Joan P. Schwartz

University of Houston - Downtown

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E. Costa

Universidade Federal de Minas Gerais

Takeshi Yabe

Setsunan University

Takayuki Taniwaki

Kurume University

Gerald J. Chader

Keck Hospital of USC

S. Patricia Becerra

National Eye Institute

Janet V. Passonneau

National Institute on Alcohol Abuse and Alcoholism

Dahlia Minc‐Golomb

National Institutes of Health

E Costa

New York University

Vivian W. Wu

National Institute of Neurological Disorders and Stroke

Ann M. Marini

Uniformed Services University of the Health Sciences

Cooperative Institutions

National Institutes of Health

National Institute of Neurological Disorders and Stroke

National Institute of Mental Health

National Cancer Institute

Harvard University

St. Elizabeths Hospital

Massachusetts General Hospital

University of Gothenburg

National Institutes of Health Clinical Center

Mayo Clinic in Arizona

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Expression of Both Constitutive and Inducible Nitric Oxide Synthases in Neuronal and Astrocyte Cultures

Annals of the New York Academy of Sciences (1994)

Dahlia Minc‐Golomb Joan P. Schwartz

10.1111/j.1749-6632.1994.tb21838.x

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Citations (22)

Pigment epithelium-derived factor induces the production of chemokines by rat microglia

Glia (2006)

Asako Takanohashi Takeshi Yabe Joan P. Schwartz

10.1002/glia.20351

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Citations (1)

Pigment Epithelium‐Derived Factor Protects Cultured Cerebellar Granule Cells Against Glutamate‐Induced Neurotoxicity

Journal of Neurochemistry (1997)

Takayuki Taniwaki Naohide Hirashima S. Patricia Becerra Gerald J. Chader René Etcheberrigaray

Pigment epithelium-derived factor (PEDF) is a survival factor for cerebellar granule cells in culture. In the present study, we have investigated the ability of a recombinant form of PEDF (rPEDF) to protect against glutamate neurotoxicity. When rPEDF was added to cerebellar granule cell cultures 30 min before addition of 100 microM glutamate, glutamate-induced neuronal death was significantly reduced. The protective effect of rPEDF was dose-dependent in the range from 0.023 to 7.0 nM (1-500 ng/ml), with a half-maximal dose of 0.47 nM. An antibody to rPEDF blocked this protective effect. Measurement of intraneuronal free calcium levels demonstrated that rPEDF raised the basal calcium content. However, after the elevation of intracellular calcium in response to administration of glutamate, rPEDF reduced the plateau level seen in the presence of glutamate. These data show that PEDF can protect neurons against glutamate-induced neurotoxicity, possibly via a calcium-related pathway. The finding that only 30 min of preincubation is required for the neuroprotective effect, significantly faster than other known neurotrophic factors, suggests that PEDF may be useful clinically as a neuroprotective agent in the CNS.

PEDF

Neurotoxicity

Glutamic acid

Calcium in biology

Granule (geology)

10.1046/j.1471-4159.1997.68010026.x

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Citations (114)

Use of mRNA hybridization and radioimmunoassay to study mechanisms of drug-induced accumulation of enkephalins in rat brain structures.

Molecular Pharmacology (1985)

Italo Mocchetti Joan P. Schwartz E Costa

The repeated administration of haloperidol or fenfluramine for several days led to an increase of enkephalin content in specific brain areas. In order to characterize the nature of the dynamic changes underlying this increase, we measured the content of proenkephalin mRNA (PE-mRNA), of high molecular weight (HMW) enkephalin precursors, and of low molecular weight enkephalin peptides (LMW) in various brain areas. To measure PE-mRNA, we hybridized the specific mRNA with a [32P]cDNA probe for human pheochromocytoma PE. HMW and LMW enkephalin content was measured by radioimmunoassay after separation of the immunoreactive peaks by Bio-Gel P-2 column chromatography and enzymatic digestion of the precursors. Haloperidol treatment increased enkephalins, the precursor, and PE-mRNA content in the striatum, suggesting that this drug might increase enkephalin steady state by increasing transcription, translation, or both processes. In contrast, fenfluramine increased hypothalamic and striatal enkephalin content by preferentially reducing neuropeptide utilization or decreasing its catabolism without changing its synthesis.

