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PMID: 9230127 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Angiotensin II type 2 receptors mediate inhibition of mitogen-activated protein kinase cascade and functional activation of SHP-1 tyrosine phosphatase.

The Biochemical journal ·Vol. 325 ( Pt 2) ·1997-07-15 ·Pages 449-54

Bedecs K, Elbaz N, Sutren M, Masson M, Susini C, Strosberg AD, Nahmias C

Abstract

Angiotensin II type 2 (AT2) receptors are involved in the inhibition of cell proliferation as well as in apoptosis and neuronal differentiation, through intracellular signalling pathways that remain poorly defined. The present study examines the effect of AT2-receptor stimulation on growth-factor-induced pathways leading to the activation of mitogen-activated protein (MAP) kinases. In N1E-115 neuroblastoma cells, AT2 receptors inhibit the activity of MAP kinases induced by serum as well as by epidermal growth factor. The inhibitory effect of angiotensin II (Ang II) is rapid and transient, and affects both ERK1 and ERK2 (extracellular signal-related protein kinase) isoforms of the enzyme. AT2-mediated MAP kinase inactivation is not sensitive to pertussis toxin or okadaic acid, but involves a vanadate-sensitive protein tyrosine phosphatase (PTP). Expression of MAP kinase phosphatase-1 (MKP-1) is not significantly modified upon AT2-receptor activation, and insensitivity to actinomycin D also rules out transcriptional induction of other MKPs as a possible mechanism for AT2-mediated inactivation of MAP kinases. In addition, we report here that both in N1E-115 cells and in Chinese hamster ovary cells expressing recombinant human AT2 receptors, Ang II rapidly stimulates the catalytic activity of SHP-1, a soluble PTP that has been implicated in termination of signalling by cytokine and growth-factor receptors. These findings thus demonstrate functional negative cross-talk between heptahelical AT2 receptors and receptor tyrosine kinases, and suggest that SHP-1 tyrosine phosphatase is an early transducer of the AT2 receptor signalling pathway.

MeSH Terms
Angiotensin II/pharmacology Animals Blood Proteins/pharmacology CHO Cells Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors,metabolism Cell Cycle Proteins Cricetinae Dactinomycin/pharmacology Dual Specificity Phosphatase 1 Enzyme Activation Epidermal Growth Factor/pharmacology Immediate-Early Proteins/metabolism Intracellular Signaling Peptides and Proteins Mitogen-Activated Protein Kinase 1 Mitogen-Activated Protein Kinase 3 Mitogen-Activated Protein Kinases Okadaic Acid/pharmacology Phosphoprotein Phosphatases Protein Phosphatase 1 Protein Tyrosine Phosphatase, Non-Receptor Type 11 Protein Tyrosine Phosphatase, Non-Receptor Type 6 Protein Tyrosine Phosphatases/metabolism RNA/metabolism Receptor, Angiotensin, Type 2 Receptors, Angiotensin/metabolism Recombinant Proteins/metabolism Tumor Cells, Cultured Vanadates/pharmacology
Chemicals
Blood Proteins Cell Cycle Proteins Immediate-Early Proteins Intracellular Signaling Peptides and Proteins Receptor, Angiotensin, Type 2 Receptors, Angiotensin Recombinant Proteins Angiotensin II Dactinomycin Okadaic Acid Vanadates Epidermal Growth Factor RNA Calcium-Calmodulin-Dependent Protein Kinases Mitogen-Activated Protein Kinase 1 Mitogen-Activated Protein Kinase 3 Mitogen-Activated Protein Kinases Phosphoprotein Phosphatases Protein Phosphatase 1 DUSP1 protein, human Dual Specificity Phosphatase 1 PTPN11 protein, human PTPN6 protein, human Protein Tyrosine Phosphatase, Non-Receptor Type 11 Protein Tyrosine Phosphatase, Non-Receptor Type 6 Protein Tyrosine Phosphatases
Authors & Affiliations
7 authors, click to expand affiliations / ORCID
Bedecs K
Institut Cochin de Génétique Moléculaire, CNRS UPR 0415, 22, rue Méchain, 75014 Paris, France.
Elbaz N
Sutren M
Masson M
Susini C
Strosberg A D
Nahmias C
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Article Info
Journal
The Biochemical journal
Abbr.
Biochem J
ISSN
0264-6021
DOI
10.1042/bj3250449
Published
1997-07-15
Pages
449-54
Language
English
Region
England
NLM ID
2984726R
PMCID
PMC1218581
Subset
IM
External Links
PubMed source DOI: 10.1042/bj3250449 PMC Full Text View journal details
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