Angiotensin II-induced insulin resistance and protein tyrosine phosphatases

Mario B. Marrero, David J Fulton, David W Stepp, David M. Stern

Research output: Contribution to journalShort survey

29 Citations (Scopus)

Abstract

Although the importance of protein tyrosine phosphorylation by tyrosine kinases in mitogenic signaling is well-accepted, recent studies also suggest that tyrosine dephosphorylation by protein tyrosine phosphatases (PTPases) play an equally important role. For example, both angiotensin II (Ang II) and insulin are known to mediate protein tyrosine phosphorylation and dephosphorylation events. These apparently paradoxical effects of Ang II and insulin suggest that both convergent and divergent intracellular signaling cascades are stimulated downstream of their respective receptors, producing diverse cellular responses. In this review, we discuss the hypothesis that the protein tyrosine phosphatase (PTPase), PTP-1B, plays a central role in Ang II-induced insulin resistance by inhibiting activation of the insulin receptor. We hypothesize that Ang II-induced PTP-1B activation leads to dephosphorylation of the insulin receptor and that this signaling pathway underlies the maladaptive responses observed in diabetic vascular and renal tissue during type II diabetes.

Original languageEnglish (US)
Pages (from-to)2009-2013
Number of pages5
JournalArteriosclerosis, Thrombosis, and Vascular Biology
Volume24
Issue number11
DOIs
StatePublished - Nov 1 2004

Fingerprint

Protein Tyrosine Phosphatases
Angiotensin II
Insulin Resistance
Tyrosine
Insulin Receptor
Non-Receptor Type 1 Protein Tyrosine Phosphatase
Phosphorylation
Insulin
Protein-Tyrosine Kinases
Type 2 Diabetes Mellitus
Blood Vessels
Proteins
Kidney

Keywords

  • Angiotensin II
  • Insulin resistance
  • PTB-1B

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Angiotensin II-induced insulin resistance and protein tyrosine phosphatases. / Marrero, Mario B.; Fulton, David J; Stepp, David W; Stern, David M.

In: Arteriosclerosis, Thrombosis, and Vascular Biology, Vol. 24, No. 11, 01.11.2004, p. 2009-2013.

Research output: Contribution to journalShort survey

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