Expression of Plasma Membrane Calcium ATPases in Phenotypically Distinct Canine Vascular Smooth Muscle Cells

Abramowitz, Joel; Aydemir-Koksoy, Aslihan; Helgason, Thorunn; Jemelka, Sandra; Odebunmi, Timothy; Seidel, Charles L.; Allen, Jeffrey C.

doi:10.1006/jmcc.2000.1120

Cited by 14 publications

(15 citation statements)

References 38 publications

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“…Reciprocally, inhibition of PMCA4a upregulation with Wortmannin inhibited cell proliferation [3]. These results may appear incompatible with the general concept whereby decreased PMCA1 and SERCA2a, increased TRPC channels and IP 3 -mediated Ca 2+ release contribute to the sustained increase in cytoplasmic Ca 2+ levels that are necessary to drive cell proliferation.…”

Section: Role Of Pmcamentioning

confidence: 78%

“…In fact, 2-APB, at much lower concentrations (30 µM) is a potent inhibitor of SOC channels and is also known to partially inhibit TRPC channels [137], while U-73122 acts upstream to inhibit PLC, and would thus consequently inhibit the activation of receptor-operated channels, including all TRPC channels. Nonetheless, in serum-stimulated VSMC, proliferation is associated with a sustained increase in intracellular Ca 2+ partially due to enhanced excitability of IP 3 R following binding of IP 3 . In addition, a recent report showed a sixfold increase in the expression level of IP 3 R1 as VSMC progressed from G0 to G1/S of the cell cycle [5].…”

Section: Role Of Ip 3 R Ca 2+ Release Channelsmentioning

confidence: 99%

“…In the vasculature, medial smooth muscle cells appear to express multiple isoforms of both PMCA1 and 4 [3,131] and cell lines from canine carotid artery or saphenous vein medial wall express PMCA1b, 4a and 4b [3]. The role of PMCA1 might be to repress VSMC proliferation as cells in the G1/S phase of the cell cycle experienced lower levels of PMCA1 mediated through repression by the transcription factor c-Myb [61,62].…”

Section: Role Of Pmcamentioning

confidence: 99%

See 2 more Smart Citations

The non-excitable smooth muscle: Calcium signaling and phenotypic switching during vascular disease

House

Potier

Bisaillon

et al. 2008

Pflugers Arch - Eur J Physiol

217

207

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Calcium (Ca 2+ ) is a highly versatile second messenger that controls vascular smooth muscle cell (VSMC) contraction, proliferation, and migration. By means of Ca 2+ permeable channels, Ca 2+ pumps and channels conducting other ions such as potassium and chloride, VSMC keep intracellular Ca 2+ levels under tight control. In healthy quiescent contractile VSMC, two important components of the Ca 2+ signaling pathways that regulate VSMC contraction are the plasma membrane voltageoperated Ca 2+ channel of the high voltage-activated type (L-type) and the sarcoplasmic reticulum Ca 2+ release channel, Ryanodine Receptor (RyR). Injury to the vessel wall is accompanied by VSMC phenotype switch from a contractile quiescent to a proliferative motile phenotype (synthetic phenotype) and by alteration of many components of VSMC Ca 2+ signaling pathways. Specifically, this switch that culminates in a VSMC phenotype reminiscent of a non-excitable cell is characterized by loss of L-type channels expression and increased expression of the low voltage-activated (T-type) Ca 2+ channels and the canonical transient receptor potential (TRPC) channels. The expression levels of intracellular Ca 2+ release channels, pumps and Ca 2+ -activated proteins are also altered: the proliferative VSMC lose the RyR3 and the sarcoplasmic/endoplasmic reticulum Ca 2+ ATPase isoform 2a pump and reciprocally regulate isoforms of the ca 2+ /calmodulin-dependent protein kinase II. This review focuses on the changes in expression of Ca 2+ signaling proteins associated with VSMC proliferation both in vitro and in vivo. The physiological implications of the altered expression of these Ca 2+ signaling molecules, their contribution to VSMC dysfunction during vascular disease and their potential as targets for drug therapy will be discussed.

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Section: Role Of Pmcamentioning

confidence: 78%

Section: Role Of Ip 3 R Ca 2+ Release Channelsmentioning

confidence: 99%

Section: Role Of Pmcamentioning

confidence: 99%

See 1 more Smart Citation

The non-excitable smooth muscle: Calcium signaling and phenotypic switching during vascular disease

House

Potier

Bisaillon

et al. 2008

Pflugers Arch - Eur J Physiol

217

207

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“…Then, the resulting spontaneous transient outward currents (STOC) hyperpolarize the membrane and decrease the open probability of Ltype Ca 2+ channels [23]. Cytosolic calcium is extruded at the level of plasma membrane by plasma membrane Ca 2+ ATPase (PMCA) and the Na + /Ca 2+ exchanger (NCX) [24,25]. The principal amount of cytosolic Ca 2+ (> 70%) is re-uploaded to the internal store.…”

Section: Calcium Handling By the Plasma Membrane's Calcium Channels Amentioning

confidence: 99%

Calcium Cycling in Synthetic and Contractile Phasic or Tonic Vascular Smooth Muscle Cells

Lipskaia¹,

Limon²,

Bobe³

et al. 2012

Current Basic and Pathological Approaches to the Function of Muscle Cells and Tissues - From Molecules to Humans

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“…Due to their widespread distribution, they are thought to be important "housekeeping" Ca 2+ -pumps, but their function in smooth muscle is less well known. In addition to Ca 2+ homeostasis, it has been suggested that PMCA is associated with vascular smooth muscle proliferation (Abramowitz et al, 2000) and signal transduction (Hammes et al, 1998). The latter is based on the PDZ domains in PMCA4b which lead to a complex with nitric oxide synthase I in caveolae of vascular smooth muscle (Schuh et al, 2001).…”

Section: Plasma Membrane Ca 2+ Pumpsmentioning

confidence: 99%

Ca2+ clearance in smooth muscle: lessons from gene-altered mice

Ishida

Rutgeerts

2005

J. Smooth Muscle Res.

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Expression of Plasma Membrane Calcium ATPases in Phenotypically Distinct Canine Vascular Smooth Muscle Cells

Cited by 14 publications

References 38 publications

The non-excitable smooth muscle: Calcium signaling and phenotypic switching during vascular disease

The non-excitable smooth muscle: Calcium signaling and phenotypic switching during vascular disease

Calcium Cycling in Synthetic and Contractile Phasic or Tonic Vascular Smooth Muscle Cells

Ca2+ clearance in smooth muscle: lessons from gene-altered mice

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