edu.ar/handle/123456789/14036
dc.language.none.fl_str_mv	eng
language	eng
dc.rights.none.fl_str_mv	info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by-nc-sa/4.0/
eu_rights_str_mv	openAccess
rights_invalid_str_mv	https://creativecommons.org/licenses/by-nc-sa/4.0/
dc.format.none.fl_str_mv	application/pdf
dc.source.none.fl_str_mv	Postprint de artículo publicado en Biochemistry and Cell Biology. 2021, 99 (4) reponame:Repositorio Institucional (UCA) instname:Pontificia Universidad Católica Argentina
reponame_str	Repositorio Institucional (UCA)
collection	Repositorio Institucional (UCA)
instname_str	Pontificia Universidad Católica Argentina
repository.name.fl_str_mv	Repositorio Institucional (UCA) - Pontificia Universidad Católica Argentina
repository.mail.fl_str_mv	claudia_fernandez@uca.edu.ar
_version_	1836638362017988608
score	13.22299

Epidermal growth factor receptor activity upregulates lactate dehydrogenase a expression, lactate dehydrogenase activity, and lactate secretion in cultured ib3-1 cystic fibrosis lu...

Publicaciones similares