scholarly journals Overexpression of UCP2 Protects Thalamic Neurons following Global Ischemia in the Mouse

2008 ◽  
Vol 28 (6) ◽  
pp. 1186-1195 ◽  
Author(s):  
Tomas Deierborg Olsson ◽  
Tadeusz Wieloch ◽  
Sabrina Diano ◽  
Craig H Warden ◽  
Tamas L Horvath ◽  
...  
Keyword(s):  
Cell Death ◽  
Neuronal Damage ◽  
Uncoupling Protein ◽  
Global Ischemia ◽  
Thalamic Nuclei ◽  
Global Brain Ischemia ◽  
Ucp2 Expression ◽  
Extensive Cell Death ◽  
Extensive Cell ◽  
Global Brain

Uncoupling protein 2 (UCP2) is upregulated in the brain after sublethal ischemia, and overexpression of UCP2 is neuroprotective in several models of neurodegenerative disease. We investigated if increased levels of UCP2 diminished neuronal damage after global brain ischemia by subjecting mice overexpressing UCP2 (UCP2/3tg) and wild-type littermates (wt) to a 12-min global ischemia. The histopathological outcome in the cortex, hippocampus, striatum, and thalamus was evaluated at 4 days of recovery, allowing maturation of the selective neuronal death. Global ischemia led to extensive cell death in the striatum, thalamus, and in the CA1 and CA2, and less-pronounced cell death in the CA3 and dentate gyrus (DG) hippocampal subfields. Histologic damage was significantly lower in the ventral posterolateral VPL and medial VPM thalamic nuclei in UCP2/3tg animals compared with wt. These thalamic regions showed a larger increase in UCP2 expression in UCP2/3tg compared with wt animals relative to the nonprotected DG. In the other regions studied, the histologic damage was lower or equal in UCP2/3tg animals compared with wt. Consequently, neuroprotection in the thalamus correlated with a high expression of UCP2, which is neuroprotective in a number of models of neurodegenerative diseases.

Neuroprotection and Enhancement of Spatial Memory by Herbal Mixture HT008-1 in Rat Global Brain Ischemia Model

2008 ◽  
Vol 36 (02) ◽  
pp. 287-299 ◽  
Author(s):  
Yun Tai Kim ◽  
Youn-Ju Yi ◽  
Mi-Yeon Kim ◽  
Youngmin Bu ◽  
Zhen Hua Jin ◽  
...  
Keyword(s):  
Spatial Memory ◽  
Brain Ischemia ◽  
Neuronal Damage ◽  
Memory Function ◽  
Neuronal Cell ◽  
Memory Deficit ◽  
Global Brain Ischemia ◽  
Herbal Mixture ◽  
Y Maze ◽  
Global Brain

To investigate whether HT008-1, a prescription used in traditional Korean medicine to treat mental and physical weakness, has a neuroprotective effect on a rat model of global brain ischemia and an enhancing effect against memory deficit following ischemia. Global brain ischemia was induced for 10 min by using 4-vessel occlusion (4-VO). HT008-1 was orally administered at doses of 30, 100, and 300 mg/kg respectively twice at 0 and 90 min after ischemia. The effect on memory deficit was investigated by using a Y-maze neurobehavioral test 4 days after brain ischemia, and the effect on neuronal damage was measured 7 days after ischemia. The mechanism of action was studied immunohistochemically using an anti-CD11b (OX-42) antibody. The oral administration of HT008-1 at 100 and 300 mg/kg significantly reduced hippocampal neuronal cell death by 49% and 53%, respectively, compared with a vehicle-treated group, and also improved spatial memory function in the Y-maze test. Immunohistochemically, HT008-1 inhibited OX-42 expression in the hippocampus. The effects of HT008-1 were more pronounced than those of its individual herb components. The herbal mixture HT008-1 protects the most vulnerable CA1 pyramidal cells of the hippocampus and enhances spatial memory function against global brain ischemia; an anti-inflammatory effect may be one of the mechanisms of action.

scholarly journals Cells differentiating into neuroectoderm undergo apoptosis in the absence of functional retinoblastoma family proteins.

1995 ◽  
Vol 129 (3) ◽  
pp. 779-788 ◽  
Author(s):  
R S Slack ◽  
I S Skerjanc ◽  
B Lach ◽  
J Craig ◽  
K Jardine ◽  
...  
Keyword(s):  
Cell Death ◽  
P19 Cells ◽  
Adenovirus E1a ◽  
Genes Encoding ◽  
Extensive Cell Death ◽  
Extensive Cell ◽  
Early Mouse ◽  
Dying Cells ◽  
Related Proteins ◽  
E1a Protein

The retinoblastoma (RB) protein is present at low levels in early mouse embryos and in pluripotent P19 embryonal carcinoma cells; however, the levels of RB rise dramatically in neuroectoderm formed both in embryos and in differentiating cultures of P19 cells. To investigate the effect of inactivating RB and related proteins p107 and p130, we transfected P19 cells with genes encoding mutated versions of the adenovirus E1A protein that bind RB and related proteins. When these E1A-expressing P19 cells were induced to differentiate into neuroectoderm, there was a striking rise in the expression of c-fos and extensive cell death. The ultrastructural and biochemical characteristics of the dying cells were indicative of apoptosis. The dying cells were those committed to the neural lineages because neurons and astrocytes were lost from differentiating cultures. Cell death was dependent on the ability of the E1A protein to bind RB and related proteins. Our results suggest that proteins of the RB family are essential for the development of the neural lineages and that the absence of functional RB activity triggers apoptosis of differentiating neuroectodermal cells.

