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Ca2+/Calmodulin-Dependent Protein Kinase II in Vascular Smooth Muscle.

F Z Saddouk1, R Ginnan1, H A Singer1

  • 1Department of Molecular and Cellular Physiology, Albany Medical College, Albany, NY, United States.

Advances in Pharmacology (San Diego, Calif.)
|February 19, 2017
PubMed
Summary

Calcium/calmodulin-dependent protein kinase II (CaMKII) isoforms, gamma and delta, play opposing roles in vascular smooth muscle (VSM) cell function. CaMKII delta drives synthetic VSM proliferation in vascular disease, while CaMKII gamma supports differentiated VSM function.

Keywords:
CaM kinase IICaMKIICamk2dCamk2gExcitation–contraction couplingGene transcriptionIsoformsMigrationProliferationRestenosisVascular remodelingVascular smooth muscle

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Area of Science:

  • Vascular Biology
  • Molecular Cell Biology
  • Biochemistry

Background:

  • Calcium (Ca2+)-dependent signaling pathways are crucial for vascular smooth muscle (VSM) cell function, regulating both differentiated contractile activity and synthetic phenotype processes like gene transcription, proliferation, and migration.
  • Synthetic VSM growth and hyperplasia are key features of major vascular diseases, including hypertension, atherosclerosis, and restenosis.
  • Ca2+/calmodulin-dependent protein kinase II (CaMKII) is a central mediator of intracellular Ca2+ signals, known for its complexity, autoregulation, and potential to integrate Ca2+ with reactive oxygen/nitrogen species signaling.

Purpose of the Study:

  • To elucidate the distinct roles of CaMKII isoforms in regulating vascular smooth muscle cell phenotypes and their contribution to vascular remodeling.
  • To understand how CaMKII isoform expression and function differ between differentiated and synthetic VSM cells.
  • To investigate the functional consequences of CaMKII isoform switching in the context of vascular injury and disease.

Main Methods:

  • Analysis of CaMKII isoform expression in differentiated versus synthetic VSM cells.
  • Utilizing genetically engineered mouse models with smooth muscle-specific deletion of CaMKII isoforms.
  • Employing transgenic models expressing endogenous CaMKII inhibitors (CAMK2N) to assess CaMKII function in vivo.
  • In vitro studies examining the effects of CaMKII on VSM cell cycle regulation, proliferation, and migration.

Main Results:

  • Differentiated VSM primarily expresses CaMKII gamma, linked to contractile activity and Ca2+ homeostasis.
  • Synthetic VSM cells predominantly express CaMKII delta, which is associated with VSM gene transcription, proliferation, and migration.
  • CaMKII delta and gamma isoforms exhibit opposing functions in regulating VSM cell cycle, proliferation, and hyperplasia.
  • Isoform switching of CaMKII following vascular injury is identified as a critical event promoting vascular remodeling.

Conclusions:

  • CaMKII isoforms, particularly delta and gamma, play distinct and often opposing roles in regulating VSM cell phenotype and function.
  • CaMKII delta is implicated in promoting the synthetic VSM phenotype and vascular hyperplasia characteristic of vascular diseases.
  • CaMKII gamma is associated with the differentiated VSM phenotype and contractile function.
  • Understanding CaMKII isoform dynamics is crucial for developing therapeutic strategies targeting vascular remodeling and disease.