摘要:

AbstractEndothelial cells elaborate growth promoting activities in culture medium that support limited smooth muscle cell and fibroblast growth in vitro in the absence of serum. We investigated whether insulin‐like growth factor‐I (IGF‐I) was synthesized and secreted by bovine aortic endothelial cells in vitro. Subconfluent endothelial cell cultures in serum‐free medium secreted severalfold higher IGF‐I levels than confluent cultures by acid‐sizing chromatography and IGF‐I radioimmunoassay. The IGF‐I secretory level was not sustained during a second serum‐free incubation. In contrast, secretion of IGF binding proteins persisted and was maintained at constant levels throughout the same observation periods. Analysis of poly (A+)RNA by northern blots revealed hybridization of an IGF‐I cDNA to a 7.5‐ to 7.0‐kb transcript and superinduction of the 7.5–7.0‐kb mRNA by the translational inhibitor, cyclohexamide. However, no endogenously labeled IGF‐I was detected in conditioned media after incubation of cultures with [35S]cysteine or [3H]leucine. When cultures were incubated in the presence of serum supplemented with IGF‐I, subconfluent cultures sequestered and released more IGF‐I than confluent cultures. We concluded that the majority of IGF‐I secreted in vitro was sequestered

ISSN:0021-9541    

DOI:10.1002/jcp.1041540122

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY

摘要:

AbstractThe induction of apoptosis in leukemic cells by dexamethasone is well known, but the mechanism of this type of cell death and of dexamethasone resistance by some variants is still poorly understood. Apoptotic cell death is preceded by many changes in cellular properties, such as glucose metabolism, cell size, cell density, and others. In this study,19F‐NMR has been used to characterize changes in cell membrane potential and intracellular accessible volume during dexamethasone induced apoptosis. One dex‐sensitive (CEM‐C7) and three dex‐resistant variants (CEM‐C1, CEM‐ICR27, and CEM‐4R4) were examined. We have observed separate intracellular and extracellular resonances for trifluoroacetate and trifluoroacetamide added to suspended leukemic cells. From the equilibrium distribution of these fluoro‐compounds between intra and extracellular spaces, the changes in membrane potential and intracellular accessible volume were calculated. The membrane potential for CEM‐C7 cells was found to significantly decrease in the presence of dexamethasone (9‐mV decrease within 18 h of dexamethasone treatment), while that of CEM‐ICR27 was found in some samples to increase on dexamethasone incubation. The membrane potential for CEM‐C1 decreased slightly, while that of CEM‐4R4 was not appreciably affected by dexamethasone. The reduction of membrane potential seems to be an early step in the mechanism of dexamethasone induced apoptosis. Although the intracellular volume varied with cell type and dexamethasone incubation (for CEM‐C7), the fractional intracellular volume (α = Vin/Vcellwas found to be the same (0.82 ± 0.06) for all the cell lines in the presence and absence of dexameth

ISSN:0021-9541    

DOI:10.1002/jcp.1041540123

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY

摘要:

AbstractElevated cellular plasminogen activator activity has been associated with significant alterations in the in vitro phenotype of both malignant cell lines and nonmalignant endothelial cells. To examine the role of elevated cellular plasminogen activator activity in the production of altered endothelial cell behavior, bovine coronary artery endothelial cells were transduced with a retroviral vector expressing large amounts of tissue plasminogen activator. Cells transduced with the tissue plasminogen activator vector were compared with both untransduced cells and cells transduced with a control vector in a series of in vitro assays of cellular attachment, proliferation, migration, and invasion. The morphology of the 2 transduced populations was unchanged. There was a small decrease (5–15%) in the horizontal migration rate of both transduced cell populations, as compared with that of untransduced cells. No significant differences were detected among the three cell populations in any of the other assays. We conclude that expression of high levels of tissue plasminogen activator does not specifically affect endothelial cell phenotype in vitro. These data lend support to the hypothesis that elevated plasminogen activator activity is necessary but not sufficient to produce alterations in endothelial cell behavior. © 1993 Wiley‐Liss,

ISSN:0021-9541    

DOI:10.1002/jcp.1041540124

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY

ISSN:0021-9541    

DOI:10.1002/jcp.1041540101

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY