Nox4 mediates TGF-beta1-induced retinoblastoma protein phosphorylation, proliferation, and hypertrophy in human airway smooth muscle cells.

Nox4 mediates TGF-beta1-induced retinoblastoma protein phosphorylation, proliferation, and hypertrophy in human airway smooth muscle cells. Research Abstract Details 

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Nox4 mediates TGF-beta1-induced retinoblastoma protein phosphorylation, proliferation, and hypertrophy in human airway smooth muscle cells. Abstract Text:

Anne Sturrock,Thomas P Huecksteadt,Kimberly Norman,Karl Sanders,Thomas M Murphy,Pasquale Chitano,Kimberly Wilson,John R Hoidal,Thomas P Kennedy,

Transforming growth factor-beta1 (TGF-beta1) plays a pivotal role in increasing airway smooth muscle mass in severe asthma by inducing proliferation and hypertrophy of human airway smooth muscle. The mechanism(s) for these effects of TGF-beta1 have not been fully elucidated. In this study, we demonstrate that TGF-beta1 is a potent inducer of expression of the nonphagocyte NAD(P)H oxidase catalytic homolog Nox4, diphenylene iodonium-inhibitable reactive oxygen species production, proliferation, and hypertrophy in cultured human airway smooth muscle cells. By confocal microscopy, TGF-beta1-induced Nox4 was localized with the endoplasmic reticulum and the nucleus, implying a role for Nox4 in regulation of both the cell cycle and protein synthesis. Consistent with this hypothesis, TGF-beta1 increased retinoblastoma protein phosphorylation at both Ser807/811 and Ser780. Silencing Nox4 prevented TGF-beta1-mediated retinoblastoma protein phosphorylation, proliferation, and cell hypertrophy. TGF-beta1 also increased phosphorylation of eukaryotic translation initiation factor 4E binding protein-1 at Thr37/46, and this was likewise blocked by silencing Nox4. This is the first report to suggest a functional role for Nox4 in cell cycle transition and to demonstrate that Nox4 influences the pathobiochemistry of asthma by generating reactive oxygen species that promote TGF-beta1-induced proliferation and hypertrophy of human airway smooth muscle.

Nox4 mediates TGF-beta1-induced retinoblastoma protein phosphorylation, proliferation, and hypertrophy in human airway smooth muscle cells. Publishing Authors By Initials

A Sturrock,TP Huecksteadt,K Norman,K Sanders,TM Murphy,P Chitano,K Wilson,JR Hoidal,TP Kennedy,

For similar peptides: intercellular signaling peptides and proteins: cytokines: transforming growth factor beta: transforming growth factor beta1 research abstracts see: peptides: intercellular signaling peptides and proteins: cytokines: transforming growth factor beta: transforming growth factor beta1 research

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Nox4 mediates TGF-beta1-induced retinoblastoma protein phosphorylation, proliferation, and hypertrophy in human airway smooth muscle cells. Journal Published:

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

Journal: American journal of physiology. Lung cellular and

VOLUME: 292

Page Numbers: L1543-55

Journal Abbreviation: Am. J. Physiol. Lung Cell Mol.

ISSN: 1040-0605

DAY: 16

MONTH: 03

YEAR: 2007

Nox4 mediates TGF-beta1-induced retinoblastoma protein phosphorylation, proliferation, and hypertrophy in human airway smooth muscle cells. Information

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LANGUAGE: eng

NlmUniqueID: 100901229

Nox4 mediates TGF-beta1-induced retinoblastoma protein phosphorylation, proliferation, and hypertrophy in human airway smooth muscle cells. Keywords Mesh Terms:

KEYWORDS: Transforming Growth Factor beta1

MESH TERMS: pharmacology

Chemical & Substance for Abstract: Nox4 mediates TGF-beta1-induced retinoblastoma protein phosphorylation, proliferation, and hypertrophy in human airway smooth muscle cells. Information

Substance Name: CDC2 Protein Kinase

Registry Number: EC 2.7.1.37

Grant and Affiliation Information for Nox4 mediates TGF-beta1-induced retinoblastoma protein phosphorylation, proliferation, and hypertrophy in human airway smooth muscle cells.

AFFILIATION: Division of Respiratory, Critical Care and Occupational Pulmonary Medicine, University of Utah Health Sciences Center and Veterans Administration Medical Center, Salt Lake City, Utah 84132, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: HL-67281

ACRONYM: HL

MEDLINETA: Am J Physiol Lung Cell Mol Phy

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