The Cell Cycle in the Central Nervous System

2006 ◽  
Keyword(s):  
Cell Cycle ◽  
Central Nervous System ◽  
Nervous System ◽  
The Central Nervous System

scholarly journals Conditional Mutation of Rb Causes Cell Cycle Defects without Apoptosis in the Central Nervous System

2003 ◽  
Vol 23 (3) ◽  
pp. 1044-1053 ◽  
Author(s):  
D. MacPherson ◽  
J. Sage ◽  
D. Crowley ◽  
A. Trumpp ◽  
R. T. Bronson ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Central Nervous System ◽  
Nervous System ◽  
Muscle Development ◽  
Brain Size ◽  
Targeted Disruption ◽  
Show Evidence ◽  
The Central Nervous System ◽  
P53 Activation ◽  
Phase Entry

ABSTRACT Targeted disruption of the retinoblastoma gene in mice leads to embryonic lethality in midgestation accompanied by defective erythropoiesis. Rb −/− embryos also exhibit inappropriate cell cycle activity and apoptosis in the central nervous system (CNS), peripheral nervous system (PNS), and ocular lens. Loss of p53 can prevent the apoptosis in the CNS and lens; however, the specific signals leading to p53 activation have not been determined. Here we test the hypothesis that hypoxia caused by defective erythropoiesis in Rb-null embryos contributes to p53-dependent apoptosis. We show evidence of hypoxia in CNS tissue from Rb −/− embryos. The Cre-loxP system was then used to generate embryos in which Rb was deleted in the CNS, PNS and lens, in the presence of normal erythropoiesis. In contrast to the massive CNS apoptosis in Rb-null embryos at embryonic day 13.5 (E13.5), conditional mutants did not have elevated apoptosis in this tissue. There was still significant apoptosis in the PNS and lens, however. Rb −/− cells in the CNS, PNS, and lens underwent inappropriate S-phase entry in the conditional mutants at E13.5. By E18.5, conditional mutants had increased brain size and weight as well as defects in skeletal muscle development. These data support a model in which hypoxia is a necessary cofactor in the death of CNS neurons in the developing Rb mutant embryo.

Multiparameter Flow Cytometric Analysis of Neoplasms of the Central Nervous System: Correlation of Nuclear Antigen p105 and DNA Content with Clinical Behavior

Neurosurgery ◽  
1990 ◽  
Vol 27 (1) ◽  
pp. 83-96 ◽  
Author(s):  
Alan J. Appley ◽  
Patrick L. Fitzgibbons ◽  
Parakrama T. Chandrasoma ◽  
David R. Hinton ◽  
Michael L. J. Apuzzo
Keyword(s):  
Cell Cycle ◽  
Central Nervous System ◽  
Nervous System ◽  
Dna Content ◽  
Proliferative Activity ◽  
Pituitary Tumors ◽  
Nuclear Antigen ◽  
Clinical Behavior ◽  
The Central Nervous System ◽  
Well Differentiated

Abstract Analysis of the DNA content of various solid tumors and hematological malignancies may provide useful prognostic information. To date, however, there has been a striking lack of correlation between DNA content in neoplasms of the central nervous system and clinical behavior. Simultaneous quantitation of DNA content and proliferation-associated nuclear antigen (p105) by flow cytometry was performed on paraffin-embedded tissues representing three major groups of central nervous system neoplasms—1) 21 astrocytic tumors, 2) 13 pituitary tumors, and 3) 19 meningiomas-and the results were correlated with clinical behavior. All 4 well-differentiated gliomas were diploid, while 3 of 9 anaplastic astrocytomas and 1 of 8 glioblastomas had a demonstrable aneuploid peak. Three of 13 pituitary tumors had an identifiable aneuploid peak, while only 2 of 19 meningiomas had an aneuploid DNA content. Cell-cycle analysis of the malignant gliomas revealed a significantly higher proliferative index (PI, %S + G2M) compared with the well-differentiated astrocytomas (P< 0.05). Within the subgroup of diploid anaplastic astrocytomas, however, extended patient survival appeared to be associated with a higher PI. For diploid pituitary adenomas, the PI was consistently lower in the 3 tumors that recurred than it was in the remaining 8 adenomas. Nuclear antigen quantitation of diploid tumors showed a wide range of p105 expression in G0G1cells, suggesting that, within each tumor, the cells are heterogeneous with respect to proliferative activity. Aneuploid nuclei of glial tumors showed enhanced expression of p105 relative to diploid cells of the same specimen. In pituitary tumors, the median G2M/G0G1fluorescence ratio for p105 was significantly higher (P< 0.05) for the 3 diploid recurrent tumors than for those that did not recur. These data support the assumption that the aggressive clinical course of malignant glial neoplasms may be related to an abnormal DNA stemline and/or an alteration in cell proliferative activity. Cell cycle analysis and measurement of p105 by this technique may provide information useful from both a prognostic standpoint and in directing adjuvant therapy.

