PMID- 21109762
OWN - NLM
STAT- MEDLINE
DCOM- 20110411
LR  - 20181201
IS  - 1423-0313 (Electronic)
IS  - 0031-7012 (Linking)
VI  - 86
IP  - 5-6
DP  - 2010
TI  - COMP-Ang1, a variant of angiopoietin 1, inhibits serum-deprived apoptosis of 
      mesenchymal cells via PI3K/Akt and mitogen-activated protein kinase pathways.
PG  - 327-35
LID - 10.1159/000321885 [doi]
AB  - 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.
CI  - Copyright (c) 2010 S. Karger AG, Basel.
FAU - Lee, Kkot-Nim
AU  - Lee KN
AD  - Dental Science Research Institute and the BK21 Project, School of Dentistry, 
      Chonnam National University, Republic of Korea.
FAU - Seo, Min-Chul
AU  - Seo MC
FAU - Bae, In-Ho
AU  - Bae IH
FAU - Oh, Sin-Hye
AU  - Oh SH
FAU - Jang, Won Gu
AU  - Jang WG
FAU - Jeong, Byung-Chul
AU  - Jeong BC
FAU - Oh, Won-Mann
AU  - Oh WM
FAU - Kim, Sun-Hun
AU  - Kim SH
FAU - Lee, Shee-Eun
AU  - Lee SE
FAU - Shim, Kyung Mi
AU  - Shim KM
FAU - Park, Bae-Keun
AU  - Park BK
FAU - Koh, Jeong-Tae
AU  - Koh JT
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20101129
PL  - Switzerland
TA  - Pharmacology
JT  - Pharmacology
JID - 0152016
RN  - 0 (COMP-Ang1 fusion protein)
RN  - 0 (RNA, Messenger)
RN  - 0 (Recombinant Fusion Proteins)
RN  - 136601-57-5 (Cyclin D1)
RN  - EC 2.7.1.137 (Phosphatidylinositol 3-Kinase)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Animals
MH  - Apoptosis/*drug effects
MH  - Blotting, Western
MH  - Cell Survival/drug effects
MH  - Cells, Cultured
MH  - Cyclin D1/genetics
MH  - Humans
MH  - Mesenchymal Stem Cells/*drug effects/metabolism
MH  - Mice
MH  - Mitogen-Activated Protein Kinases/metabolism
MH  - Phosphatidylinositol 3-Kinase/metabolism
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - RNA, Messenger/metabolism
MH  - Recombinant Fusion Proteins/*pharmacology
MH  - Reverse Transcriptase Polymerase Chain Reaction
EDAT- 2010/11/27 06:00
MHDA- 2011/04/13 06:00
CRDT- 2010/11/27 06:00
PHST- 2010/03/23 00:00 [received]
PHST- 2010/10/08 00:00 [accepted]
PHST- 2010/11/27 06:00 [entrez]
PHST- 2010/11/27 06:00 [pubmed]
PHST- 2011/04/13 06:00 [medline]
AID - 000321885 [pii]
AID - 10.1159/000321885 [doi]
PST - ppublish
SO  - Pharmacology. 2010;86(5-6):327-35. doi: 10.1159/000321885. Epub 2010 Nov 29.