PMID- 20979529
OWN - NLM
STAT- MEDLINE
DCOM- 20110503
LR  - 20110302
IS  - 1557-7430 (Electronic)
IS  - 1044-5498 (Linking)
VI  - 30
IP  - 3
DP  - 2011 Mar
TI  - C-reactive protein can influence the proliferation, apoptosis, and monocyte 
      chemotactic protein-1 production of human umbilical vein endothelial cells.
PG  - 157-62
LID - 10.1089/dna.2010.1093 [doi]
AB  - C-reactive protein (CRP) has been shown to be closely associated with coronary 
      heart disease. The serum CRP concentrations of chronic periodontitis (CP) 
      patients were increased due to periodontal inflammation. CRP may be a potential 
      key mediator associating CP with coronary heart disease. This study aimed to 
      investigate the effects of CRP on human endothelial cells in vitro. CRP ranging 
      from 0 to 10 mug/mL was adopted to imitate the chronic inflammatory conditions of 
      periodontitis. The influences of CRP on proliferation, apoptosis, and monocyte 
      chemotactic protein-1 (MCP-1) production of human umbilical vein endothelial 
      cells (HUVECs) were studied through 
      3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, flow 
      cytometry, and enzyme-linked immunosorbent assay analysis, respectively. Compared 
      to the blank control, 2.5 and 5.0 mug/mL CRP significantly suppressed cell 
      proliferation by 6.9% and increased apoptosis by 10.2% and 14.6%, respectively 
      (p<0.05). Concentrations of 7.5 and 10.0 mug/mL CRP also induced 2.3% HUVEC 
      proliferation suppression (p>0.05) and significantly increased apoptosis ratio 
      compared to that of the blank control. CRP could promote MCP-1 production of 
      HUVECs in a concentration-dependent manner. The MCP-1 production of 10.0 mug/mL 
      CRP group was about 15.3% higher than that of the control group. It is concluded 
      that low concentrations of CRP, which appears in CP, inhibits cell proliferation, 
      promotes cell apoptosis, and increases MCP-1 production in endothelium, which may 
      initiate self-repairing function of vascular endothelium following vascular 
      injury process.
FAU - Guo, Shujuan
AU  - Guo S
AD  - State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, 
      Sichuan University, Chengdu, Sichuan, China.
FAU - Meng, Shu
AU  - Meng S
FAU - Chen, Bin
AU  - Chen B
FAU - Liu, Juan
AU  - Liu J
FAU - Gao, Li
AU  - Gao L
FAU - Wu, Yafei
AU  - Wu Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20101027
PL  - United States
TA  - DNA Cell Biol
JT  - DNA and cell biology
JID - 9004522
RN  - 0 (Chemokine CCL2)
RN  - 9007-41-4 (C-Reactive Protein)
SB  - IM
MH  - Apoptosis/*drug effects
MH  - C-Reactive Protein/*pharmacology
MH  - Cell Proliferation/*drug effects
MH  - Cell Survival/drug effects
MH  - Cells, Cultured
MH  - Chemokine CCL2/*metabolism
MH  - Dose-Response Relationship, Drug
MH  - Endothelial Cells/cytology/*drug effects/metabolism
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Female
MH  - Flow Cytometry
MH  - Humans
MH  - Umbilical Veins/cytology
EDAT- 2010/10/29 06:00
MHDA- 2011/05/04 06:00
CRDT- 2010/10/29 06:00
PHST- 2010/10/29 06:00 [entrez]
PHST- 2010/10/29 06:00 [pubmed]
PHST- 2011/05/04 06:00 [medline]
AID - 10.1089/dna.2010.1093 [doi]
PST - ppublish
SO  - DNA Cell Biol. 2011 Mar;30(3):157-62. doi: 10.1089/dna.2010.1093. Epub 2010 Oct 
      27.