Interplay between calcium and reactive Oxygen/Nitrogen species: An essential paradigm for vascular smooth muscle signaling

Mohamed Trebak, Roman Ginnan, Harold A. Singer, David Jourd'Heuil

Research output: Contribution to journalReview article

73 Citations (Scopus)

Abstract

Signaling cascades initiated or regulated by calcium (Ca2+), reactive oxygen (ROS), and nitrogen (RNS) species are essential to diverse physiological and pathological processes in vascular smooth muscle. Stimuli-induced changes in intracellular Ca2+ regulate the activity of primary ROS and RNS, producing enzymes including NADPH oxidases (Nox) and nitric oxide synthases (NOS). At the same time, alteration in intracellular ROS and RNS production reciprocates through redox-based post-translational modifications altering Ca2+ signaling networks. These may include Ca2+ pumps such as sarcoplasmic endoplasmic reticulum Ca 2+-ATPase (SERCA), voltage-gated channels, transient receptor potential canonical (TRPC), melastatin2 (TRPM2), and ankyrin1 (TRPA1) channels, store operated Ca2+ channels such as Orai1/stromal interaction molecule 1 (STIM1), and Ca2+ effectors such as Ca2+/ calmodulin-dependent protein kinase II (CaMKII). In this review, we summarize and highlight current experimental evidence supporting the idea that cross-talk between Ca2+ and ROS/RNS may represent a well-integrated signaling network in vascular smooth muscle. Antioxid.

Original languageEnglish (US)
Pages (from-to)657-674
Number of pages18
JournalAntioxidants and Redox Signaling
Volume12
Issue number5
DOIs
StatePublished - Mar 1 2010

Fingerprint

Reactive Nitrogen Species
Vascular Smooth Muscle
Muscle
Reactive Oxygen Species
Nitrogen
Sarcoplasmic Reticulum Calcium-Transporting ATPases
Physiological Phenomena
Oxygen
Calcium
Transient Receptor Potential Channels
Calcium-Calmodulin-Dependent Protein Kinase Type 2
NADPH Oxidase
Pathologic Processes
Post Translational Protein Processing
Nitric Oxide Synthase
Endoplasmic Reticulum
Oxidation-Reduction
Adenosine Triphosphatases
Enzymes
Pumps

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Physiology
  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology

Cite this

@article{72f87d59fb86493a8792fe696f595711,
title = "Interplay between calcium and reactive Oxygen/Nitrogen species: An essential paradigm for vascular smooth muscle signaling",
abstract = "Signaling cascades initiated or regulated by calcium (Ca2+), reactive oxygen (ROS), and nitrogen (RNS) species are essential to diverse physiological and pathological processes in vascular smooth muscle. Stimuli-induced changes in intracellular Ca2+ regulate the activity of primary ROS and RNS, producing enzymes including NADPH oxidases (Nox) and nitric oxide synthases (NOS). At the same time, alteration in intracellular ROS and RNS production reciprocates through redox-based post-translational modifications altering Ca2+ signaling networks. These may include Ca2+ pumps such as sarcoplasmic endoplasmic reticulum Ca 2+-ATPase (SERCA), voltage-gated channels, transient receptor potential canonical (TRPC), melastatin2 (TRPM2), and ankyrin1 (TRPA1) channels, store operated Ca2+ channels such as Orai1/stromal interaction molecule 1 (STIM1), and Ca2+ effectors such as Ca2+/ calmodulin-dependent protein kinase II (CaMKII). In this review, we summarize and highlight current experimental evidence supporting the idea that cross-talk between Ca2+ and ROS/RNS may represent a well-integrated signaling network in vascular smooth muscle. Antioxid.",
author = "Mohamed Trebak and Roman Ginnan and Singer, {Harold A.} and David Jourd'Heuil",
year = "2010",
month = "3",
day = "1",
doi = "10.1089/ars.2009.2842",
language = "English (US)",
volume = "12",
pages = "657--674",
journal = "Antioxidants and Redox Signaling",
issn = "1523-0864",
publisher = "Mary Ann Liebert Inc.",
number = "5",

}

Interplay between calcium and reactive Oxygen/Nitrogen species : An essential paradigm for vascular smooth muscle signaling. / Trebak, Mohamed; Ginnan, Roman; Singer, Harold A.; Jourd'Heuil, David.

In: Antioxidants and Redox Signaling, Vol. 12, No. 5, 01.03.2010, p. 657-674.

Research output: Contribution to journalReview article

TY - JOUR

T1 - Interplay between calcium and reactive Oxygen/Nitrogen species

T2 - An essential paradigm for vascular smooth muscle signaling

AU - Trebak, Mohamed

AU - Ginnan, Roman

AU - Singer, Harold A.

AU - Jourd'Heuil, David

PY - 2010/3/1

Y1 - 2010/3/1

N2 - Signaling cascades initiated or regulated by calcium (Ca2+), reactive oxygen (ROS), and nitrogen (RNS) species are essential to diverse physiological and pathological processes in vascular smooth muscle. Stimuli-induced changes in intracellular Ca2+ regulate the activity of primary ROS and RNS, producing enzymes including NADPH oxidases (Nox) and nitric oxide synthases (NOS). At the same time, alteration in intracellular ROS and RNS production reciprocates through redox-based post-translational modifications altering Ca2+ signaling networks. These may include Ca2+ pumps such as sarcoplasmic endoplasmic reticulum Ca 2+-ATPase (SERCA), voltage-gated channels, transient receptor potential canonical (TRPC), melastatin2 (TRPM2), and ankyrin1 (TRPA1) channels, store operated Ca2+ channels such as Orai1/stromal interaction molecule 1 (STIM1), and Ca2+ effectors such as Ca2+/ calmodulin-dependent protein kinase II (CaMKII). In this review, we summarize and highlight current experimental evidence supporting the idea that cross-talk between Ca2+ and ROS/RNS may represent a well-integrated signaling network in vascular smooth muscle. Antioxid.

AB - Signaling cascades initiated or regulated by calcium (Ca2+), reactive oxygen (ROS), and nitrogen (RNS) species are essential to diverse physiological and pathological processes in vascular smooth muscle. Stimuli-induced changes in intracellular Ca2+ regulate the activity of primary ROS and RNS, producing enzymes including NADPH oxidases (Nox) and nitric oxide synthases (NOS). At the same time, alteration in intracellular ROS and RNS production reciprocates through redox-based post-translational modifications altering Ca2+ signaling networks. These may include Ca2+ pumps such as sarcoplasmic endoplasmic reticulum Ca 2+-ATPase (SERCA), voltage-gated channels, transient receptor potential canonical (TRPC), melastatin2 (TRPM2), and ankyrin1 (TRPA1) channels, store operated Ca2+ channels such as Orai1/stromal interaction molecule 1 (STIM1), and Ca2+ effectors such as Ca2+/ calmodulin-dependent protein kinase II (CaMKII). In this review, we summarize and highlight current experimental evidence supporting the idea that cross-talk between Ca2+ and ROS/RNS may represent a well-integrated signaling network in vascular smooth muscle. Antioxid.

UR - http://www.scopus.com/inward/record.url?scp=76249129516&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=76249129516&partnerID=8YFLogxK

U2 - 10.1089/ars.2009.2842

DO - 10.1089/ars.2009.2842

M3 - Review article

C2 - 19719386

AN - SCOPUS:76249129516

VL - 12

SP - 657

EP - 674

JO - Antioxidants and Redox Signaling

JF - Antioxidants and Redox Signaling

SN - 1523-0864

IS - 5

ER -