Hydrogen peroxide down-regulates inositol 1,4,5-trisphosphate receptor content through proteasome activation

Martín-Garrido, Abel; Boyano-Adánez, M.C.; Alique, Matilde; Calleros, Laura; Serrano, Isabel; Griera, Mercedes; Rodríguez‐Puyol, Diego; Griendling, Kathy K.; Rodrı́guez-Puyol, Manuel

doi:10.1016/j.freeradbiomed.2009.07.006

Cited by 15 publications

(15 citation statements)

References 52 publications

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“…IP 3 binds to receptors in the SR to release Ca 2+ into the cytosol. Of note, the IP 3 R is targeted to proteasome degradation by H 2 O 2 [332], resulting in a decrease in Ca 2+ efflux from the SR. DAG, along with Ca 2+ , activates the redox-sensitive PKC to promote downstream contractile signaling [95] (Figure 3). How oxidants interact with PKC during contraction is unknown.…”

Section: Redox Regulation Of the Actin Cytoskeleton In Cell Physiologymentioning

confidence: 99%

Redox regulation of the actin cytoskeleton and its role in the vascular system

Huff

Fujii

et al. 2017

Free Radical Biology and Medicine

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The actin cytoskeleton is critical for form and function of vascular cells, serving mechanical, organizational and signaling roles. Because many cytoskeletal proteins are sensitive to reactive oxygen species, redox regulation has emerged as a pivotal modulator of the actin cytoskeleton and its associated proteins. Here, we summarize work implicating oxidants in altering actin cytoskeletal proteins and focus on how these alterations affect cell migration, proliferation and contraction of vascular cells. Finally, we discuss the role of oxidative modification of the actin cytoskeleton in vivo and highlight its importance for vascular diseases.

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Section: Redox Regulation Of the Actin Cytoskeleton In Cell Physiologymentioning

confidence: 99%

Redox regulation of the actin cytoskeleton and its role in the vascular system

Huff

Fujii

et al. 2017

Free Radical Biology and Medicine

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“…Evidence for redox modulation of the IP3R comes only from noncardiac tissue or in a heterologous system. For example, IP3Rs are downregulated when vascular smooth muscle cells are stimulated by H 2 O 2 (177). This decrease in IP3R by H 2 O 2 is accompanied by a reduction in calcium efflux induced by IP3 (177).…”

Section: A Ip3r Receptorsmentioning

confidence: 99%

Redox Control of Cardiac Excitability

Aggarwal

Makielski

2013

Antioxidants & Redox Signaling

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Reactive oxygen species (ROS) have been associated with various human diseases, and considerable attention has been paid to investigate their physiological effects. Various ROS are synthesized in the mitochondria and accumulate in the cytoplasm if the cellular antioxidant defense mechanism fails. The critical balance of this ROS synthesis and antioxidant defense systems is termed the redox system of the cell. Various cardiovascular diseases have also been affected by redox to different degrees. ROS have been indicated as both detrimental and protective, via different cellular pathways, for cardiac myocyte functions, electrophysiology, and pharmacology. Mostly, the ROS functions depend on the type and amount of ROS synthesized. While the literature clearly indicates ROS effects on cardiac contractility, their effects on cardiac excitability are relatively under appreciated. Cardiac excitability depends on the functions of various cardiac sarcolemal or mitochondrial ion channels carrying various depolarizing or repolarizing currents that also maintain cellular ionic homeostasis. ROS alter the functions of these ion channels to various degrees to determine excitability by affecting the cellular resting potential and the morphology of the cardiac action potential. Thus, redox balance regulates cardiac excitability, and under pathological regulation, may alter action potential propagation to cause arrhythmia. Understanding how redox affects cellular excitability may lead to potential prophylaxis or treatment for various arrhythmias. This review will focus on the studies of redox and cardiac excitation. Antioxid. Redox Signal. 18, 432-468.

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“…Cellular levels of IP 3 Rs in SMCs are determined by an equilibrium between gene transcription and protein degradation (3,129,171,227). c-Myb, a transcription factor, binds to the IP 3 R1 promoter and stimulates transcription in cultured aortic SMCs (3).…”

Section: Cellular Expression and Localization Of Smc Ip 3 Rsmentioning

confidence: 99%

“…In A7r5 cells, retinoic acid inhibited IP 3 R1 gene transcription through a mechanism mediated by activator protein-2, another transcription factor (45). In cultured aortic SMCs, hydrogen peroxide (H 2 O 2 ) stimulated proteasomal degradation of IP 3 R1 and IP 3 R3, whereas Jak2, a tyrosine kinase, phosphorylated IP 3 R1 and prevented proteasomal degradation (129,227). Transforming growth factor-␤ (TGF-␤) reduced IP 3 R1 and IP 3 R3 protein in renal arteriolar SMCs, although it was not determined if this was due to protein degradation (138).…”

Section: Cellular Expression and Localization Of Smc Ip 3 Rsmentioning

confidence: 99%

Inositol trisphosphate receptors in smooth muscle cells

Narayanan

Adebiyi

Jaggar

2012

American Journal of Physiology-Heart and Circulatory Physiology

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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.

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Hydrogen peroxide down-regulates inositol 1,4,5-trisphosphate receptor content through proteasome activation

Cited by 15 publications

References 52 publications

Redox regulation of the actin cytoskeleton and its role in the vascular system

Redox regulation of the actin cytoskeleton and its role in the vascular system

Redox Control of Cardiac Excitability

Inositol trisphosphate receptors in smooth muscle cells

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