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51.
Lee OK Ko YC Kuo TK Chou SH Li HJ Chen WM Chen TH Su Y 《Journal of cellular biochemistry》2004,93(5):917-928
Recent studies have shown that statins, the most potent inhibitors of 3-hydroxy-2-methylglutaryl coenzyme A (HMG-CoA) reductase, stimulate bone formation in vitro and in rodents by activating the expression of bone morphogenetic protein-2 (BMP-2), one of the most critical osteoblast differentiation-inducing factors. However, the effect of statins on mesenchymal stem cells (MSCs) is yet to be reported. The purpose of this study is to investigate the influence of fluvastatin, lovastatin, and pravastatin, three commonly prescribed lipid-lowering agents, on the proliferation and differentiation of human MSCs. To our surprise, even though fluvastatin and lovastatin effectively suppressed the growth of human MSCs, a neuroglia rather than osteoblast-like morphology was observed after treatment. Interestingly, such morphological change was inhibited by the co-addition of geranylgeranyl pyrophosphate (GGPP). Immunofluorescence staining with antibodies against neuron-, astrocyte-, as well as oligodendrocyte-specific markers confirmed the neuroglial identity of the differentiated cells. However, BMP-2 is unlikely to play a positive role in neuroglial differentiation of MSCs since its expression was down-regulated in fluvastatin-treated cells. Taken together, our results suggest that fluvastatin and lovastatin induce neuroglial differentiation of human MSCs and that these cholesterol-lowering agents might be used in conjunction with MSC transplantation in the future for treating neurological disorders and injuries. 相似文献
52.
Chang WW Yu CY Lin TW Wang PH Tsai YC 《Biochemical and biophysical research communications》2006,341(2):614-619
The transfer of sialic acids to the non-reducing terminal positions on sugar chains of glycoconjugates is catalyzed by sialyltransferases (STs). Increased sialylation is correlated with oncogenic transformation and metastatic potential. ST inhibitors may be potentially valuable as anti-cancer and anti-metastatic agents. In this study, we evaluated the effects of soyasaponin I (Ssa I), a known inhibitor of STs, on tumor metastasis through studying a highly metastatic cancer cell line B16F10. Ssa I specifically inhibited the expression of alpha2,3-linked sialic acids without affecting other glycans on the B16F10 cell surface. We also found that Ssa I decreased the migratory ability of cells, enhanced cell adhesion to extracellular matrix proteins. Finally, a pulmonary metastasis assay demonstrated that alteration of glycosylation in this way significantly reduced the ability of tumor cells to distribute to the lungs of mice. Collectively, these findings suggested that alpha2,3-linked sialic acids may play an important role in metastasis potential of B16F10 cells. 相似文献
53.
Wen-Cheng Chen Yi-Shiuan Tzeng Hung Li Wei-Sheng Tien Ying-Chieh Tsai 《Cell and tissue research》2010,342(1):75-85
Stromal-derived factor (SDF)-1/CXCL12 is a cytokine that is involved in organogenesis, hematopoiesis, chemoattraction, and
wound healing. An SDF-1 knockout mouse (SDF-1-/-) has provided important insights into the role of SDF-1 in fetal development. Because the SDF-1 knockout is lethal in the
perinatal period, we have created a conditional SDF-1 knockout mouse. In the present study, we induced conditionally knocked
out SDF-1 in neonatal mice and found that lung development was compromised; neonatal lungs showed increased alveolar airspace
and abnormal ultrastructure. Conditional knockout of SDF-1 in adult mice resulted in an emphysemic morphology, with increased
alveolar airspace and thickened alveolar septa. Fluorescence angiography showed pulmonary vessel hyperdilation. To determine
whether the hyperdilation involved nitric oxide, we inhibited endothelial nitric oxide synthase (eNOS) with N (G)-nitro-L-
arginine methyl ester. This resulted in the inhibition of pulmonary vessel hyperdilation. Western blot results showed increased
phosphorylation of eNOS in our induced SDF-1 knockout mice, indicating that eNOS is normally repressed in the presence of
SDF-1, and that activation of eNOS contributes to pulmonary pathology. Thus, a conditional knockout mouse has been successsfully
created for SDF-1; initial characterization indicates that SDF-1 is intimately involved in lung development and physiology. 相似文献