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
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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