scholarly journals Control of proliferation activation in quiescent neuroblasts of the Drosophila central nervous system

Development ◽  
1995 ◽  
Vol 121 (4) ◽  
pp. 1173-1182 ◽  
Author(s):  
S. Datta
Keyword(s):  
Cell Cycle ◽  
Central Nervous System ◽  
Nervous System ◽  
Spatial And Temporal Patterns ◽  
Larval Brain ◽  
Cycle Arrest ◽  
Dividing Cells ◽  
The Central Nervous System ◽  
Neuroblast Proliferation ◽  
Dependent Pathway

Stem cell proliferation is controlled through cell cycle arrest and activation. In the central nervous system of Drosophila melanogaster, neuroblast quiescence and activation takes place in defined spatial and temporal patterns. Two genes have been identified that regulate the pattern of neuroblast quiescence and proliferation. ana, which has been previously described by Ebens and coworkers (Ebens, A., Garren, H., Cheyette, B. N. R. and Zipursky, S. L. (1993). Cell 74, 15–28), encodes a secreted glial glycoprotein that inhibits premature neuroblast proliferation. We previously showed that trolsd causes a dramatic drop in the number of dividing cells in the larval brain late in development. This study presents evidence that this decrease results from a failure to activate proliferation in the quiescent neuroblast population at the appropriate time. However, trolsd does not affect the maintenance of cell division in already dividing mushroom body neuroblasts. The quiescent optic lobe and thoracic neuroblasts affected by trolsd proliferate in a trol mutant background if they have been activated by a lack of the ana proliferation repressor, demonstrating that trolsd does not affect cellular viability, nor does trol represent a celltype-specific mitotic factor. This also shows that trol acts downstream of ana to activate proliferation of quiescent neuroblasts in an ana-dependent pathway, possibly by inactivating or bypassing the ana repressor. These results suggest that trol and ana are components of a novel developmental pathway for the control of cell cycle activation in quiescent neuroblasts.

Effects of Hyperoxia on Lung Utrastructure

1970 ◽  
Vol 28 ◽  
pp. 26-27
Author(s):  
Gladys Harrison
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Light Microscopy ◽  
Oxygen Effects ◽  
Age Dependent ◽  
The Central Nervous System ◽  
The Subject ◽  
Space Age ◽  
Alveolar Septa ◽  
Extensive Damage

With the advent of the space age and the need to determine the requirements for a space cabin atmosphere, oxygen effects came into increased importance, even though these effects have been the subject of continuous research for many years. In fact, Priestly initiated oxygen research when in 1775 he published his results of isolating oxygen and described the effects of breathing it on himself and two mice, the only creatures to have had the “privilege” of breathing this “pure air”.Early studies had demonstrated the central nervous system effects at pressures above one atmosphere. Light microscopy revealed extensive damage to the lungs at one atmosphere. These changes which included perivascular and peribronchial edema, focal hemorrhage, rupture of the alveolar septa, and widespread edema, resulted in death of the animal in less than one week. The severity of the symptoms differed between species and was age dependent, with young animals being more resistant.

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