Dopamine activates ERKs in alveolar epithelial cells via Ras-PKC-dependent and Grb2/Sos-independent mechanisms

Carmen Guerrero; Liuska Pesce; Emilia Lecuona; Karen M Ridge; Jacob I Sznajder

doi:10.1152/ajplung.00178.2001

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Dopamine activates ERKs in alveolar epithelial cells via Ras-PKC-dependent and Grb2/Sos-independent mechanisms

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Dopamine activates ERKs in alveolar epithelial cells via Ras-PKC-dependent and Grb2/Sos-independent mechanisms

Carmen Guerrero, Liuska Pesce, Emilia Lecuona, Karen M Ridge and Jacob I Sznajder

American journal of physiology. Lung cellular and molecular physiology, Vol.282(5), pp.L1099-L1107

05/01/2002

DOI: 10.1152/ajplung.00178.2001

PMID: 11943676

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Abstract

Recently it has been described that dopamine (DA), via dopaminergic type 2 receptors (D2R), activates the mitogen-activated protein kinase extracellular signal-regulated kinase (MAPK/ERK) proteins in alveolar epithelial cells (AEC), which results in the upregulation of Na+-K+-ATPase. In the present report, we used AEC to investigate the signaling pathway that links DA with ERK activation. Incubation of AEC with DA resulted in rapid and transient stimulation of ERK activity, which was mediated by Ras proteins and the serine/threonine kinase Raf-1. Pretreatment of AEC with Src homology 3 binding peptide, which blocks the interaction between Grb2 and Sos, did not prevent DA activation of ERK. Diacylglycerol (DAG)-dependent protein kinase C (PKC) isoenzymes, involved in the DA-mediated activation of ERK proteins as pretreatment with either bisindolylmaleimide or Ro-31-8220, prevented the phosphorylation of Elk-1, and quinpirole, a D2R activator, stimulates the translocation of PKCε. Together, the data suggest that DA activated MAPK/ERK via Ras, Raf-1 kinase, and DAG-dependent PKC isoenzymes, but, importantly and contrary to the classical model, this pathway did not involve the Grb2-Sos complex formation.

Details

Title: Subtitle: Dopamine activates ERKs in alveolar epithelial cells via Ras-PKC-dependent and Grb2/Sos-independent mechanisms
Creators: Carmen Guerrero - Division of Pulmonary and Critical Care Medicine, Northwestern University, Chicago, Illinois 60611; and, Centro de Investigación del Cáncer, Universidad de Salamanca, 37007 Salamanca, Spain
Liuska Pesce - Division of Pulmonary and Critical Care Medicine, Northwestern University, Chicago, Illinois 60611; and
Emilia Lecuona - Division of Pulmonary and Critical Care Medicine, Northwestern University, Chicago, Illinois 60611; and
Karen M Ridge - Division of Pulmonary and Critical Care Medicine, Northwestern University, Chicago, Illinois 60611; and
Jacob I Sznajder - Division of Pulmonary and Critical Care Medicine, Northwestern University, Chicago, Illinois 60611; and
Resource Type: Journal article
Publication Details: American journal of physiology. Lung cellular and molecular physiology, Vol.282(5), pp.L1099-L1107
DOI: 10.1152/ajplung.00178.2001
PMID: 11943676
NLM abbreviation: Am J Physiol Lung Cell Mol Physiol
ISSN: 1040-0605
eISSN: 1522-1504
Language: English
Date published: 05/01/2002
Academic Unit: Endocrinology and Diabetes; Stead Family Department of Pediatrics
Record Identifier: 9984093218202771

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