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JNK as a positive regulator of angiogenic potential in endothelial cells by Cassandra Uchida; Eric Gee; Eric Ispanovic; Tara L. Haas is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.
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## Abstract Angiogenesis (the growth of new capillaries) occurs in adults in response to physiological stimuli such as wound healing and exercise. The mitogen‐activated protein kinase c‐jun N‐terminal kinase (JNK) has a controversial role in the process of angiogenesis, with previous evidence supporting JNK as both a positive and negative regulator of blood vessel growth. The purpose of this study was to clarify the role of JNK in the angiogenesis process. Phosphorylated JNK was observed in cultured endothelial cells, and levels were constant regardless of extracellular matrix composition. Using SP600125, inhibition of JNK attenuated sprout growth in 3D capillary sprout cultures. Inhibition of JNK reduced endothelial cell proliferation and migration __in vitro__. JNK inhibition and siRNA knockdown of c‐jun (a downstream target of JNK) decreased protein levels of the transcription factor Egr‐1, a regulator of genes involved in proliferation and migration. Matrix metalloproteinase‐2 (MMP‐2) production, and activity also, was reduced in sprout cultures treated with SP600125. c‐Jun silencing decreased both MMP‐2 and membrane type‐1 (MT1)‐MMP mRNA in endothelial cells, implicating both
Who reads JNK as a positive regulator of angiogenic potential in endothelial cells?
It is typically read by researchers, students, and practitioners in Biochemistry, Genetics and Molecular Biology.
- Author
- Cassandra Uchida; Eric Gee; Eric Ispanovic; Tara L. Haas
- Publisher
- Elsevier Science; Wiley (John Wiley & Sons); Wiley-Blackwell; Wiley (ISSN 1065-6995)
- Published
- 2008
- Language
- EN
- Field
- Biochemistry, Genetics and Molecular Biology (Life Sciences)
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