Sequence of a cDNA clone encoding mouse glial fibrillary acidic protein: structural conservation of intermediate filaments.

Lewis, Sally A.; Balcarek, J M; Krek, Veronica; Shelanski, Michael L.; Cowan, Nicholas J.

doi:10.1073/pnas.81.9.2743

Cited by 301 publications

(197 citation statements)

References 22 publications

(20 reference statements)

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“…There was no evidence of binding to either '5 or % RNA. This is consistent with previous studies using probes prepared from this vector (Lewis et al, 1984). Dot blot analyses of GFAP mRNA levels after lesions of the entorhinal cortex Quantification of GFAP mRNA levels in whole hippocampus by dot blot hybridization revealed that there were substantial increases in the levels of GFAP mRNA in the hippocampus after lesions of the entorhinal cortex (Fig.…”

Section: Resultssupporting

confidence: 79%

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The process of reinnervation in the dentate gyrus of adult rats: An ultrastructural study of changes in presynaptic terminals as a result of sprouting

Steward

Vinsant

Davis

1988

J of Comparative Neurology

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The present study was undertaken to define the ultrastructure of synapses of the crossed temporodentate pathway after they had sprouted to reinnervate the dentate gyrus following the destruction of the normal ipsilateral temporodentate pathway. The synapses of the sprouted crossed temporodentate pathway were identified at the EM level by using autoradiographic techniques and by evaluating the degeneration of the pathway following secondary lesions. Both EM autoradiography and EM degeneration revealed that the terminals of the sprouted crossed temporodentate pathway formed asymmetric synapses on spines; individual terminals appeared to make more synaptic contacts per terminal (multiple synapses) than in the case of the normal crossed pathway. In the two lesioned animals exhibiting the best labeling, labeled terminals made an average of 3.0 ± 2.2 and 2.0 ± 1.3 contacts per terminal. In contrast, labeled terminals in normal animals exhibited only one contact per terminal. The terminals of the sprouted pathway were also larger than those of the normal crossed pathway. The synapses of the crossed temporodentate pathway that degenerated after a secondary lesion of the entorhinal cortex exhibited both electron‐lucent and electron‐dense forms of degeneration at 2 days postlesion. In two animals that were quantitatively analyzed, the density of degenerating synaptic terminals was 281 and 218/10,000 μm2 in the terminal field of the sprouted crossed pathway. These values are much higher than in normal animals, where the density of degenerating synaptic terminals was only 2.12/10,000 μm2 at 2 days postlesion. Because degenerating terminals were evident at 2 days postlesion, the sprouted crossed pathway does not appear to exhibit the very rapid degeneration that is characteristic of the normal crossed pathway. We conclude that sprouting in this pathway involves terminal proliferation (an increase in the number of presynaptic elements), and terminal hypertrophy (an increase in the size of presynaptic terminals, together with an increase in the number of synaptic contacts formed by individual terminals).

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Section: Resultssupporting

confidence: 79%

“…The probes used in this study were derived from a cDNA for mouse GFAP that has been characterized previously (Lewis et al, 1984). The original cDNA clone was 2.5 kilobases (kb) in length, which specified over 97% of the GFAP amino acid sequence, and also included a 1.4 kb long portion of the 3' untranslated region.…”

Section: Methodsmentioning

confidence: 99%

The process of reinnervation in the dentate gyrus of adult rats: An ultrastructural study of changes in presynaptic terminals as a result of sprouting

Steward

Vinsant

Davis

1988

J of Comparative Neurology

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“…Sense and antisense RNA probes were transcribed in vitro with T3 and T7 RNA polymerase from linearized pBlusescript vectors carrying cDNAs for v-src, GFAP (Lewis et al, 1984), synaptophysin (Leube et al, 1989), proteolipid protein (Milner et al, 1985), VEGF (Breier et al, 1992),¯k-1 and¯t-1 (Breier et al, 1995) in the presence of digoxigenin-11-dUTP (Boehringer Mannheim). 50 ± 200 ng of labeled transcripts (0.7 ± 1.2 kb) were hybridized to tissue sections at 658C as described (Marino et al, 1995).…”

