scholarly journals The C60(FeCp2)2-Based Cell Proliferation Accelerator

2013 ◽  
Vol 2013 ◽  
pp. 1-4 ◽  
Author(s):  
Andrei Soldatov ◽  
Edward Shpilevsky ◽  
Vitaliy Goranov ◽  
Vladimir Kulchitsky ◽  
Floriana Tuna

We studied structural and magnetic proprieties of the fulleride C60(FeCp2)2. The influence of fulleride particles on the cell proliferative activity was also investigated. We found that the proliferative activity of the RINmF5 cells increases (53% versus control) in presence of the C60(FeCp2)2nanosized particles. Moreover, it was registered that the cell culture became multilayered and secreted basophile matrix.

2013 ◽  
Vol 2013 ◽  
pp. 1-5 ◽  
Author(s):  
B. Yahaya ◽  
G. McLachlan ◽  
D. D. S. Collie

The response of S-phase cells labelled with bromodeoxyuridine (BrdU) in sheep airways undergoing repair in response to endobronchial brush biopsy was investigated in this study. Separate sites within the airway tree of anaesthetised sheep were biopsied at intervals prior to pulse labelling with BrdU, which was administered one hour prior to euthanasia. Both brushed and spatially disparate unbrushed (control) sites were carefully mapped, dissected, and processed to facilitate histological analysis of BrdU labelling. Our study indicated that the number and location of BrdU-labelled cells varied according to the age of the repairing injury. There was little evidence of cell proliferation in either control airway tissues or airway tissues examined six hours after injury. However, by days 1 and 3, BrdU-labelled cells were increased in number in the airway wall, both at the damaged site and in the regions flanking either side of the injury. Thereafter, cell proliferative activity largely declined by day 7 after injury, when consistent evidence of remodelling in the airway wall could be appreciated. This study successfully demonstrated the effectiveness ofin vivopulse labelling in tracking cell proliferation during repair which has a potential value in exploring the therapeutic utility of stem cell approaches in relevant lung disease models.


2021 ◽  
Vol 23 (Supplement_2) ◽  
pp. ii22-ii22
Author(s):  
V Kolesnikova ◽  
N Samoylenkova ◽  
S Drozd ◽  
A Revishchin ◽  
D Y Usachev ◽  
...  

Abstract BACKGROUND According to one of the theories, gliomas can occur as a result of dysregulation of stem cell division in the subventricular region of the brain. The CD133 membrane marker is a characteristic of both normal and tumor neural stem cells therefore it can be used to isolate a stem cell population from tumor tissue. Tumor cells actively proliferate which suggests that their possible differentiation may be achieved by inhibiting of their division as these two processes are mutually exclusive. For this purpose, G-quadruplex oligonucleotides together with neural-inducers such as a brain-derived neurotrophic factor (BDNF) may be used. MATERIAL AND METHODS Five cell cultures obtained from human glioblastoma tissues were analyzed for expression of CD133 using RT-qPCR. From cell culture with the highest level of CD133 using immunomagnetic separation CD133+ and CD133- cultures were received. CD133fr/peGFP-c1 recombinant DNA consisted of a CD133 second extracellular loop fragment and a peGFP-c1 vector was constructed to determine the localization of prominin-1, that is known as CD133 when found on cell membrane, using confocal microscopy. On chosen cell cultures an oligonucleotide bi-(AID-1-T) and its combination with BDNF were tested. The mechanism of GQ’s action is cytostatic and its non-toxicity properties were proved by flow cytometry. For evaluating the proliferative activity of cells MTT assay was performed on 10th and 20th days after exposure to the factors. RESULTS Cell culture G01 was chosen for further research as it had the highest level of the CD133. Colocalization of CD133 and GFP demonstrated a membrane localization of CD133 in cells with high expression level of this marker. MTT assay on 10th day after exposure to bi-(AID-1-T) as well as its combination with BDNF on cell culture G01 CD133- showed total inhibition of cell proliferation. The same combinations tested on G01 CD133+ cell culture demonstrated no difference in proliferative activity. After 20 days after exposure to bi-(AID-1-T) and combination of bi-(AID-1-T) with BDNF the significant decrease of G01 CD133+ cells’ proliferation was observed. When tested on whole glioblastoma cell culture G01 these combinations also showed significant inhibition of cell proliferation. CONCLUSION We showed that glioblastoma cells upon transfection with recombinant DNA, that contains a fragment of CD133, mainly have a membrane localization of this marker. It was observed that CD133+ cells are more stable to external influence that can be a proof of the fact that CD133 is charactered for glioblastoma stem cells. We tested the effect of an GQ bi-(AID-1-T) and its combination with BDNF and showed that BDNF is necessary for blocking proliferation of glioblastoma cells. Altogether, the results may be used for further research as it reveals a potential treatment for patients with glioblastoma. Grant №075-15-2020-809 (13.1902.21.0030).


2015 ◽  
Vol 30 (1) ◽  
pp. 120-127 ◽  
Author(s):  
Binh Cao Quan Nguyen ◽  
Nozomi Taira ◽  
Hiroshi Maruta ◽  
Shinkichi Tawata

1999 ◽  
Vol 112 (10) ◽  
pp. 1599-1609 ◽  
Author(s):  
B.M. Kraling ◽  
D.G. Wiederschain ◽  
T. Boehm ◽  
M. Rehn ◽  
J.B. Mulliken ◽  
...  

Vessel maturation during angiogenesis (the formation of new blood vessels) is characterized by the deposition of new basement membrane and the downregulation of endothelial cell proliferation in the new vessels. Matrix remodeling plays a crucial, but still poorly understood role, in angiogenesis regulation. We present here a novel assay system with which to study the maturation of human capillary endothelial cells in vitro. When human dermal microvascular endothelial cells (HDMEC) were cultured in the presence of dibutyryl cAMP (Bt2) and hydrocortisone (HC), the deposition of a fibrous lattice of matrix molecules consisting of collagens type IV, type XVIII, laminin and thrombospondin was induced. In basal medium (without Bt2 and HC), HDMEC released active matrix metalloproteinases (MMPs) into the culture medium. However, MMP protein levels were significantly reduced by treatment with Bt2 and HC, while protein levels and activity of endogenous tissue inhibitor of MMPs (TIMP) increased. This shift in the proteolytic balance and matrix deposition was inhibited by the specific protein kinase A inhibitors RpcAMP and KT5720 or by substituting analogues without reported glucocorticoid activity for HC. The addition of MMP inhibitors human recombinant TIMP-1 or 1,10-phenanthroline to cultures under basal conditions induced matrix deposition in a dose-dependent manner, which was not observed with the serine protease inhibitor epsilon-amino-n-caproic acid (ACA). The deposited basement membrane-type of matrix reproducibly suppressed HDMEC proliferation and increased HDMEC adhesion to the substratum. These processes of matrix deposition and downregulation of endothelial cell proliferation, hallmarks of differentiating new capillaries in the end of angiogenesis, were recapitulated in our cell culture system by decreasing the matrix-degrading activity. These data suggest that our cell culture assay provides a simple and feasible model system for the study of capillary endothelial cell differentiation and vessel maturation in vitro.


2001 ◽  
Vol 51 (11) ◽  
pp. 853-860 ◽  
Author(s):  
Aihua Li ◽  
Masamichi Goto ◽  
Michiko Horinouchi ◽  
Sadao Tanaka ◽  
Kohzoh Imai ◽  
...  

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