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- Title
COMP-Ang1, a Variant of Angiopoietin 1, Inhibits Serum-Deprived Apoptosis of Mesenchymal Cells via PI3K/Akt and Mitogen-Activated Protein Kinase Pathways.
- Authors
Lee, Kkot-Nim; Seo, Min-Chul; Bae, In-Ho; Oh, Sin-Hye; Jang, Won Gu; Jeong, Byung-Chul; Oh, Won-Mann; Kim, Sun-Hun; Lee, Shee-Eun; Shim, Kyung Mi; Park, Bae-Keun; Koh, Jeong-Tae
- Abstract
Background/Aims: Cartilage oligomeric matrix protein (COMP)-angiopoietin 1 (Ang1) is a soluble and stable form of Ang1 which plays important roles in vessel formation and the survival of endothelial cells, neurons and cardiomyocytes. However, the effects of COMP-Ang1 on the survival of mesenchymal cells are unknown. Mesenchymal cells have been transplanted with some scaffolds for bone tissue regeneration, but they occasionally underwent cell death due to a lack of nutrient supply. This study examined the effects of COMP-Ang1 on the survival of mesenchymal cells under nutrient-deprived conditions. Methods: Primary and C3H10T1/2 mesenchymal cells were cultured under serum deprivation with or without COMP-Ang1. The effects of COMP-Ang1 on mesenchymal cell survival and its molecular mechanism were determined using a viability test, RT-PCR, Western blotting and fluorescence-activated cell sorting analysis. Results and Conclusion: COMP-Ang1 inhibited the nutrient-deprived apoptotic cell death of mesenchymal cells through the Akt, p38 and extracellular-signal-regulated kinase (ERK) pathways. In addition, COMP-Ang1 reversed the nutrient-deprived suppression of cyclin D1 mRNA expression. These results suggest that COMP-Ang1 has a protective role in the survival of nutrient-deprived mesenchymal cells. The use of COMP-Ang1 with some scaffolds might be useful for bone tissue engineering. Copyright © 2010 S. Karger AG, Basel
- Subjects
GROWTH factors; APOPTOSIS; SERUM; MESENCHYMAL stem cells; MITOGEN-activated protein kinases; CARTILAGE; NEURONS; HEART cells; REVERSE transcriptase polymerase chain reaction
- Publication
Pharmacology, 2010, Vol 86, Issue 5/6, p327
- ISSN
0031-7012
- Publication type
Article
- DOI
10.1159/000321885