alpha(1)-Adrenergic receptor stimulation of cell motility requires phospholipase D-mediated extracellular signal-regulated kinase activation.

alpha(1)-Adrenergic receptor stimulation of cell motility requires phospholipase D-mediated extracellular signal-regulated kinase activation. Research Abstract Details 

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alpha(1)-Adrenergic receptor stimulation of cell motility requires phospholipase D-mediated extracellular signal-regulated kinase activation. Abstract Text:

Rachel L Sang,Jessica F Johnson,Jennifer Taves,Callie Nguyen,Mark A Wallert,Joseph J Provost,

Phospholipase D is suspected to play a role in tumorigenesis, and the inhibition of phospholipase D has been associated with changes in several cellular events including invasion and migration. We report here that the specific alpha(1)-adrenergic receptor agonist, phenylepherine, signals to a growth factor pathway in a manner that requires phospholipase D activity in CCL39 fibroblasts. Phenylepherine increased extracellular signal-regulated kinase phosphorylation eightfold and promoted stress fiber formation threefold. Stress fiber formation was blocked when extracellular signal-regulated kinase activation was inhibited. Stimulation of CCL39 fibroblasts by phenylepherine increased the rate of wound healing fourfold in a wounding assay, while treatment with the MEK inhibitor, PD98059 reduced the closure of phenylepherine-induced wound healing to control levels. Addition of 1-butanol but not 2-butanol inhibited extracellular signal-regulated kinase activation by phenylepherine, presumably by blocking the formation of phosphatidic acid. Exogenously added cell permeable phosphatidic acid increased extracellular signal-regulated kinase activation in a time- and dose-dependent manner as well as stimulated the formation of stress fibers. 1-butanol also significantly inhibited the ability of phenylepherine to stimulate stress fiber formation and wound healing. Taken together, these results indicate a novel role for phospholipase D in the activation of the extracellular signal-regulated kinase growth factor pathway to stimulate early cellular events induced by phenylepherine.

alpha(1)-Adrenergic receptor stimulation of cell motility requires phospholipase D-mediated extracellular signal-regulated kinase activation. Publishing Authors By Initials

RL Sang,JF Johnson,J Taves,C Nguyen,MA Wallert,JJ Provost,

For similar biological phenomena, cell phenomena, and immunity: biological phenomena: regeneration: wound healing research abstracts see: biological phenomena, cell phenomena, and immunity: biological phenomena: regeneration: wound healing research

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alpha(1)-Adrenergic receptor stimulation of cell motility requires phospholipase D-mediated extracellular signal-regulated kinase activation. Journal Published:

PUBLICATION TYPE: Research Support, U.S. Gov't,

Journal: Chemical biology & drug design

VOLUME: 69

Page Numbers: 240-50

Journal Abbreviation:

ISSN: 1747-0277

DAY: 3

MONTH: Apr

YEAR: 2007

alpha(1)-Adrenergic receptor stimulation of cell motility requires phospholipase D-mediated extracellular signal-regulated kinase activation. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 101262549

alpha(1)-Adrenergic receptor stimulation of cell motility requires phospholipase D-mediated extracellular signal-regulated kinase activation. Keywords Mesh Terms:

KEYWORDS: Wound Healing

MESH TERMS: metabolism

Chemical & Substance for Abstract: alpha(1)-Adrenergic receptor stimulation of cell motility requires phospholipase D-mediated extracellular signal-regulated kinase activation. Information

Substance Name: Phospholipase D

Registry Number: EC 3.1.4.4

Grant and Affiliation Information for alpha(1)-Adrenergic receptor stimulation of cell motility requires phospholipase D-mediated extracellular signal-regulated kinase activation.

AFFILIATION: Department of Bioscience, Minnesota State University Moorhead, Moorhead, MN 56563, USA.

Country: England

AGENCY: United States NHLBI

GRANT: R15-HL074924-01A1

ACRONYM: HL

MEDLINETA: Chem Biol Drug Des

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