ENaC proteins contribute to VSMC migration

Grifoni, S.; Gannon, Kimberly Anita; Stec, David E.; Drummond, Heather A.

doi:10.1152/ajpheart.00333.2006

Cited by 57 publications

(66 citation statements)

References 60 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous studies have shown that VSMC migration, from the media into the intima, plays a significant role following arterial injury, and blocking VSMC migration can reduce the neointimal lesion size (Rutherford et al, 1997;Slepian et al, 1998). A role for DEG/ ENaC/ASIC proteins in cellular migration has been suggested in recent reports (Chifflet et al, 2005;Grifoni et al, 2006;Vila-Carriles et al, 2006). Our previous study showed that DEG/ ENaC/ASIC pharmacological inhibition with amiloride and its analog benzamil inhibit VSMC migration.…”

Section: Discussionmentioning

confidence: 93%

“…We have used this approach previously to silence ENaC/ASIC expression Grifoni et al, 2006;Jernigan and Drummond, 2006). For migration assays, VSMCs were plated and allowed to grow to 90% confluence before transfection with siRNA molecules.…”

Section: Sirnamentioning

confidence: 99%

“…To determine extent of siRNA suppression ASIC expression, we used quantitative immunostaining, an approach that we have used previously Grifoni et al, 2006;Jernigan and Drummond, 2006). For immunostaining experiments, cells were plated on fibronectin coated glass slides, treated with siRNA molecules for 4 hours, grown 72 hours, and then prepared for ASIC immunolabeling as described before.…”

Section: Sirnamentioning

confidence: 99%

“…Recently, others and we have shown members of the Degenerin/Epithelial Sodium (Na + ) Channel/Acid Sensing-Ion Channel (DEG/ENaC/ASIC) protein family, contribute to cellular migration in glial, epithelial and VSM cells (Chifflet et al, 2005;Grifoni et al, 2006;VilaCarriles et al, 2006). Members of this family share a similar structure, two membrane spanning domains separated by a large extracellular domain and intracellular N-and C-termini.…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

ASIC proteins regulate smooth muscle cell migration

Grifoni

Jernigan

Hamilton

et al. 2008

Microvascular Research

Self Cite

View full text Add to dashboard Cite

The purpose of the present study was to investigate Acid Sensing Ion Channel (ASIC) protein expression and importance in cellular migration. We recently demonstrated Epithelial Na + Channel (ENaC) proteins are required for vascular smooth muscle cell (VSMC) migration, however the role of the closely related ASIC proteins has not been addressed. We used RT-PCR and immunolabeling to determine expression of ASIC1, ASIC2, ASIC3 and ASIC4 in A10 cells. We used small interference RNA to silence individual ASIC expression and determine the importance of ASIC proteins in wound healing and chemotaxis (PDGF-bb) initiated migration. We found ASIC1, ASIC2, and ASIC3, but not ASIC4, expression in A10 cells. ASIC1, ASIC2, and ASIC3 siRNA molecules significantly suppressed expression of their respective proteins compared to non-targeting siRNA (RISC) transfected controls by 63%, 44%, and 55%, respectively. Wound healing was inhibited by 10, 20 and 26% compared to RISC controls following suppression of ASIC1, ASIC2, and ASIC3, respectively. Chemotactic migration was inhibited by 30% and 45%, respectively following suppression of ASIC1 and ASIC3. ASIC2 suppression produced a small, but significant, increase in chemotactic migration (4%). Our data indicate ASIC expression is required for normal migration and may suggest a novel role for ASIC proteins in cellular migration.

show abstract

Section: Discussionmentioning

confidence: 93%

Section: Sirnamentioning

confidence: 99%

Section: Sirnamentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

ASIC proteins regulate smooth muscle cell migration

Grifoni

Jernigan

Hamilton

et al. 2008

Microvascular Research

Self Cite

View full text Add to dashboard Cite

show abstract

“…It has previously been suggested that in addition ENaC plays an important role in wound healing (33,34) and proliferation (35). Both ASIC and ENaC channels contribute to migration of vascular smooth muscle cells (36,37), although in neither case are the underlying mechanisms well understood.…”

Section: Discussionmentioning

confidence: 99%

Glioma-specific Cation Conductance Regulates Migration and Cell Cycle Progression

Rooj

McNicholas

Bartoszewski

et al. 2012

Journal of Biological Chemistry

View full text Add to dashboard Cite

Background: Cation transport contributes to migration and proliferation of tumor cells. Results: Sodium current block decreased ERK phosphorylation and increased expression of cell cycle inhibitors. Conclusion: Activity of an ENaC/ASIC cation channel is required to maintain the glioma cell phenotype. Significance: Activity of a membrane cation channel influences signaling pathways to effect changes in migration and proliferation of glioma cells.

show abstract

Roles of Ion Transport in Control of Cell Motility

Stock

Ludwig

Hanley

et al. 2013

Comprehensive Physiology

View full text Add to dashboard Cite

Cell motility is an essential feature of life. It is essential for reproduction, propagation, embryonic development, and healing processes such as wound closure and a successful immune defense. If out of control, cell motility can become life-threatening as, for example, in metastasis or autoimmune diseases. Regardless of whether ciliary/flagellar or amoeboid movement, controlled motility always requires a concerted action of ion channels and transporters, cytoskeletal elements, and signaling cascades. Ion transport across the plasma membrane contributes to cell motility by affecting the membrane potential and voltage-sensitive ion channels, by inducing local volume changes with the help of aquaporins and by modulating cytosolic Ca(2+) and H(+) concentrations. Voltage-sensitive ion channels serve as voltage detectors in electric fields thus enabling galvanotaxis; local swelling facilitates the outgrowth of protrusions at the leading edge while local shrinkage accompanies the retraction of the cell rear; the cytosolic Ca(2+) concentration exerts its main effect on cytoskeletal dynamics via motor proteins such as myosin or dynein; and both, the intracellular and the extracellular H(+) concentration modulate cell migration and adhesion by tuning the activity of enzymes and signaling molecules in the cytosol as well as the activation state of adhesion molecules at the cell surface. In addition to the actual process of ion transport, both, channels and transporters contribute to cell migration by being part of focal adhesion complexes and/or physically interacting with components of the cytoskeleton. The present article provides an overview of how the numerous ion-transport mechanisms contribute to the various modes of cell motility.

show abstract

ENaC proteins contribute to VSMC migration

Cited by 57 publications

References 60 publications

ASIC proteins regulate smooth muscle cell migration

ASIC proteins regulate smooth muscle cell migration

Glioma-specific Cation Conductance Regulates Migration and Cell Cycle Progression

Roles of Ion Transport in Control of Cell Motility

Contact Info

Product

Resources

About