Adrenomedullin provokes endothelial Akt activation and promotes vascular regeneration both in vitro and in vivo
Autor: | Takami Yurugi-Kobayashi, Kazuwa Nakao, Yasutomo Fukunaga, Kwijun Park, Kenichi Yamahara, Masakatsu Sone, Kazutoshi Miyashita, Naoki Sawada, Hiroshi Itoh |
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Jazyk: | angličtina |
Předmět: |
Time Factors
Angiogenesis Biocompatible Materials Biochemistry Umbilical vein Mice Phosphatidylinositol 3-Kinases Adrenomedullin Cell Movement Structural Biology Cyclic AMP Phosphorylation Cells Cultured Re-endothelialization Cell biology Drug Combinations medicine.anatomical_structure Proteoglycans Collagen Cell Division Protein Binding medicine.medical_specialty Endothelium Blotting Western Biophysics Neovascularization Physiologic Protein Serine-Threonine Kinases Biology Proto-Oncogene Proteins Internal medicine cAMP Genetics medicine Animals Humans Regeneration Protein kinase A Molecular Biology Protein kinase B PI3K/AKT/mTOR pathway Wound Healing Dose-Response Relationship Drug Akt Cell Biology Cyclic AMP-Dependent Protein Kinases Vascular regeneration Enzyme Activation Endocrinology Endothelium Vascular Laminin Peptides Wound healing Proto-Oncogene Proteins c-akt |
Zdroj: | FEBS Letters. (1-3):86-92 |
ISSN: | 0014-5793 |
DOI: | 10.1016/S0014-5793(03)00484-8 |
Popis: | We previously reported that adrenomedullin (AM), a vasodilating hormone secreted from blood vessels, promotes proliferation and migration of human umbilical vein endothelial cells (HUVECs). In this study, we examined the ability of AM to promote vascular regeneration. AM increased the phosphorylation of Akt in HUVECs and the effect was inhibited by the AM antagonists and the inhibitors for protein kinase A (PKA) or phosphatidylinositol 3-kinase (PI3K). AM promoted re-endothelialization in vitro of wounded monolayer of HUVECs and neo-vascularization in vivo in murine gel plugs. These effects were also inhibited by the AM antagonists and the inhibitors for PKA or PI3K. The findings suggest that AM plays significant roles in vascular regeneration, associated with PKA- and PI3K-dependent activation of Akt in endothelial cells, and possesses therapeutic potential for vascular injury and tissue ischemia. |
Databáze: | OpenAIRE |
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