Invasion of Vascular Endothelium and Organ Tissue in Vitro by B16 Melanoma Variants

1986 ◽  
pp. 275-297 ◽  
Author(s):  
Garth L. Nicolson ◽  
Motowo Nakajima ◽  
Tatsuro Irimura
Keyword(s):  
Vascular Endothelium ◽  
B16 Melanoma ◽  
Organ Tissue

Interactions Between Blood Platelets and Vascular Endothelium in vitro Studies

1979 ◽  
Author(s):  
M.A. Gimbrone ◽  
K.D. Curwen ◽  
R. I. Handin
Keyword(s):  
Platelet Aggregation ◽  
Vascular Endothelium ◽  
Potent Inhibitor ◽  
Platelet Reactivity ◽  
Blood Platelets ◽  
Primary Cultures ◽  
Adenosine Diphosphate ◽  
Human Platelets ◽  
Platelet Adherence

Endothelial cells (EC) can actively influence the hemostatic response at sites of vascular injury through multiple mechanisms. For example, EC can degrade adenosine diphosphate, release plasminogen activator, and synthesize prostacyclin (PGI2), a potent inhibitor of platelet aggregation. We have examined whether PGI2 also might account for the normal lack of platelet adherence to the uninjured EC surface. In a monolayer adherence assay, radiolabeled human platelets in citrated plasma showed minimal interaction with primary cultures of human EC (<1 platelet adhering per cell). Platelets from aspirin-treated and untreated donors behaved similarly. However, aspirin pretreatment of EC consistently resulted in ~2-fold increases in platelet adherence which could be completely abolished by exogenous PGI2 (0.5–1.0 μg/ml). SV40-transformed human EC (SVHEC), which are deficient in PGI2 production compared to primary EC, showed 10-30 times more platelet adherence. Exogenous PGI2 produced a dose - related (.001-1.0 μg/ml) decrease in platelet adherence to SVHEC but did not result in the basal levels observed with normal EC monolayers. These data suggest that : 1) In addition to its effects on platelet aggregation, PGI2 can influence platelet endothelial cell interactions; 2) The increased platelet reactivity of transformed EC is associated with, but not completely attributable, to decreased PGI2 production; and 3) Factors other than PGI2 may play a role in the thromboresistance of normal vascular endothelium.

B16 melanoma secretomes and in vitro invasiveness: syntenin as an invasion modulator

2010 ◽  
Vol 20 (2) ◽  
pp. 77-84 ◽  
Author(s):  
Fabien Rondepierre ◽  
Bernadette Bouchon ◽  
Mathilde Bonnet ◽  
Nicole Moins ◽  
Jean M. Chezal ◽  
...  
Keyword(s):  
B16 Melanoma ◽  
In Vitro Invasiveness

Comparative Studies on Vascular Endothelium in vitro

Pathobiology ◽  
1995 ◽  
Vol 63 (2) ◽  
pp. 83-92 ◽  
Author(s):  
Christoph L. Klein ◽  
Fernando Bittinger ◽  
Holger K&ouml;hler ◽  
Mechthild Wagner ◽  
Mike Otto ◽  
...  
Keyword(s):  
Vascular Endothelium ◽  
Comparative Studies

Exercise effects on lung tumor metastases and in vitro alveolar macrophage antitumor cytotoxicity

1998 ◽  
Vol 274 (5) ◽  
pp. R1454-R1459 ◽  
Author(s):  
J. M. Davis ◽  
M. L. Kohut ◽  
D. A. Jackson ◽  
L. H. Colbert ◽  
E. P. Mayer ◽  
...  
Keyword(s):  
Alveolar Macrophage ◽  
Prolonged Exercise ◽  
Lung Tumor ◽  
Melanoma Cells ◽  
B16 Melanoma ◽  
Intravenous Injections ◽  
B16 Melanoma Cells ◽  
Strong Trend ◽  
Tumor Metastases

This study examined the effects of moderate and prolonged exercise on 1) lung tumor metastases and 2) alveolar macrophage antitumor response in vitro. C57Bl/6 mice were assigned to either Ex-30 (30-min run), Ex-F (run to fatigue), Ex-F-24 h (run to fatigue 24 h before tumor injection), or Con (rested in lanes above the treadmill). Mice received intravenous injections of syngeneic B16 melanoma cells 30 min postexercise. Lungs were removed 7 or 10 days later, and tumor foci were counted. Ex-F had fewer tumors than either Ex-30 or Con, whereas Ex-F-24 h also showed a strong trend toward fewer tumors. The initial localization of tumor cells in the lungs after injection was not different among groups. For the in vitro experiment, mice were killed immediately after exercise or 8 h later. Alveolar macrophages were removed and cultured in vitro with B16 melanoma cells. The growth of the tumors cultured with macrophages from Ex-F was lower than Con after exercise and, to a lesser extent, 8 h later. In Ex-30, this effect was only found immediately after exercise. The data suggest that prolonged exercise has a protective effect on lung tumor metastases and enhances alveolar macrophage antitumor cytotoxicity.

scholarly journals STAT3 Knockdown in B16 Melanoma by siRNA Lipopolyplexes Induces Bystander Immune Response In Vitro and In Vivo

2011 ◽  
Vol 4 (3) ◽  
pp. 178-188 ◽  
Author(s):  
Aws Alshamsan ◽  
Samar Hamdy ◽  
Azita Haddadi ◽  
John Samuel ◽  
Ayman O.S. El-Kadi ◽  
...  
Keyword(s):  
Immune Response ◽  
B16 Melanoma ◽  
Immune Response In Vitro

scholarly journals Radiocontrast agents induce endothelin release in vivo and in vitro.

