Neurotrophins and Their Receptors in Nerve Injury and Repair

Ebadi, Manuchair; Bashir, Rumaisa; Heidrick, Margaret L.; Hamada, Fumihiko; Refaey, E El; Hamed, Ahmed R.; Helal, Gouda K.; Baxi, Mayur D.; Cerutis, D. Roselyn; Lassi, N.K

doi:10.1016/s0197-0186(96)00071-x

Cited by 225 publications

(131 citation statements)

References 238 publications

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“…1A) (62)(63)(64)(65)(66). However, NGF has been shown to synergistically trans-activate the HIV-1 LTR with Tat to promote viral replication (67,68), and NGF is an autocrine/ paracrine survival factor for HIV-1-infected macrophages and monocytes ( Fig.…”

Section: Hiv-1 Tat-coactivator Interactions Inhibitmentioning

confidence: 99%

HIV-1 Tat Interactions with p300 and PCAF Transcriptional Coactivators Inhibit Histone Acetylation and Neurotrophin Signaling through CREB

Wong

Sharma

Awasthi

et al. 2005

Journal of Biological Chemistry

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The human immunodeficiency virus type-1 (HIV-1) infects microglia, macrophages, and astrocytes in the central nervous system (CNS) and may cause severe neurological diseases, such as AIDS-related dementias or progressive encephalopathies, as a result of CNS inflammation and neurotrophin signaling defects associated with expression of viral antigens and HIV-1 replication in the brain. The HIV Tat protein can be endocytosed by surrounding uninfected cells; interacts with transcriptional coactivators/acetyltransferases,

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Section: Hiv-1 Tat-coactivator Interactions Inhibitmentioning

confidence: 99%

HIV-1 Tat Interactions with p300 and PCAF Transcriptional Coactivators Inhibit Histone Acetylation and Neurotrophin Signaling through CREB

Wong

Sharma

Awasthi

et al. 2005

Journal of Biological Chemistry

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“…Other results have shown that the neurotrophic factors, such as basic fibroblast growth factor (bFGF; Grothe and Unsicker, 1992), brain-derived neurotrophin factor (BDNF; Yan et al, 1992), and ciliary neurotrophic factor (CNTF; Sendtner et al, 1992), reduce experimental axotomy-induced death of facial or hypoglossal motoneurons in neonatal or immature rats similarly to the reduction produced by selegiline. Neurotropic factors in dopaminergic neurons may represent a potential neuroprotective therapy for PD (for reviews and references see Moller et al, 1996;Ebadi et al, 1997). studied the effects of metallothionein, neurotrophins, and selegiline in providing neuroprotection in PD.…”

Section: Selegiline Possesses Neurotrophic-like Action and Rescues Axmentioning

confidence: 99%

Neuroprotective actions of selegiline

Ebadi

Sharma

Shaik

et al. 2002

J of Neuroscience Research

122

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Selegiline, a selective inhibitor of monoamine oxidase-B (MAO-B), was one of the first adjunct therapies in clinical neurology. A retrospective analysis of data from patients with Parkinson's disease found a significant increase in survival in those treated with selegiline plus L-dopa compared with L-dopa alone. The mechanism of action of selegiline is complex and cannot be explained solely by its MAO-B inhibitory action. Pretreatment with selegiline can protect neurons against a variety of neurotoxins, such as 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP), 6-hydroxydopamine, N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4), methyl-␤-acetoxyethyl-2-chloroethylamine (AF64A), and 5,6-dihydroxyserotonin, which damage dopaminergic, adrenergic, cholinergic, and sertoninergic neurons, respectively. Selegiline produces an amphetamine-like effect, enhances the release of dopamine, and blocks the reuptake of dopamine. It stimulates gene expression of L-aromatic amino acid decarboxylase, increases striatal phenylethylamine levels, and activates dopamine receptors. Selegiline reduces the production of oxidative radicals, up-regulates superoxide dismutase and catalase, and suppresses nonenzymatic and iron-catalyzed autooxidation of dopamine. Selegiline compensates for loss of target-derived trophic support, delays apoptosis in serum-deprived cells, and blocks apoptosis-related fall in the mitochondrial membrane potential. Most of the aforementioned properties occur independently of selegiline's efficacy to inhibit MAO-B. © 2002 Wiley-Liss, Inc.Selegiline (deprenyl; Jumex), a noncompetitive monoamine oxidase-B (MAO-B) inhibitor, has continued to hold a fascination for clinicians and researchers since it was first synthesized as a "psychic energizer." The "neuroprotective effects" of selegiline became evident when it was found that it blocked the parkinsonism-inducing effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP; see Langston and Tanner, 2000).MPTP as a neurotoxin has attracted the attention of many investigators owing to its capacity in humans and nonhuman primates to induce neuropathologic abnormalities (rigidity, resting tremor, akinesia, etc.) similar to those observed in patients with idiopathic Parkinson's disease (PD). As in PD also after administration of MPTP, the observed symptoms are caused by depletion of dopamine in the neostriatum following selective degeneration of the dopaminergic neurons of the substantia nigra pars compacta (SNpc).MPTP's capacity to induce PD was discovered accidentally when several drug addicts in California developed numerous symptoms of PD after self-administration of a "synthetic heroin" containing MPTP as a contaminant byproduct. Numerous investigations have since been carried out in which MPTP was administered in vivo to primates and rodents as well as in vitro using cell cultures. Today, MPTP-induced toxicity represents one of the most interesting models for investigating the pathogenesis of the parkinsonian syndrome. However, its mechanism of action is stil...

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“…As an injury ensues, the signal is sensed by nearby Schwann cells, which then produce and release neurotrophins that promote regeneration of the injured axon. [2][3][4] Four neurotrophins have been characterized in mammals: nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4 (NT-4). Although similar in sequence and structure, different neurotrophins play distinctive roles during neuronal development and regeneration.…”

Section: Introductionmentioning

confidence: 99%

Growth factor therapy and neuronal nitric oxide synthase

Lin

2004

Int J Impot Res

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Trauma to the cavernous nerve is a known cause of erectile dysfunction, with lengthy and often incomplete recovery. Using rat models, we have previously shown that injury to the cavernous nerves or ligation of pudendal arteries causes a significant decrease of neuronal nitric oxide synthase (nNOS) in the dorsal nerve of the penis and intracavernosal tissue as well as loss of erectile response to neurostimulation. Intracavernous injection of vascular endothelial growth factor or brain-derived neurotrophic factor facilitates the recovery of nNOS and erectile function. Studies are underway to elucidate the molecular mechanism of cavernous nerve regeneration and the potential of using growth factors to enhance the recovery of erectile function in patients after radical pelvic surgery.

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Neurotrophins and Their Receptors in Nerve Injury and Repair

Cited by 225 publications

References 238 publications

HIV-1 Tat Interactions with p300 and PCAF Transcriptional Coactivators Inhibit Histone Acetylation and Neurotrophin Signaling through CREB

HIV-1 Tat Interactions with p300 and PCAF Transcriptional Coactivators Inhibit Histone Acetylation and Neurotrophin Signaling through CREB

Neuroprotective actions of selegiline

Growth factor therapy and neuronal nitric oxide synthase

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