RÉSUMÉ
<p><b>BACKGROUND AND OBJECTIVE</b>Endothelial progenitor cells (EPCs) play an important role in hypoxia-triggered tumor vasculogenesis. However, the homing of exogenous EPCs in tumors is still unclear. In this study, we investigated the recruitment of exogenous EPCs in human lung adenocarcinoma model of nude mice.</p><p><b>METHODS</b>EPCs labeled with green fluorescence protein (GFP) were transplanted into nude mice bearing human lung adenocarcinoma. The growth of tumor was observed. After the mice were killed, GFP-EPCs in different tissues were examined by fluorescence. The tumor tissues were stained for CD133, hypoxia-inducible factor-1alpha (HIF-1α), stromal cell-derived factor-1α (SDF-1α), and vascular endothelial growth factor receptor (KDR). Real-time polymerase chain reaction of CD133, HIF-1α, SDF-1α, and VEGF-1 were also performed.</p><p><b>RESULTS</b>The growth of tumor in EPC group was significantly faster than that in saline solution group (P <0.05). Under fluorescence microscope, GFP-EPCs were strongly expressed in both tumor and bone marrow. EPCs were recruited to the tumor periphery to participate in tumor vasculogenesis. The expression of CD133, HIF-1α, and SDF-1 mRNA in tumor and bone marrow were significantly higher than that in the liver, spleen, and skin (P<0.05).</p><p><b>CONCLUSIONS</b>Exogenous EPCs can be recruited to tumor and accelerate tumor growth. Except tumor, bone marrow can also recruit EPCs.</p>
Sujet(s)
Animaux , Femelle , Humains , Souris , Antigène AC133 , Adénocarcinome , Métabolisme , Anatomopathologie , Antigènes CD , Génétique , Métabolisme , Moelle osseuse , Métabolisme , Anatomopathologie , Lignée cellulaire tumorale , Chimiokine CXCL12 , Génétique , Métabolisme , Cellules endothéliales , Anatomopathologie , Transplantation , Glycoprotéines , Génétique , Métabolisme , Protéines à fluorescence verte , Métabolisme , Sous-unité alpha du facteur-1 induit par l'hypoxie , Génétique , Métabolisme , Tumeurs du poumon , Métabolisme , Anatomopathologie , Souris nude , Transplantation tumorale , Néovascularisation pathologique , Peptides , Génétique , Métabolisme , ARN messager , Métabolisme , Transplantation de cellules souches , Cellules souches , Anatomopathologie , Transfection , Charge tumorale , Facteur de croissance endothéliale vasculaire de type A , Génétique , MétabolismeRÉSUMÉ
<p><b>OBJECTIVE</b>To investigate the effects of mineral trioxide aggregate (MTA) and calcium hydroxide on the proliferation and differentiation capacity of pulp cells of primary teeth.</p><p><b>METHODS</b>Pulp cells were isolated from the retained primary teeth without apparent root resorption and cultured. The cells of 4 - 8 passages were used in the study. Cell proliferation was detected by MTT array, von Kossa staining employed to observe the formation of mineralized nodules and mRNA expression of alkaline phosphatase (ALP) and dentin sialophosphoprotein (DSPP) determined by real time PCR.</p><p><b>RESULTS</b>MTA-treated cells proliferated significantly faster than the other two groups (F = 1835.065, P < 0.01), while calcium hydroxide-treated cells grew slower than the control significantly (F = 1792.301, P < 0.01). The formation of mineralized nodules was found in both MTA-treated and calcium hydroxide-treated pulp cells. The number of mineralized nodules showed no significant difference between the two groups (P > 0.05). Either ALP or DSPP mRNA expression showed significant difference among the three groups (F = 349.651, P < 0.01; F = 1653.001, P < 0.01). MTA increased mRNA expression of ALP and DSPP in pulp cells (P < 0.01), whereas calcium hydroxide down-regulated them (P < 0.01).</p><p><b>CONCLUSIONS</b>MTA is more suitable than calcium hydroxide as pulp-capping agent in primary teeth.</p>