Induction of adenylate cyclase sensitive dopamine D2-receptors in retinoic acid induced differentiated human neuroblastoma SHSY-5Y cells

Farooqui, Shakeel M.

doi:10.1016/0024-3205(94)00520-6

Cited by 50 publications

(23 citation statements)

References 29 publications

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“…It had been previously reported that RA differentiation of SH-SY5Y cells followed by treatment with the phorbol ester TPA significantly elevates production of DA synthetic enzymes (Pennypacker et al, 1989), D 2 receptors (Farooqui 1994) and its G-proteins (Ammer and Schulz 1994). We confirmed this by identifying that SH-SY5Y cells were immunoreactive to TH and DAT antibodies, and that membranes prepared from the SH-SY5Y cells were also immunopositive using western blotting.…”

Section: Pretreatment With Pramipexole Is Neuroprotective Against Mppsupporting

confidence: 80%

Terminally differentiated SH-SY5Y cells provide a model system for studying neuroprotective effects of dopamine agonists

et al. 2003

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Section: Pretreatment With Pramipexole Is Neuroprotective Against Mppsupporting

confidence: 80%

Terminally differentiated SH-SY5Y cells provide a model system for studying neuroprotective effects of dopamine agonists

et al. 2003

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“…These human neuroblastoma cells were chosen for this study because they have been widely used to investigate neuronal cell damage and death and they serve as an in vitro model for Parkinson's disease [17]. They produce dopamine [24], express dopamine receptors [25], and are able to introduce dopamine and MPP + through the norepinephrine transporter [26]. Furthermore, a fully functional endocannabinoid system is present in this cell line that markedly expresses enzymes involved in endocannabinoid production and more modest amounts of CB 1 and CB 2 receptors [18].…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effect of JZL184 in MPP+-Treated SH-SY5Y Cells Through CB2 Receptors

et al. 2015

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Growing evidence suggests that the endocannabinoid system plays a role in neuroprotection in Parkinson's disease. Recently, we have shown the neuroprotective effect of monoacylglycerol lipase (MAGL) inhibition with JZL184 in the chronic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model. However, further investigation is needed to determine the neuroprotective mechanisms of the endocannabinoid system on the nigrostriatal pathway. The aim of this work was to investigate whether the neuroprotective effect of JZL184 in mice could be extended to an in vitro cellular model to further understand the mechanism of action of the drug. The SH-SY5Y cell line was selected based on its dopaminergic-like phenotype and its susceptibility to 1-methyl-4-phenylpyridinium iodide (MPP(+)) toxicity. Furthermore, SH-SY5Y cells express both cannabinoid receptors, CB1 and CB2. The present study describes the neuroprotective effect of MAGL inhibition with JZL184 in SH-SY5Y cells treated with MPP(+). The effect of JZL184 in cell survival was blocked by AM630, a CB2 receptor antagonist, and it was mimicked with JWH133, a CB2 receptor agonist. Rimonabant, a CB1 receptor antagonist, did not affect JZL184-induced cell survival. These results demonstrate that the neuroprotective effect of MAGL inhibition with JZL184 described in animal models of Parkinson's disease could be extended to in vitro models such as SH-SY5Y cells treated with MPP(+). This represents a useful tool to study mechanisms of neuroprotection mediated by MAGL inhibition, and we provide evidence for the possible involvement of CB2 receptors in the improvement of cell survival.

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“…Membrane association of UCH-L1 may be important to facilitate its interaction with other membrane-associated proteins, such as Lamp-2A (38), to promote its oligomerization (26,28), and/or to induce enzymatic activity (22). Although multiple forms of UCH-L1 have been identified in cell culture and in tissue (16,(55)(56)(57), the possibility that one could be farnesylated had not been entertained previously (58). For example, one previous study showed that membrane-associated UCH-L1 is more abundant (and the sol- SH-SY5Y cells were transfected with either nonspecific (NS) or UCH-L1-specific siRNA oligos, followed by infection with ␣-synuclein-expressing virus and treatment with either DMSO or 100 nM FTI-277.…”

Section: Discussionmentioning

confidence: 99%

Membrane-associated farnesylated UCH-L1 promotes α-synuclein neurotoxicity and is a therapeutic target for Parkinson's disease

Liu

Meray

Grammatopoulos³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

126

131

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Ubiquitin C-terminal hydrolase-L1 (UCH-L1) is linked to Parkinson's disease (PD) and memory and is selectively expressed in neurons at high levels. Its expression pattern suggests a function distinct from that of its widely expressed homolog UCH-L3. We report here that, in contrast to UCH-L3, UCH-L1 exists in a membrane-associated form (UCH-L1 M ) in addition to the commonly studied soluble form. C-terminal farnesylation promotes the association of UCH-L1 with cellular membranes, including the endoplasmic reticulum. The amount of UCH-L1 M in transfected cells is shown to correlate with the intracellular level of ␣-synuclein, a protein whose accumulation is associated with neurotoxicity and the development of PD. Reduction of UCH-L1 M in cell culture models of ␣-synuclein toxicity by treatment with a farnesyltransferase inhibitor (FTI-277) reduces ␣-synuclein levels and increases cell viability. Proteasome function is not affected by UCH-L1 M , suggesting that it may negatively regulate the lysosomal degradation of ␣-synuclein. Therefore, inhibition of UCH-L1 farnesylation may be a therapeutic strategy for slowing the progression of PD and related synucleinopathies.farnesylation ͉ synuclein

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Induction of adenylate cyclase sensitive dopamine D2-receptors in retinoic acid induced differentiated human neuroblastoma SHSY-5Y cells

Cited by 50 publications

References 29 publications

Terminally differentiated SH-SY5Y cells provide a model system for studying neuroprotective effects of dopamine agonists

Terminally differentiated SH-SY5Y cells provide a model system for studying neuroprotective effects of dopamine agonists

Neuroprotective Effect of JZL184 in MPP+-Treated SH-SY5Y Cells Through CB2 Receptors

Membrane-associated farnesylated UCH-L1 promotes α-synuclein neurotoxicity and is a therapeutic target for Parkinson's disease

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