Effect of colcemid on cell migration, mitosis, and DNA synthesis in mouse embryonic fibroblast cultures

1972 ◽  
Vol 73 (6) ◽  
pp. 706-708
Author(s):  
V. I. Gel'shtein ◽  
A. A. Stavrovskaya
2010 ◽  
Vol 3 (1) ◽  
pp. 8-14 ◽  
Author(s):  
Liyuan Li ◽  
Chikezie O. Madu ◽  
Andrew Lu ◽  
Yi Lu

Hypoxia-inducible factor-1α (HIF-1α) is known as a transactivator for VEGF gene promoter. It can be induced by hypoxia. However, no study has been done so far to dissect HIF-1α-mediated effects from hypoxia or VEGF-mediated effects. By using a HIF-1α knockout (HIF-1α KO) cell system in mouse embryonic fibroblast (MEF) cells, this study analyzes cell migration and HIF-1α, hypoxia and VEGF activation. A hypoxia-mediated HIF-1α induction and VEGF transactivation were observed: both HIF-1α WT lines had significantly increased VEGF transactivation, as an indicator for HIF-1α induction, in hypoxia compared to normoxia; in contrast, HIF-1α KO line had no increased VEGF transactivation under hypoxia. HIF-1α promotes cell migration: HIF-1α-KO cells had a significantly reduced migration compared to that of the HIF-1α WT cells under both normoxia and hypoxia. The significantly reduced cell migration in HIF-1α KO cells can be partially rescued by the restoration of WT HIF-1α expression mediated by adenoviral-mediated gene transfer. Interestingly, hypoxia has no effect on cell migration: the cells had a similar cell migration rate under hypoxic and normoxic conditions for both HIF-1α WT and HIF-1α KO lines, respectively. Collectively, these data suggest that HIF-1α plays a role in MEF cell migration that is independent from hypoxia-mediated effects.


2020 ◽  
Vol 47 (7) ◽  
pp. 5377-5383
Author(s):  
Şehnaz Yilmaz ◽  
Oguz Yoldas ◽  
Aysin Dumani ◽  
Gizem Guler ◽  
Seda Ilgaz ◽  
...  

2020 ◽  
Vol 13 (12) ◽  
pp. 450
Author(s):  
Fatima Bianca A. Dessouki ◽  
Rakesh C. Kukreja ◽  
Dinender K. Singla

Doxorubicin (Dox)-induced muscle toxicity (DIMT) is a common occurrence in cancer patients; however, the cause of its development and progression is not established. We tested whether inflammation-triggered cell death, “pyroptosis” plays a role in DIMT. We also examined the potential role of exosomes derived from embryonic stem cells (ES-Exos) in attenuating DIMT. C57BL/6J mice (10 ± 2 wks age) underwent the following treatments: Control (saline), Dox, Dox+ES-Exos, and Dox+MEF-Exos (mouse-embryonic fibroblast-derived exosomes, negative control). Our results demonstrated that Dox significantly reduced muscle function in mice, which was associated with a significant increase in NLRP3 inflammasome and initiation marker TLR4 as compared with controls. Pyroptosis activator, ASC, was significantly increased compared to controls with an upregulation of specific markers (caspase-1, IL-1β, and IL-18). Treatment with ES-Exos but not MEF-Exos showed a significant reduction in inflammasome and pyroptosis along with improved muscle function. Additionally, we detected a significant increase in pro-inflammatory cytokines (TNF-α and IL-6) and inflammatory M1 macrophages in Dox-treated animals. Treatment with ES-Exos decreased M1 macrophages and upregulated anti-inflammatory M2 macrophages. Furthermore, ES-Exos showed a significant reduction in muscular atrophy and fibrosis. In conclusion, these results suggest that DIMT is mediated through inflammation and pyroptosis, which is attenuated following treatment with ES-Exos.


FEBS Letters ◽  
2013 ◽  
Vol 587 (14) ◽  
pp. 2112-2117 ◽  
Author(s):  
Bai-Wei Gu ◽  
Jingping Ge ◽  
Jian-Meng Fan ◽  
Monica Bessler ◽  
Philip J. Mason

2015 ◽  
Vol 35 (5) ◽  
Author(s):  
Peng Chen ◽  
Jian-Feng Yao ◽  
Rong-Fu Huang ◽  
Fang-Fang Zheng ◽  
Xiao-Hong Jiang ◽  
...  

BIX-01294 (a diazepin-quinazolin-amine derivative) has important biological effects and its epigenetic regulation at imprinting control regions is highly complex. BIX-01294 may reduce global H3K9me2 levels and affect epigenetic modifications of small nuclear ribonucleoprotein N (Snrpn) in MEFs.


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