期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 116, 期 11, 页码 2955-2963出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI27392
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资金
- NHLBI NIH HHS [HL55413, HL62454, R01 HL055413, R01 HL062454] Funding Source: Medline
- NIAID NIH HHS [P01 AI050514, AI50514] Funding Source: Medline
The transcription factor NF-kappa B is an important regulator of homeostatic growth and inflammation. Although gene-targeting studies have revealed important roles for NF-kappa B, they have been complicated by component redundancy and lethal phenotypes. To examine the role of NF-kappa B in endothelial tissues, Tie2 promoter/enhancer-I kappa B alpha(S32A/S36A) transgenic mice were generated. These mice grew normally but exhibited enhanced sensitivity to LPS-induced toxemia, notable for an increase in vascular permeability and apoptosis. Moreover, B16-BL6 tumors grew significantly more aggressively in transgenic mice, underscoring a new role for NF-kappa B in the homeostatic response to cancer. Tumor vasculature in transgenic mice was extensive and disorganized. This correlated with a marked loss in tight junction formation and suggests that NF-kappa B plays an important role in the maintenance of vascular integrity and response to stress.
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