The development of fused− embryos of Drosophila melanogaster

Development ◽  
1985 ◽  
Vol 87 (1) ◽  
pp. 99-114
Author(s):  
Alfonso Martinez-Arias
Keyword(s):  
Cell Death ◽  
Drosophila Melanogaster ◽  
Embryonic Development ◽  
Mature Embryo ◽  
Lethal Mutations ◽  
Extensive Cell Death ◽  
Extensive Cell ◽  
Secondary Consequence

The mutant fused (1–59·5) belongs to a class of lethal mutations in Drosophila melanogaster that produce pattern duplications in every segment of the mature embryo. A study of the embryonic development of fused'− embryos derived horn fused− mothers shows that extensive cell death occurs early in development. This cell death accounts for the smaller size of the segments in fused− embryos. The pattern duplication observed is, probably, a secondary consequence of the pattern deletion.

scholarly journals Uncoupled Cerebral Blood Flow and Metabolism after Severe Global Ischemia in Rats

1992 ◽  
Vol 12 (5) ◽  
pp. 802-808 ◽  
Author(s):  
Narendra C. Singh ◽  
Patrick M. Kochanek ◽  
Joanne K. Schiding ◽  
John A. Melick ◽  
Edwin M. Nemoto
Keyword(s):  
Blood Flow ◽  
Cardiac Arrest ◽  
Cerebral Blood Flow ◽  
Brain Ischemia ◽  
Global Ischemia ◽  
Global Brain Ischemia ◽  
Sagittal Sinus ◽  
Postischemic Period ◽  
Baseline Values ◽  
Global Brain

In a rat model of complete global brain ischemia (neck tourniquet) lasting either 3 min or 20 min, we monitored global CBF (sagittal sinus H2 clearance) and CMRO2 for 6 h to test the hypothesis that delayed postischemic hyperemia and uncoupling of CBF and CMRO2 occur depending on the severity of the insult. Early postischemic hyperemia occurred in both the 3-min and 20-min groups ( p < 0.05 vs. baseline values) and resolved by 15 min. Hypoperfusion occurred in the 3-min group between 15 and 60 min postischemia (≈23% reduction), and in the 20-min group from 15 to 120 min postischemia (≈50% reduction) ( p < 0.05), and then resolved. CMRO2 was not significantly different from baseline at any time after ischemia in the 3-min group. After 20 min of ischemia, however, CMRO2 was decreased (≈60%) throughout the postischemic period ( p < 0.05). At 5 min after ischemia, CBF/CMRO2 was increased in both groups but returned to baseline from 60 to 120 min postischemia. In the 3-min group, CBF/CMRO2 remained at baseline throughout the rest of the experiment. However, in the 20-min group, CBF/CMRO2 once again increased (≈100%), reaching a significant level at 180 min and remaining so for the rest of the 6-h period ( p < 0.05). These data demonstrate biphasic uncoupling of CBF and CMRO2 after severe (20 min) global ischemia in rats. This relatively early reemergence of CBF/CMRO2 uncoupling after 180 min of reperfusion is similar to that observed after prolonged cardiac arrest and resuscitation in humans.

Autoimmune bone marrow environment severely inhibits B cell development by inducing extensive cell death and inhibiting proliferation

Autoimmunity ◽  
2012 ◽  
Vol 45 (3) ◽  
pp. 210-217 ◽  
Author(s):  
Shih-En Chang ◽  
Linjie Guo ◽  
Jun Tian ◽  
Yang Liu ◽  
Zhuxiu Guo ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Cell Death ◽  
B Cell ◽  
Cell Development ◽  
B Cell Development ◽  
Extensive Cell Death ◽  
Extensive Cell

Calcium ionophore-induced de-encryption of tissue factor in monocytes is associated with extensive cell death

2007 ◽  
Vol 119 (5) ◽  
pp. 621-630 ◽  
Author(s):  
C.E. Henriksson ◽  
O. Klingenberg ◽  
M. Hellum ◽  
K.S. Landsverk ◽  
G.B. Joø ◽  
...  
Keyword(s):  
Cell Death ◽  
Tissue Factor ◽  
Calcium Ionophore ◽  
Extensive Cell Death ◽  
Extensive Cell

scholarly journals Phenotype of the Triplo-lethal locus of Drosophila melanogaster and its suppression by hyperoxia

2003 ◽  
Vol 82 (3) ◽  
pp. 163-170 ◽  
Author(s):  
LAURA K. SMOYER ◽  
DOUGLAS R. DORER ◽  
KENNETH W. NICKERSON ◽  
ALAN C. CHRISTENSEN
Keyword(s):  
Cell Death ◽  
Drosophila Melanogaster ◽  
Environmental Condition ◽  
Reporter Strain ◽  
First Report ◽  
Extensive Cell Death ◽  
Extensive Cell

The Triplo-lethal locus (Tpl) of Drosophila is both triplo-lethal and haploinsufficient, but the function of the locus is unknown. We have examined Tpl-aneuploid embryos and find that, in both trisomics and monosomics, the midgut shows extensive cell death and the tracheae are abnormal. Shortly thereafter, all tissues die. PCR-based genotyping of individual embryos and larvae show that this phenotype occurs in the trisomics after hatching and in the monosomics before hatching. Weak alleles of the interacting gene Su(Tpl) delay the death of Tpl trisomics, but they still show the same tracheal and midgut phenotypes before dying. Hyperoxia (45% oxygen) partially suppresses the phenotype of Tpl aneuploids, even though the use of a hypoxia reporter strain shows that dying Tpl aneuploids are not hypoxic. This is the first report of a phenotype associated with the Tpl locus and the first report of an environmental condition that suppresses the phenotype.

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