Cyclic stretch activates ERK1/2 via G proteins and EGFR in alveolar epithelial cells

Eduardo Correa-Meyer; Liuska Pesce; Carmen Guerrero; Jacob I Sznajder

doi:10.1152/ajplung.00203.2001

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Cyclic stretch activates ERK1/2 via G proteins and EGFR in alveolar epithelial cells

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Cyclic stretch activates ERK1/2 via G proteins and EGFR in alveolar epithelial cells

Eduardo Correa-Meyer, Liuska Pesce, Carmen Guerrero and Jacob I Sznajder

American journal of physiology. Lung cellular and molecular physiology, Vol.282(5), pp.L883-L891

05/01/2002

DOI: 10.1152/ajplung.00203.2001

PMID: 11943650

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Abstract

Mechanical stimuli are transduced into intracellular signals in lung alveolar epithelial cells (AEC). We studied whether mitogen-activated protein kinase (MAPK) pathways are activated during cyclic stretch of AEC. Cyclic stretch induced a rapid (within 5 min) increase in extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation in AEC. The inhibition of Na+, L-type Ca2+ and stretch-activated ion channels with amiloride, nifedipine, and gadolinium did not prevent the stretch-induced ERK1/2 activation. The inhibition of Grb2-SOS interaction with an SH3 binding sequence peptide, Ras with a farnesyl transferase inhibitor, and Raf-1 with forskolin did not affect the stretch-induced ERK1/2 phosphorylation. Moreover, cyclic stretch did not increase Ras activity, suggesting that stretch-induced ERK1/2 activation is independent of the classical receptor tyrosine kinase-MAPK pathway. Pertussis toxin and two specific epidermal growth factor receptor (EGFR) inhibitors (AG-1478 and PD-153035) prevented the stretch-induced ERK1/2 activation. Accordingly, in primary AEC, cyclic stretch activates ERK1/2 via G proteins and EGFR, in Na+ and Ca2+ influxes and Grb2-SOS-, Ras-, and Raf-1-independent pathways.

Details

Title: Subtitle: Cyclic stretch activates ERK1/2 via G proteins and EGFR in alveolar epithelial cells
Creators: Eduardo Correa-Meyer - Division of Pulmonary and Critical Care Medicine, Northwestern University, Chicago, Illinois 60611; and
Liuska Pesce - Division of Pulmonary and Critical Care Medicine, Northwestern University, Chicago, Illinois 60611; and
Carmen Guerrero - Centro de Investigación del Cáncer, Universidad de Salamanca, 37007 Salamanca, Spain
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.L883-L891
DOI: 10.1152/ajplung.00203.2001
PMID: 11943650
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: 9984093234202771

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