c-Myb–Dependent Inositol 1,4,5-Trisphosphate Receptor Type-1 Expression in Vascular Smooth Muscle Cells

Afroze, Talat; Sadi, Al Muktafi; Momen, M. Abdul; Gu, Steven; Heximer, Scott P.; Husain, Mansoor

doi:10.1161/atvbaha.107.142059

Cited by 16 publications

(35 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…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]. This increase was mediated by the cell cycle-associated transcription factor c-Myb and was accompanied by increased intracellular Ca 2+ at the G1/S transition [5].…”

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

confidence: 94%

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

218

207

View full text Add to dashboard Cite

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.

show abstract

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

confidence: 94%

“…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]. This increase was mediated by the cell cycle-associated transcription factor c-Myb and was accompanied by increased intracellular Ca 2+ at the G1/S transition [5].…”

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

confidence: 94%

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

House

Potier

Bisaillon

et al. 2008

Pflugers Arch - Eur J Physiol

218

207

View full text Add to dashboard Cite

show abstract

“…IP 3 binds to and activates SR-localized IP 3 receptors (IP 3 Rs) (21, 57). SMC IP 3 Rs were first purified from aorta and, following reconstitution into phospholipid vesicles, were identified as Ca 2ϩ release channels (34, 52, 134). IP 3 Rs regulate many cellular processes in SMCs, including contractility, gene expression, migration, and proliferation (2,60,149,156,234,237).…”

mentioning

confidence: 99%

Inositol trisphosphate receptors in smooth muscle cells

Narayanan

Adebiyi

Jaggar

2012

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Inositol 1,4,5-trisphosphate receptors (IP3Rs) are a family of tetrameric intracellular calcium (Ca2+) release channels that are located on the sarcoplasmic reticulum (SR) membrane of virtually all mammalian cell types, including smooth muscle cells (SMC). Here, we have reviewed literature investigating IP3R expression, cellular localization, tissue distribution, activity regulation, communication with ion channels and organelles, generation of Ca2+ signals, modulation of physiological functions, and alterations in pathologies in SMCs. Three IP3R isoforms have been identified, with relative expression and cellular localization of each contributing to signaling differences in diverse SMC types. Several endogenous ligands, kinases, proteins, and other modulators control SMC IP3R channel activity. SMC IP3Rs communicate with nearby ryanodine-sensitive Ca2+ channels and mitochondria to influence SR Ca2+ release and reactive oxygen species generation. IP3R-mediated Ca2+ release can stimulate plasma membrane-localized channels, including transient receptor potential (TRP) channels and store-operated Ca2+ channels. SMC IP3Rs also signal to other proteins via SR Ca2+ release-independent mechanisms through physical coupling to TRP channels and local communication with large-conductance Ca2+-activated potassium channels. IP3R-mediated Ca2+ release generates a wide variety of intracellular Ca2+ signals, which vary with respect to frequency, amplitude, spatial, and temporal properties. IP3R signaling controls multiple SMC functions, including contraction, gene expression, migration, and proliferation. IP3R expression and cellular signaling are altered in several SMC diseases, notably asthma, atherosclerosis, diabetes, and hypertension. In summary, IP3R-mediated pathways control diverse SMC physiological functions, with pathological alterations in IP3R signaling contributing to disease.

show abstract

“…It has been established that c-myb regulates the proliferation of VSMCs and the differentiation of VSMCs from ESCderived progenitors in vitro [18][19][20]29,30 ; however, it remained unknown if c-myb has a similar role in adult vessel-resident VSMC progenitor cells in vivo. Here, we show that a mouse harboring a point-mutated c-myb has defects in vessel remodeling in response to wire denudation injury and that this is a vessel-intrinsic defect associated with defective proliferation of Sca1 + adventitial VSMC progenitor cells.…”

Section: Discussionmentioning

confidence: 99%

c-Myb Regulates Proliferation and Differentiation of Adventitial Sca1 ⁺ Vascular Smooth Muscle Cell Progenitors by Transactivation of Myocardin

Shikatani

Chandy

Besla

et al. 2016

ATVB

Self Cite

View full text Add to dashboard Cite

c-Myb–Dependent Inositol 1,4,5-Trisphosphate Receptor Type-1 Expression in Vascular Smooth Muscle Cells

Cited by 16 publications

References 50 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

Inositol trisphosphate receptors in smooth muscle cells

c-Myb Regulates Proliferation and Differentiation of Adventitial Sca1 ⁺ Vascular Smooth Muscle Cell Progenitors by Transactivation of Myocardin

Contact Info

Product

Resources

About

c-Myb–Dependent Inositol 1,4,5-Trisphosphate Receptor Type-1 Expression in Vascular Smooth Muscle Cells

Cited by 16 publications

References 50 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

Inositol trisphosphate receptors in smooth muscle cells

c-Myb Regulates Proliferation and Differentiation of Adventitial Sca1 + Vascular Smooth Muscle Cell Progenitors by Transactivation of Myocardin

Contact Info

Product

Resources

About

c-Myb Regulates Proliferation and Differentiation of Adventitial Sca1 ⁺ Vascular Smooth Muscle Cell Progenitors by Transactivation of Myocardin