1992 ◽  
Vol 3 (1) ◽  
pp. 58-65 ◽  
Author(s):  
S N Heyman ◽  
B A Clark ◽  
N Kaiser ◽  
K Spokes ◽  
S Rosen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Plasma Concentration ◽  
Plasma Level ◽  
Vascular Endothelium ◽  
Radiocontrast Agent ◽  
Transient Rise ◽  
Bovine Endothelial Cells ◽  
Radiocontrast Agents

The intravascular administration of the ionic radiocontrast agent sodium iothalamate (2.9 g of iodine/kg body wt) to rats induced an increase in plasma concentration of immunoreactive endothelin from 21.3 +/- 1.2 to 36 +/- 3 fmol/mL, preceded by a transient rise in the plasma level of atrial natriuretic peptide and associated with a fall in RBF. Equi-iodine amounts of the nonionic agents ioxaglate and iohexol elicited similar or more marked changes in plasma endothelin, but hypertonic solutions of NaCl, mannitol, or glucose did not. Comparable levels of endothelin produced by infusions of endothelin-1 induced a reduction of up to 29% in RBF. Iothalamate and iohexol stimulated endothelin release from cultured bovine endothelial cells, suggesting a direct effect of ionic and nonionic agents on vascular endothelium. The data invite speculation that under some circumstances endothelin release might play a role in the circulatory changes caused by these compounds and in the pathogenesis of radiocontrast nephropathy.

scholarly journals Deciphering Repertoire of B16 Melanoma Reactive TCRs by Immunization, In Vitro Restimulation and Sequencing of IFNγ-Secreting T Cells

2021 ◽  
Vol 22 (18) ◽  
pp. 9859
Author(s):  
Anna V. Izosimova ◽  
Diana V. Yuzhakova ◽  
Valeria D. Skatova ◽  
Lilia N. Volchkova ◽  
Elena V. Zagainova ◽  
...  
Keyword(s):  
Cell Receptor ◽  
B16 Melanoma ◽  
Adoptive Cell Transfer ◽  
Limiting Factors ◽  
Great Promise ◽  
T Helper ◽  
Cell Therapies ◽  
Optimized Protocol ◽  
Tumor Specificity

Recent advances in cancer immunotherapy have great promise for the treatment of solid tumors. One of the key limiting factors that hamper the decoding of physiological responses to these therapies is the inability to distinguish between specific and nonspecific responses. The identification of tumor-specific lymphocytes is also the most challenging step in cancer cell therapies such as adoptive cell transfer and T cell receptor (TCR) cloning. Here, we have elaborated a protocol for the identification of tumor-specific T lymphocytes and the deciphering of their repertoires. B16 melanoma engraftment following anti-PD1 checkpoint therapy provides better antitumor immunity compared to repetitive immunization with heat-shocked tumor cells. We have also revealed that the most error-prone part of dendritic cell (DC) generation, i.e., their maturation step, can be omitted if DCs are cultured at a sufficiently high density. Using this optimized protocol, we have achieved a robust IFNγ response to B16F0 antigens, but only within CD4+ T helper cells. A comparison of the repertoires of IFNγ-positive and -negative cells shows a prominent enrichment of certain clones with putative tumor specificity among the IFNγ+ fraction. In summary, our optimized protocol and the data provided here will aid in the acquisition of broad statistical data and the creation of a meaningful database of B16-specific TCRs.

scholarly journals Protection of the vascular endothelium in experimental situations

2011 ◽  
Vol 4 (1) ◽  
pp. 20-26 ◽  
Author(s):  
Ružena Sotníková ◽  
Jana Nedelčevová ◽  
Jana Navarová ◽  
Viera Nosáľová ◽  
Katarína Drábiková ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vascular Endothelium ◽  
Vascular Dysfunction ◽  
Antioxidant Properties ◽  
Pharmacological Intervention ◽  
Ros Production ◽  
Nitric Oxide Radical ◽  
Endothelium Dependent Relaxation

Protection of the vascular endothelium in experimental situationsOne of the factors proposed as mediators of vascular dysfunction observed in diabetes is the increased generation of reactive oxygen species (ROS). This provides support for the use of antioxidants as early and appropriate pharmacological intervention in the development of late diabetic complications. In streptozotocin (STZ)-induced diabetes in rats we observed endothelial dysfuction manifested by reduced endothelium-dependent response to acetylcholine of the superior mesenteric artery (SMA) and aorta, as well as by increased endothelaemia. Changes in endothelium-dependent relaxation of SMA were induced by injury of the nitric oxide radical (·NO)-signalling pathway since the endothelium-derived hyperpolarising factor (EDHF)-component of relaxation was not impaired by diabetes. The endothelial dysfunction was accompanied by decreased ·NO bioavailabity as a consequence of reduced activity of eNOS rather than its reduced expression. The results obtained using the chemiluminiscence method (CL) argue for increased oxidative stress and increased ROS production. The enzyme NAD(P)H-oxidase problably participates in ROS production in the later phases of diabetes. Oxidative stress was also connected with decreased levels of reduced glutathione (GSH) in the early phase of diabetes. After 10 weeks of diabetes, adaptational mechanisms probably took place because GSH levels were not changed compared to controls. Antioxidant properties of SMe1EC2 foundin vitrowere partly confirmedin vivo.Administration of SMe1EC2 protected endothelial function. It significantly decreased endothelaemia of diabetic rats and improved endothelium-dependent relaxation of arteries, slightly decreased ROS-production and increased bioavailability of ·NO in the aorta. Further studies with higher doses of SMe1EC2 may clarify the mechanism of its endothelium-protective effectin vivo.

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