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Ang II attenuates IGF-1-stimulated Na+, K(+)-ATPase activity via PI3K/Akt pathway in vascular smooth muscle cells.
Int J Mol Med. 2004 Jun; 13(6):915-22.IJ

Abstract

We have investigated the role of phosphatidylinositol 3-kinase (PI3K) and serine/threonine protein kinase B (Akt) in mediating vascular smooth muscle cells (VSMC) sodium pump (Na+, K(+)-ATPase) regulatory interactions between insulin-like growth factor-1 (IGF-1) and angiotensin II (Ang II). Treatment with IGF-1 (100 nM) for 30 min or Ang II (100 nM) for 10 min increased sodium pump activity. Pretreatment with Ang II for 10 min, abolished IGF-1 increased sodium pump activity. Given separately for 6 h, Ang II and IGF-1 stimulated alpha1 mRNA accumulation. Phosphorylation on Ser473 of Akt was increased after treatment with both IGF-1 and Ang II. Pretreatment with 100 nM of PI3K inhibitor Wortmannin (WT) for 30 min decreased: IGF-1 and Ang II-stimulated pump activity, phosphorylation of Akt and PI3K protein expression. Pretreatment with Ang II attenuated IGF-1-stimulated sodium pump activity, phosphorylation of Akt and PI3K protein expression. IGF-1 increased the association between IRS-1 and p85, and Ang II as well as PI3K inhibition decreased this IGF-1 effect. These results suggest that Ang II, which increases pump activity alone, reduces the IGF-1 stimulation of sodium pump activity by attenuating PI3K/Akt signaling. These results implicate PI3K/Akt pathways in Ang II/IGF-1 regulation of the sodium pump in VSMC.

Authors+Show Affiliations

Departments of Cell Biology, Biochemistry and Medicine, SUNY-Health Science Center and VA Medical Center, Brooklyn, NY 11203, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15138635

Citation

Isenovic, Esma R., et al. "Ang II Attenuates IGF-1-stimulated Na+, K(+)-ATPase Activity Via PI3K/Akt Pathway in Vascular Smooth Muscle Cells." International Journal of Molecular Medicine, vol. 13, no. 6, 2004, pp. 915-22.
Isenovic ER, Meng Y, Jamali N, et al. Ang II attenuates IGF-1-stimulated Na+, K(+)-ATPase activity via PI3K/Akt pathway in vascular smooth muscle cells. Int J Mol Med. 2004;13(6):915-22.
Isenovic, E. R., Meng, Y., Jamali, N., Milivojevic, N., & Sowers, J. R. (2004). Ang II attenuates IGF-1-stimulated Na+, K(+)-ATPase activity via PI3K/Akt pathway in vascular smooth muscle cells. International Journal of Molecular Medicine, 13(6), 915-22.
Isenovic ER, et al. Ang II Attenuates IGF-1-stimulated Na+, K(+)-ATPase Activity Via PI3K/Akt Pathway in Vascular Smooth Muscle Cells. Int J Mol Med. 2004;13(6):915-22. PubMed PMID: 15138635.
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TY - JOUR T1 - Ang II attenuates IGF-1-stimulated Na+, K(+)-ATPase activity via PI3K/Akt pathway in vascular smooth muscle cells. AU - Isenovic,Esma R, AU - Meng,Yong, AU - Jamali,Nasir, AU - Milivojevic,Nikola, AU - Sowers,James R, PY - 2004/5/13/pubmed PY - 2004/11/17/medline PY - 2004/5/13/entrez SP - 915 EP - 22 JF - International journal of molecular medicine JO - Int J Mol Med VL - 13 IS - 6 N2 - We have investigated the role of phosphatidylinositol 3-kinase (PI3K) and serine/threonine protein kinase B (Akt) in mediating vascular smooth muscle cells (VSMC) sodium pump (Na+, K(+)-ATPase) regulatory interactions between insulin-like growth factor-1 (IGF-1) and angiotensin II (Ang II). Treatment with IGF-1 (100 nM) for 30 min or Ang II (100 nM) for 10 min increased sodium pump activity. Pretreatment with Ang II for 10 min, abolished IGF-1 increased sodium pump activity. Given separately for 6 h, Ang II and IGF-1 stimulated alpha1 mRNA accumulation. Phosphorylation on Ser473 of Akt was increased after treatment with both IGF-1 and Ang II. Pretreatment with 100 nM of PI3K inhibitor Wortmannin (WT) for 30 min decreased: IGF-1 and Ang II-stimulated pump activity, phosphorylation of Akt and PI3K protein expression. Pretreatment with Ang II attenuated IGF-1-stimulated sodium pump activity, phosphorylation of Akt and PI3K protein expression. IGF-1 increased the association between IRS-1 and p85, and Ang II as well as PI3K inhibition decreased this IGF-1 effect. These results suggest that Ang II, which increases pump activity alone, reduces the IGF-1 stimulation of sodium pump activity by attenuating PI3K/Akt signaling. These results implicate PI3K/Akt pathways in Ang II/IGF-1 regulation of the sodium pump in VSMC. SN - 1107-3756 UR - https://www.unboundmedicine.com/medline/citation/15138635/Ang_II_attenuates_IGF_1_stimulated_Na+_K_+__ATPase_activity_via_PI3K/Akt_pathway_in_vascular_smooth_muscle_cells_ L2 - http://www.spandidos-publications.com/ijmm/13/6/915 DB - PRIME DP - Unbound Medicine ER -