Endocrine Abstracts (2007) 13 P152

Effect of SOM230 on the proliferation of adult human vascular endothelial cells

Chao Li, Wenwen Zhong, Shang-Zhong Xu & Stephen L Atkin

Postgraduate Medical Institute & Hull York Medical School, University of Hull, Hull, United Kingdom.

SOM230 is one of the long-acting somatostatin analogues, which has been developed for the treatment of neuroendocrine tumours. Recently we found that SOM230 inhibits the proliferation of human umbilical vein endothelial cells (HUVECs). The aim of this study is to further investigate its antiproliferative effect using adult human aortic endothelial cells (HAECs) and human dermal microvessel endothelial cells (HDMECs). The expression of SSTRs and the potential mechanism were observed.

Methods: The human vascular endothelial cells and the cell culture medium were purchased from Promocell Co. Cells were cultured in a CO2 incubator at 37  °C. The mRNA of SSTRs was detected by RT-PCR and real-time RT-PCR, and the proteins were detected by western blotting. The WST-1 kit for cell proliferation assay was purchased from Roche Co. Intracellular Ca2+ was measured with Fura-2. Data were presented as mean±S.E.M. and the statistic difference was analysed with ANOVA or student t test where appropriate.

Results: The mRNAs of SSTR1-5 were detected in the HAECs and HDMECs. The proteins of SSTR1, SSTR2, SSTR3 and SSTR5 were also detected in HAECs with western blotting. SOM230 at the concentrations from 10−11 M to 10−6 M significantly inhibited the proliferation of HAECs. The absorbance for proliferation was inhibited by 55.2±4.1% (P<0.001) after incubation with SOM230 (10−10 M) for 48 h. The proliferation of HDMECs was also changed. SOM230 (10−6 M) had no effect on the intracellular Ca2+ release in HAECs and HEK-293 cells, but slightly increased the sustained phase of calcium influx in the SSTR3-transfected cells.

Conclusions: We demonstrated that the five isoforms of SSTRs exist in adult vascular endothelial cells. SOM230 inhibited the adult human endothelial cell proliferation. The mechanism seems to be not related to the intracellular Ca2+ release, but may relate to the sustained phase of calcium influx via receptor activation pathways.

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