Transgenic mice expressing β-galactosidase in mature neurons under neuron-specific enolase promoter control

Forss‐Petter, Sonja; Danielson, Patria E.; Catsicas, Stefan; Battenberg, Elena; Price, Jennifer A.; Nerenberg, Michael; Sutcliffe, Gregor

doi:10.1016/0896-6273(90)90308-3

Cited by 353 publications

(227 citation statements)

References 28 publications

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“…23 To explore a potential role for Bag1 in the control of neuronal death, we stably over-expressed mouse Bag1 in CSM14.1 cells under the control of the neuron-specific NSE promoter. 24 Over-expression of Bag1 significantly reduced apoptotic cell death induced by serum deprivation in cultures of CSM14.1 cells. Similarly, Bag1 has been shown to reduce cell death following growth factor withdrawal in 3T3 fibroblasts, Ba/F hematopoietic cells and PC12 neural cells.…”

Section: Discussionmentioning

confidence: 99%

Bag1 is a regulator and marker of neuronal differentiation

et al. 2002

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Bag 1 acts as a co-chaperone for Hsp70/Hsc70. We report here that stable over-expression of Bag1 in immortalized neuronal CSM14.1 cells prevents death following serum deprivation. Bag1 over-expression slowed the proliferative rate of CSM14.1 cells, resulted in increased levels of phospo-MAP kinases and accelerated neuronal differentiation. Immunocytochemistry revealed mostly nuclear localization of Bag1 protein in these cells. However, during differentiation in vitro, Bag1 protein shifted from predominantly nuclear to mostly cytosolic in CSM14.1 cells. To explore in vivo parallels of these findings, we investigated Bag1 expression in the developing mouse nervous system using immunohistochemical methods. Early in brain development, Bag1 was found in nuclei of neuronal precursor cells, whereas cytosolic Bag1 staining was observed mainly after completion of neuronal precursor migration and differentiation. Taken together, these findings raise the possibility that the Bag1 protein is expressed early in neurogenesis in vivo and is capable of modulating neuronal cell survival and differentiation at least in part from a nuclear location.

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Section: Discussionmentioning

confidence: 99%

Bag1 is a regulator and marker of neuronal differentiation

et al. 2002

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“…6 A 1.8 kb NSE promoter fragment has been shown to target the expression of various transgenes to differentiated neurons in transgenic animals. 7,8 We constructed a first generation adenoviral vector containing the rat NSE promoter upstream from the LacZ reporter gene (Ad-NSE) and compared, in vitro and in vivo, the patterns of ␤-galactosidase gene expression from Ad-NSE and from an adenoviral vector containing the RSV promoter (Ad-RSV). Ad-NSE gave preferential expression of the transgene in brain neurons, with higher efficiency and lower toxicity than Ad-RSV.…”

Section: Introductionmentioning

confidence: 99%

Efficient gene transfer and long-term expression in neurons using a recombinant adenovirus with a neuron-specific promoter

et al. 1999

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“…A full-length cDNA for human VEGF 165 (provided by Dr. G. Breier, Bad Nauheim, Germany) was modified by replacing the 3Ј untranslated region with a polyadenylation signal derived from the bovine growth hormone, and placed under the control of a 1.8-kb rat NSE-promotor fragment (Forss-Petter et al, 1990), resulting in brain-specific expression. The constructs were microinjected into fertilized oocytes of (C57BL/6 X C3H/He)F1 hybrid mice.…”

Section: Generation Of Transgenic Animalsmentioning

confidence: 99%

Massive Inborn Angiogenesis in the Brain Scarcely Raises Cerebral Blood Flow

Vogel

Gehrig

Kuschinsky

et al. 2004

J Cereb Blood Flow Metab

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Summary:The functional consequences of increased capillary densities in the brain resulting from vascular endothelial growth factor (VEGF 165 ) overexpression are unknown. Therefore, the authors measured local CBF using the iodo-[ 14 C]antipyrine technique in transgenic mice expressing brain-specifically sixfold higher VEGF 165 levels and in nontransgenic littermates. To reveal possible compensatory vasoconstriction, CBF was also measured during severe hypercapnia (PaCO 2 > 130 mm Hg). Simultaneously, local capillary density, perfusion state, and blood-brain-barrier permeability were assessed. Using the 2-[ 14 C]deoxyglucose method, metabolic effects of VEGF overexpression could be excluded. In transgenic mice all capillaries showed normal morphology and a tight blood-brain barrier. However, 3% nonperfused capillaries in some brain structures indicate ongoing angiogenesis. Capillary density was drastically increased in transgenic mice in white matter structures (70% to 185%), the dentate gyrus (143%), and caudate nucleus (86%). In all other brain structures investigated, capillary densities were moderately increased by approximately 20%. Normocapnic CBF did not differ between transgenic and nontransgenic mice. During maximal hypercapnic vasodilation, CBF was 20% to 30% higher in transgenic mice, although only in brain structures where capillary density was increased more than twofold. These findings suggest that attenuated CBF in transgenic mice during normocapnia is only partly due to a compensatory vasoconstriction, and that microvascular networks in transgenic brains might be ineffectively constructed.

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Transgenic mice expressing β-galactosidase in mature neurons under neuron-specific enolase promoter control

Cited by 353 publications

References 28 publications

Bag1 is a regulator and marker of neuronal differentiation

Bag1 is a regulator and marker of neuronal differentiation

Efficient gene transfer and long-term expression in neurons using a recombinant adenovirus with a neuron-specific promoter

Massive Inborn Angiogenesis in the Brain Scarcely Raises Cerebral Blood Flow

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