Proenkephalin

Dynorphin

10.1016/s0026-895x(25)13478-0

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Citations (66)

Adenosine 3′,5′-Monophosphate in Glial Tumor Cells

Journal of Biological Chemistry (1973)

Joan P. Schwartz N. Ronald Morris Bruce McL. Breckenridge

Abstract The effect of 5-bromodeoxyuridine (BrdUrd) on the ability of the glial tumor cell line, C-6, to elevate its adenosine 3',5'-monophosphate (cAMP) content in response to norepinephrine has been examined. Increasing concentrations of BrdUrd were found to inhibit the norepinephrine response progressively, with a maximal inhibition of approximately 80%. No effect of BrdUrd was seen on basal cAMP levels. Analysis of individual enzymes demonstrated that BrdUrd increased the cAMP phosphodiesterase activities but had no effect on the adenylate cyclase or its sensitivity to norepinephrine. In addition, BrdUrd caused a change in the shape of the cells. The effect on shape also occurred in confluent cells, whereas the effect on the norepinephrine response required dividing cells, suggesting that incorporation of the BrdUrd into DNA was required. N6, O2'-Dibutyryl adenosine 3',5'-monophosphate also increased the cAMP phosphodiesterase activities of the cells, and caused a similar change in their morphology. Although BrdUrd had no effect on the adenylate cyclase, variations in the culture conditions were found to have a large effect on the enzyme's norepinephrine sensitivity. Following subculturing, there was little elevation of cAMP in response to norepinephrine until after the cells began to enter the stationary growth phase. Phosphodiesterase activity was found to remain constant throughout this period. The results suggest that cell-to-cell contact may regulate certain cellular functions.

Adenosine monophosphate

10.1016/s0021-9258(19)44062-3

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Citations (66)

beta Adrenergic receptor-mediated regulation of cyclic nucleotide phosphodiesterase in C6 glioma cells: vinblastine blockade of isoproterenol induction.

Journal of Pharmacology and Experimental Therapeutics (1980)

Joan P. Schwartz E Costa

Persistent stimulation with isoproterenol of the beta adrenergic receptor located in C6 glioma cell membranes results in a rapid rise in the cyclic AMP content, an activation of soluble cyclic AMP-dependent protein kinase, a translocation of catalytic subunits of the activated protein kinase to the nucleus and a delayed (3--4 hr later) increase of cyclic AMP phosphodiesterase activity and beta-nerve growth factor content. The phosphodiesterase increase requires new RNA and protein synthesis. A pretreatment of the cells with vinblastine in doses that fail to change protein synthesis blocks the increase in phosphodiesterase activity elicited by isoproterenol: the ED50 of vinblastine for this effect is 2.6 x 10(-7) M. In contrast, the simultaneous increase in beta-nerve growth factor content elicited by isoproterenol is not blocked by vinblastine and does not require new RNA and protein synthesis. We conclude that intact microtubules are required to transfer the catalytic subunits of activated protein kinase from cytosol to the nucleus. Hence microtubules may be operative in facilitating communication between the cell membrane and the nucleus.

Cyclic nucleotide phosphodiesterase

10.1016/s0022-3565(25)32002-1

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Citations (13)

Nerve growth factor-mediated increase of the substance P content of chick embryo dorsal root ganglia

Brain Research (1979)

Joan P. Schwartz E. Costa

10.1016/0006-8993(79)90955-7

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Citations (32)

Photography, Geography and

Encyclopedia of Human Geography (2006)

Joan P. Schwartz

10.4135/9781412952422.n219

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Survival Effects of Pigment Epithelium-Derived Factor Expressed by a Lentiviral Vector in Rat Cerebellar Granule Cells

Developmental Neuroscience (2001)

Takuo Nomura Takeshi Yabe Hideki Mochizuki Jakob Reiser S. Patricia Becerra

We have previously shown that pigment epithelium-derived factor (PEDF) acts as a survival factor for cerebellar granule cells (CGCs), by blocking apoptotic death, and can also protect these cells against glutamate-induced neurotoxicity. In preparation for gene therapy studies, pseudotyped HIV-1-based lentiviral vectors containing the PEDF gene, as well as either green fluorescent protein or β-galactosidase, were prepared. These bicistronic vectors are unique in that they express two genes efficiently under one promoter. Primary cell cultures of CGCs from postnatal day 8 rats were infected with the vectors encoding PEDF. RT-PCR demonstrated expression of mRNA and Western blot analysis confirmed that infected CGCs secrete PEDF protein to the medium. Assays for cell survival demonstrated that PEDF-infected cells were significantly more protected compared with mock-infected controls for 6–8 days in culture, as well as against induced apoptosis. The PEDF vectors expressing tat (trans-acting transcription factor) provided more protection than the tat(–) vectors. These results demonstrate that while the lentiviral vectors expressing PEDF are as neuroprotective as the protein itself for CGCs, the vectors have the advantage of providing long-lasting expression of PEDF protein, which will be more effective in in vivo studies. The present results suggest that this system may be useful for gene therapy for neurodegenerative disorders.

Granule (geology)

PEDF

10.1159/000048706

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Citations (16)

Developmental expression of the proenkephalin and prosomatostatin genes in cultured cortical and cerebellar astrocytes

Developmental Brain Research (1992)

Hisaharu Shinoda Ann M. Marini Joan P. Schwartz

Proenkephalin

Developmental profile

10.1016/0165-3806(92)90220-q

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Citations (37)