IGF-1 protects intestinal epithelial cells from oxidative stress-induced apoptosis.

IGF-1 protects intestinal epithelial cells from oxidative stress-induced apoptosis. Research Abstract Details 

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IGF-1 protects intestinal epithelial cells from oxidative stress-induced apoptosis. Abstract Text:

Naira Baregamian,Jun Song,Marc G Jeschke,B Mark Evers,Dai H Chung,

BACKGROUND: Reactive oxygen species (ROS) are involved in the pathogenesis of necrotizing enterocolitis (NEC) in premature infants. We have recently found that activation of multiple cellular signaling transduction pathways occurs during ROS-induced intestinal cell apoptosis; the phosphatidylinositol 3-kinase (PI3-K) pathway plays an anti-apoptotic role during this process. Insulin-like growth factor (IGF)-1 activates PI3-K pathway to promote cell survival; however, the effects of IGF-1 treatment during gut injury are not clearly defined. The purpose of this study was to determine whether IGF-1 protects intestinal cells from ROS-induced apoptosis. MATERIALS AND METHODS: Rat intestinal epithelial (RIE)-1 cells were treated with either IGF-1 (100 nm), hydrogen peroxide (H2O2; 500 microm), or combination. Western blotting was performed to assess phosphorylation of Akt, a downstream effector of PI3-K. Cell Death Detection ELISA, DCHF, and JC-1 assays were performed to demonstrate protective effects of IGF-1. Wortmannin, an inhibitor of PI3-K, was used to show PI3-K-dependent mechanism of action for IGF-1. RESULTS: H2O2 treatment resulted in increased intestinal epithelial cell apoptosis with intracellular ROS generation and mitochondrial membrane depolarization; IGF-1 pre-treatment attenuated this response without affecting ROS production. H2O2-induced phosphorylation of Akt was further increased with IGF-1 treatment; wortmannin abolished these effects in RIE-1 cells. CONCLUSIONS: PI3-K pathway is activated during ROS-induced intestinal epithelial cell injury; IGF-1 exerted an anti-apoptotic effect during this response by PI3-K activation. A better understanding of the exact role of IGF-1-mediated activation of PI3-K may allow us to facilitate the development of novel therapy against NEC.

IGF-1 protects intestinal epithelial cells from oxidative stress-induced apoptosis. Publishing Authors By Initials

N Baregamian,J Song,MG Jeschke,BM Evers,DH Chung,

For similar biological phenomena, cell phenomena, and immunity: cell physiology: cell communication: signal transduction research abstracts see: biological phenomena, cell phenomena, and immunity: cell physiology: cell communication: signal transduction research

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IGF-1 protects intestinal epithelial cells from oxidative stress-induced apoptosis. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: The Journal of surgical research

VOLUME: 136

Page Numbers: 31-7

Journal Abbreviation: J. Surg. Res.

ISSN: 0022-4804

DAY: 26

MONTH: 09

YEAR: 2006

IGF-1 protects intestinal epithelial cells from oxidative stress-induced apoptosis. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 376340

IGF-1 protects intestinal epithelial cells from oxidative stress-induced apoptosis. Keywords Mesh Terms:

KEYWORDS: Signal Transduction

MESH TERMS: physiology

Chemical & Substance for Abstract: IGF-1 protects intestinal epithelial cells from oxidative stress-induced apoptosis. Information

Substance Name: Proto-Oncogene Proteins c-akt

Registry Number: EC 2.7.1.37

Grant and Affiliation Information for IGF-1 protects intestinal epithelial cells from oxidative stress-induced apoptosis.

AFFILIATION: Department of Surgery, The University of Texas Medical Branch, Galveston, Texas 77555-0353, USA.

Country: United States

AGENCY: United States NIDDK

GRANT: R01 DK61470

ACRONYM: DK

MEDLINETA: J Surg Res

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