Section: In Situ Hybridizationmentioning

confidence: 99%

Development and malignant progression of astrocytomas in GFAP-v-src transgenic mice

et al. 1997

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We have generated a transgenic mouse model for astrocytoma by expressing the v-src kinase under control of the glial ®brillary acidic protein (GFAP) gene regulatory elements in astrocytes. Abnormal astrogliosis was observed in all transgenic animals already at 2 weeks postnatally, frequently followed by the development of dysplastic changes. Later, small proliferative foci arose, and overt astrocytoma developed in the brain and spinal cord in 14.4% of mice after a follow up time of 65 weeks. While early lesions were histologically consistent with low-grade astrocytoma, at later stages most tumors were highly mitotic and frankly malignant. Vascular endothelial growth factor (VEGF) was expressed by tumor cells already at early stages, suggesting induction by v-src, and it was most pronounced in pseudopalisading cells surrounding necrotic areas, implying additional upregulation by hypoxia. In larger lesions, mitotic activity and expression of¯k-1, the cognate receptor of VEGF were induced in endothelial cells. Therefore, end-stage tumors mimicked the morphological and molecular characteristics of human glioblastoma multiforme. Time course and stochastic nature of the process indicate that v-src did not su ce for malignant transformation, and that astrocytomas were the result of a multistep process necessitating co-operation of additional genetic events.

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“…A 34-mer oligonucleotide complimentary to nucleotides 358 to 391 of the mouse HSP25 sequence (Frohli et al, 1993) was used for mouse HSP25 mRNA. A 45-mer oligonucleotide complementary to nucleotides 1,119 to 1,163 of the mouse GFAP gene (Lewis et al, 1984) was used for mouse glial fibrillary acidic protein (GFAP) mRNA. A 39-mer oligonucleotide complimentary to nucleotides 1,872 to 1,910 of c-jun gene (Ryder and Nathans 1988) was used for cjun mRNA.…”

Section: In Situ Hybridizationmentioning

confidence: 99%

Overexpression of Heat Shock Protein 27 Reduces Cortical Damage after Cerebral Ischemia

Weerd

Akbar

Badin

et al. 2009

J Cereb Blood Flow Metab

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Heat shock protein 27 (HSP27) has a major role in mediating survival responses to a range of central nervous system insults, functioning as a protein chaperone, an antioxidant, and through inhibition of cell death pathways. We have used transgenic mice overexpressing HSP27 (HSP27tg) to examine the role of HSP27 in cerebral ischemia, using model of permanent middle cerebral artery occlusion (MCAO). Infarct size was evaluated using multislice T 2 -weighted anatomical magnetic resonance imaging (MRI) after 24 h. A significant reduction of 30% in infarct size was detected in HSP27tg animals compared with wild-type (WT) littermates. To gain some insight into the mechanisms contributing to cell death and its attenuation by HSP27, we monitored the effect of induction of c-jun and ATF3 on tissue survival in MCAO and their effects on the expression of endogenous mouse HSP25 and HSP70. It is important that, the c-jun induction seen at 4 h tended to be localized to regions that were salvageable in HSP27tg mice but became infarcted in WT animals. Our results provide support for the powerful neuroprotective effects of HSP27 in cerebral ischemia.

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Sequence of a cDNA clone encoding mouse glial fibrillary acidic protein: structural conservation of intermediate filaments.

Cited by 301 publications

References 22 publications

The process of reinnervation in the dentate gyrus of adult rats: An ultrastructural study of changes in presynaptic terminals as a result of sprouting

The process of reinnervation in the dentate gyrus of adult rats: An ultrastructural study of changes in presynaptic terminals as a result of sprouting

Development and malignant progression of astrocytomas in GFAP-v-src transgenic mice

Overexpression of Heat Shock Protein 27 Reduces Cortical Damage after Cerebral Ischemia

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