In vivo inhibition of angiogenesis by interleukin-13 gene therapy in a rat model of rheumatoid arthritis.

In vivo inhibition of angiogenesis by interleukin-13 gene therapy in a rat model of rheumatoid arthritis. Research Abstract Details 

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In vivo inhibition of angiogenesis by interleukin-13 gene therapy in a rat model of rheumatoid arthritis. Abstract Text:

Christian S Haas,M Asif Amin,Jeffrey H Ruth,Brittany L Allen,Salahuddin Ahmed,Angela Pakozdi,James M Woods,Shiva Shahrara,Alisa E Koch,

OBJECTIVE: Interleukin-13 (IL-13) is a pleiotropic cytokine that can affect vessel formation, an important component of the rheumatoid arthritis (RA) synovial tissue pannus. The purpose of this study was to use a gene therapy approach to investigate the role of IL-13 in angiogenesis in vivo, using a rat adjuvant-induced arthritis model of RA. METHODS: Ankle joints of female rats were injected preventatively with an adenovirus vector containing human IL-13 (AxCAIL-13), a control vector with no insert (AxCANI), or phosphate buffered saline (PBS). Joints were harvested at the peak of arthritis, and histologic and biochemical features were evaluated. RESULTS: AxCAIL-13-treated joint homogenates had lower hemoglobin levels, suggesting reduced joint vascularity, and both endothelial cell migration and tube formation were significantly inhibited (P < 0.05). Similarly, AxCAIL-13 inhibited capillary sprouting in the rat aortic ring assay and vessel growth in the Matrigel plug in vivo assay. IL-13 gene delivery resulted in up-regulation and association of phosphorylated ERK-1/2 and protein kinase Calpha/betaII, suggesting a novel pathway in IL-13-mediated angiostasis. The angiostatic effect of AxCAIL-13 was associated with down-regulation of proangiogenic cytokines (IL-18, cytokine-induced neutrophil chemoattractant 1/CXCL1, lipopolysaccharide-induced CXC chemokine/CXCL5) and up-regulation of the angiogenesis inhibitor endostatin. The expression and activity of matrix metalloproteinases 2 and 9, which participate in angiogenesis, was impaired in response to IL-13 as compared with AxCANI and PBS treatment. CONCLUSION: Our findings support a role for IL-13 as an in vivo antiangiogenic factor and provide a rationale for its use in RA to control pathologic neovascularization.

In vivo inhibition of angiogenesis by interleukin-13 gene therapy in a rat model of rheumatoid arthritis. Publishing Authors By Initials

CS Haas,MA Amin,JH Ruth,BL Allen,S Ahmed,A Pakozdi,JM Woods,S Shahrara,AE Koch,

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In vivo inhibition of angiogenesis by interleukin-13 gene therapy in a rat model of rheumatoid arthritis. Journal Published:

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

Journal: Arthritis and rheumatism

VOLUME: 56

Page Numbers: 2535-48

Journal Abbreviation: Arthritis Rheum.

ISSN: 0004-3591

DAY: 3

MONTH: Aug

YEAR: 2007

In vivo inhibition of angiogenesis by interleukin-13 gene therapy in a rat model of rheumatoid arthritis. Information

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LANGUAGE: eng

NlmUniqueID: 370605

In vivo inhibition of angiogenesis by interleukin-13 gene therapy in a rat model of rheumatoid arthritis. Keywords Mesh Terms:

KEYWORDS: Tissue Extracts

MESH TERMS: pharmacology

Chemical & Substance for Abstract: In vivo inhibition of angiogenesis by interleukin-13 gene therapy in a rat model of rheumatoid arthritis. Information

Substance Name: Matrix Metalloproteinase 9

Registry Number: EC 3.4.24.35

Grant and Affiliation Information for In vivo inhibition of angiogenesis by interleukin-13 gene therapy in a rat model of rheumatoid arthritis.

AFFILIATION: University of Michigan Medical School, 109 Zina Pitcher Place, Ann Arbor, MI 48109, USA.

Country: United States

AGENCY: United States NIAMS

GRANT: AR 48267

ACRONYM: AR

MEDLINETA: Arthritis Rheum

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