Nuclear factor of activated T cells c1 mediates p21-activated kinase 1 activation in the modulation of chemokine-induced human aortic smooth muscle cell F-actin stress fiber formation, migration, and proliferation and injury-induced vascular wall remodeling

Venkatesh Kundumani-Sridharan, Nikhlesh Singh, Sanjay Kumar, Ravisekhar Gadepalli, Rao Gadiparthi

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20 Citations (Scopus)

Abstract

Background: We explore the mechanisms by which NFATc1 mediates vascular wall remodeling. Results: MCP1 activates Pak1 in a Rac1-NFATc1-cyclin D1-CDK6-CDK4-dependent manner in the mediation of HASMC migration and proliferation. Conclusion: Downstream of Rac1, NFATc1, via the cyclin D1-CDK6-CDK4 signaling axis, mediates Pak1 activation in the modulation of vascular wall remodeling. Significance: Interference with NFATc1 activation could represent a novel therapeutic approach for the treatment of restenosis.

Original languageEnglish (US)
Pages (from-to)22150-22162
Number of pages13
JournalJournal of Biological Chemistry
Volume288
Issue number30
DOIs
StatePublished - Jul 26 2013

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p21-Activated Kinases
NFATC Transcription Factors
Stress Fibers
Cyclin D1
Chemokines
Smooth Muscle Myocytes
Muscle
Actins
Chemical activation
Cells
Modulation
Fibers
Wounds and Injuries
Vascular Remodeling
Therapeutics

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

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abstract = "Background: We explore the mechanisms by which NFATc1 mediates vascular wall remodeling. Results: MCP1 activates Pak1 in a Rac1-NFATc1-cyclin D1-CDK6-CDK4-dependent manner in the mediation of HASMC migration and proliferation. Conclusion: Downstream of Rac1, NFATc1, via the cyclin D1-CDK6-CDK4 signaling axis, mediates Pak1 activation in the modulation of vascular wall remodeling. Significance: Interference with NFATc1 activation could represent a novel therapeutic approach for the treatment of restenosis.",
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T1 - Nuclear factor of activated T cells c1 mediates p21-activated kinase 1 activation in the modulation of chemokine-induced human aortic smooth muscle cell F-actin stress fiber formation, migration, and proliferation and injury-induced vascular wall remodeling

AU - Kundumani-Sridharan, Venkatesh

AU - Singh, Nikhlesh

AU - Kumar, Sanjay

AU - Gadepalli, Ravisekhar

AU - Gadiparthi, Rao

PY - 2013/7/26

Y1 - 2013/7/26

N2 - Background: We explore the mechanisms by which NFATc1 mediates vascular wall remodeling. Results: MCP1 activates Pak1 in a Rac1-NFATc1-cyclin D1-CDK6-CDK4-dependent manner in the mediation of HASMC migration and proliferation. Conclusion: Downstream of Rac1, NFATc1, via the cyclin D1-CDK6-CDK4 signaling axis, mediates Pak1 activation in the modulation of vascular wall remodeling. Significance: Interference with NFATc1 activation could represent a novel therapeutic approach for the treatment of restenosis.

AB - Background: We explore the mechanisms by which NFATc1 mediates vascular wall remodeling. Results: MCP1 activates Pak1 in a Rac1-NFATc1-cyclin D1-CDK6-CDK4-dependent manner in the mediation of HASMC migration and proliferation. Conclusion: Downstream of Rac1, NFATc1, via the cyclin D1-CDK6-CDK4 signaling axis, mediates Pak1 activation in the modulation of vascular wall remodeling. Significance: Interference with NFATc1 activation could represent a novel therapeutic approach for the treatment of restenosis.

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