Ca2+ signaling, TRP channels, and endothelial permeability.

Ca2+ signaling, TRP channels, and endothelial permeability. Research Abstract Details 

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Ca2+ signaling, TRP channels, and endothelial permeability. Abstract Text:

Chinnaswamy Tiruppathi,Gias U Ahmmed,Stephen M Vogel,Asrar B Malik,

Increased endothelial permeability is the hallmark of inflammatory vascular edema. Inflammatory mediators that bind to heptahelical G protein-coupled receptors trigger increased endothelial permeability by increasing the intracellular Ca2+ concentration ([Ca2+]i). The rise in [Ca2+]i activates key signaling pathways that mediate cytoskeletal reorganization (through myosin-light-chain-dependent contraction) and the disassembly of VE-cadherin at the adherens junctions. The Ca2+-dependent protein kinase C (PKC) isoform PKCalpha plays a crucial role in initiating endothelial cell contraction and disassembly of VE-cadherin junctions. The increase in [Ca2+]i induced by inflammatory agonists such as thrombin and histamine is achieved by the generation of inositol 1,4,5-trisphosphate (IP3), activation of IP3-receptors, release of stored intracellular Ca2+, and Ca2+ entry through plasma membrane channels. IP3-sensitive Ca2+-store depletion activates plasma membrane cation channels (i.e., store-operated cation channels [SOCs] or Ca2+ release-activated channels [CRACs]) to cause Ca2+ influx into endothelial cells. Recent studies have identified members of Drosophila transient receptor potential (TRP) gene family of channels that encode functional SOCs in endothelial cells. These studies also suggest that the canonical TRPC homologue TRPC1 is the predominant isoform expressed in human vascular endothelial cells, and is the essential component of the SOC in this cell type. Further, evidence suggests that the inflammatory cytokine tumor necrosis factor-alpha can induce the expression of TRPC1 in human vascular endothelial cells signaling via the nuclear factor-kappaB pathway. Increased expression of TRPC1 augments Ca2+ influx via SOCs and potentiates the thrombin-induced increase in permeability in human vascular endothelial cells. Deletion of the canonical TRPC homologue in mouse, TRPC4, caused impairment in store-operated Ca2+ current and Ca2+-store release-activated Ca2+ influx in aortic and lung endothelial cells. In TRPC4 knockout (TRPC4-/-) mice, acetylcholine-induced endothelium-dependent smooth muscle relaxation was drastically reduced. In addition, TRPC4-/- mouse-lung endothelial cells exhibited lack of actin-stress fiber formation and cell retraction in response to thrombin activation of protease-activated receptor-1 (PAR-1) in endothelial cells. The increase in lung microvascular permeability in response to PAR-1 activation was inhibited in TRPC4-/- mice. These results indicate that endothelial TRP channels such as TRPC1 and TRPC4 play an important role in signaling agonist-induced increases in endothelial permeability.

Ca2+ signaling, TRP channels, and endothelial permeability. Publishing Authors By Initials

C Tiruppathi,GU Ahmmed,SM Vogel,AB Malik,

For similar proteins: carrier proteins: membrane transport proteins: ion channels: transient receptor potential channels research abstracts see: proteins: carrier proteins: membrane transport proteins: ion channels: transient receptor potential channels research

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MEDLINE DATE:

Ca2+ signaling, TRP channels, and endothelial permeability. Journal Published:

PUBLICATION TYPE: Review

Journal: Microcirculation (New York, N.Y. : 1994)

VOLUME: 13

Page Numbers: 693-708

Journal Abbreviation:

ISSN: 1073-9688

DAY: 3

MONTH: Dec

YEAR: 2006

Ca2+ signaling, TRP channels, and endothelial permeability. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 9434935

Ca2+ signaling, TRP channels, and endothelial permeability. Keywords Mesh Terms:

KEYWORDS: Transient Receptor Potential Channels

MESH TERMS: metabolism

Chemical & Substance for Abstract: Ca2+ signaling, TRP channels, and endothelial permeability. Information

Substance Name: Calcium

Registry Number: 7440-70-2

Grant and Affiliation Information for Ca2+ signaling, TRP channels, and endothelial permeability.

AFFILIATION: Department of Pharmacology and Center for Lung and Vascular Biology, College of Medicine, University of Illinois, Chicago, Illinois 60612, USA. tiruc@uic.edu

Country: United States

AGENCY: United States NHLBI

GRANT: P01 HL077806

ACRONYM: HL

MEDLINETA: Microcirculation

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ACCESSION NUMBER:

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