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Author Notes:

Address correspondence to: Kathy K. Griendling, Emory University, Division of Cardiology, 319 WMB, 1639 Pierce Dr. Atlanta, GA 30322, Telephone: 404-727-3364, Fax: 404-727-3585 kgriend@emory.edu

Acknowledgments We thank Emir Veledar for his assistance with statistical analysis of Figure 1. Confocal microscopy data for this study were acquired in the Microscopy in Medicine Core (MiM Core) at Emory University.

Live cell imaging data were acquired in the UNC Olympus Imaging Research Center. We would like to thank Giji Joseph for her assistance with immunohistochemistry.


Research Funding:

This work was supported by NIH grants HL38206, HL092120 and HL058863 to KKG, F31-HL941023 to HCW, HL093115 to ASM, GM083035 to JEB and P01 HL095070 to MiM Core.


  • vascular smooth muscle
  • coronin 1B
  • migration
  • platelet-derived growth factor

Role of Coronin 1B in PDGF-induced Migration of Vascular Smooth Muscle Cells

Journal Title:

Circulation Research


Volume 111, Number 1


, Pages 56-65

Type of Work:

Article | Post-print: After Peer Review


Rationale The type I subclass of Coronins, a family of actin binding proteins, regulates various actin dependent cellular processes including migration. However, the existence and role of coronins in vascular smooth muscle cell (VSMC) migration has yet to be determined. Objective The goal of the present study was to define the mechanism by which coronins regulate platelet-derived growth factor (PDGF)-induced VSMC migration. Methods and Results Coronin 1B (Coro1B) and 1C (Coro1C) were both found to be expressed in VSMCs at the mRNA and protein levels. Down regulation of Coro1B by siRNA increases PDGF-induced migration, while down regulation of Coro1C has no effect. We confirmed through kymograph analysis that the Coro1B-downregulation-mediated increase in migration is directly linked to increased lamellipodial protraction rate and protrusion distance in VSMC. In other cell types, coronins exert their effects on lamellipodia dynamics by an inhibitory interaction with the ARP2/3 complex, which is disrupted by the phosphorylation of Coro1B. We found that PDGF induces phosphorylation of Coro1B on serine-2 via PKCε, leading to a decrease in the interaction of Coro1B with the ARP2/3 complex. VSMCs transfected with a phospho-deficient S2A Coro1B mutant showed decreased migration in response to PDGF, suggesting that the phosphorylation of Coro1B is required for the promotion of migration by PDGF. In both the rat and mouse Coro1B phosphorylation was increased in response to vessel injury in vivo. Conclusions Our data support that phosphorylation of Coro1B and the subsequent reduced interaction with ARP2/3 complex participate in PDGF-induced VSMC migration, an important step in vascular lesion formation.

Copyright information:

© 2012 American Heart Association, Inc.

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