title: [The role of Notch signaling during the differentiation of rat bone marrow mesenchymal stem cells into endothelial cells].
abstract: OBJECTIVE
  To research the role of Notch signaling during the differentiation of bone marrow mesenchymal stem cells (MSCs) into endothelial cells and its effect on the functions of the differentiated cells.
  
  
  METHODS
  Rat bone marrow MSCs were isolated and cultured in vitro, then the cells were treated with vascular endothelial growth factor (VEGF165) and basic fibroblast growth factor (bFGF) for 2 weeks to induce it to differentiate into endothelial cells. The differentiated cells were identified by fluorescence immunoassay. The receptors and ligands of the Notch signaling were detected by reverse transcription-polymerase chain reaction (RT-PCR) before and after the differentiation. γ-secretase inhibitor was used to block Notch pathway. Migration ability of cells were assessed by scarification test. Cells were inoculated on semisolid gel to study their ability of forming the capillary-like structure.
  
  
  RESULTS
  After inducing MSCs to differentiate into endothelial cells by VEGF165 and bFGF, MSCs gained the characteristics of the endothelial cells with expression of CD31 and Flk1. There were Notch1 mRNA and Jagged1 mRNA expressions in rat bone marrow MSCs. The expression changes in the receptor Notch1 were not statistically significant on the differentiated cells (0.59±0.01 vs. 0.59±0.01, P>0.05), but there was a trend towards an increase of Jagged1 mRNA (1.01±0.02 vs. 0.99±0.03, P>0.05). When Notch pathway was blocked, the differentiated cells' migration ability was increased (number of cells on the scratched area: 44.61±4.34 vs. 40.06±2.43, P<0.05), and the ability of forming capillary-like structure was also increased (cells classification: 3.67±0.82 vs. 2.00±0.89, P<0.01).
  
  
  CONCLUSIONS
  Notch signaling may have an important role during the differentiation of MSCs into endothelial cells. The function of differentiated cells were strengthened when Notch pathway was blocked.
authors.affiliation: Central Intensive Care Unit, Guangzhou Red Cross Hospital, Fourth Affiliated Hospital, Jinan University, Guangzhou 510220, Guangdong, China. jinjinlan@163.com
authors.forename: Jin-lan
authors.initials: JL
authors.lastname: Jin
authors.forename: Han-ping
authors.initials: HP
authors.lastname: Zhuang
authors.forename: Jian-rui
authors.initials: JR
authors.lastname: Wei
authors.forename: Zhi-shun
authors.initials: ZS
authors.lastname: Feng
authors.forename: Zhe-tong
authors.initials: ZT
authors.lastname: Deng
authors.forename: Min
authors.initials: M
authors.lastname: Zhang
mesh_terms: D000818:Animals; D001854:Bone Marrow Cells / Q000166:cytology* / Q000378:metabolism; D002454:Cell Differentiation; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000378:metabolism*; D059630:Mesenchymal Stem Cells / Q000166:cytology* / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D051881:Receptor, Notch1 / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: C497763:Notch1 protein, rat; D051881:Receptor, Notch1