Static magnetic field exposure reproduces cellular effects of the Parkinson's disease drug candidate ZM241385.
This study was inspired by coalescing evidence that magnetic therapy may be a viable treatment option for certain diseases. This premise is based on the ability of moderate strength fields (i.e., 0.1 to 1 Tesla) to alter the biophysical properties of lipid bilayers and in turn modulate cellular sign...
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2010-11-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC2975637?pdf=render |
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| author | Zhiyun Wang Pao-Lin Che Jian Du Barbara Ha Kevin J Yarema |
| author_facet | Zhiyun Wang Pao-Lin Che Jian Du Barbara Ha Kevin J Yarema |
| author_sort | Zhiyun Wang |
| collection | DOAJ |
| description | This study was inspired by coalescing evidence that magnetic therapy may be a viable treatment option for certain diseases. This premise is based on the ability of moderate strength fields (i.e., 0.1 to 1 Tesla) to alter the biophysical properties of lipid bilayers and in turn modulate cellular signaling pathways. In particular, previous results from our laboratory (Wang et al., BMC Genomics, 10, 356 (2009)) established that moderate strength static magnetic field (SMF) exposure altered cellular endpoints associated with neuronal function and differentiation. Building on this background, the current paper investigated SMF by focusing on the adenosine A(2A) receptor (A(2A)R) in the PC12 rat adrenal pheochromocytoma cell line that displays metabolic features of Parkinson's disease (PD).SMF reproduced several responses elicited by ZM241385, a selective A(2A)R antagonist, in PC12 cells including altered calcium flux, increased ATP levels, reduced cAMP levels, reduced nitric oxide production, reduced p44/42 MAPK phosphorylation, inhibited proliferation, and reduced iron uptake. SMF also counteracted several PD-relevant endpoints exacerbated by A(2A)R agonist CGS21680 in a manner similar to ZM241385; these include reduction of increased expression of A(2A)R, reversal of altered calcium efflux, dampening of increased adenosine production, reduction of enhanced proliferation and associated p44/42 MAPK phosphorylation, and inhibition of neurite outgrowth.When measured against multiple endpoints, SMF elicited qualitatively similar responses as ZM241385, a PD drug candidate. Provided that the in vitro results presented in this paper apply in vivo, SMF holds promise as an intriguing non-invasive approach to treat PD and potentially other neurological disorders. |
| first_indexed | 2024-12-11T02:29:09Z |
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| id | doaj.art-6a21a470236a4102bc42d45f50013eec |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-11T02:29:09Z |
| publishDate | 2010-11-01 |
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| series | PLoS ONE |
| spelling | doaj.art-6a21a470236a4102bc42d45f50013eec2022-12-22T01:23:52ZengPublic Library of Science (PLoS)PLoS ONE1932-62032010-11-01511e1388310.1371/journal.pone.0013883Static magnetic field exposure reproduces cellular effects of the Parkinson's disease drug candidate ZM241385.Zhiyun WangPao-Lin CheJian DuBarbara HaKevin J YaremaThis study was inspired by coalescing evidence that magnetic therapy may be a viable treatment option for certain diseases. This premise is based on the ability of moderate strength fields (i.e., 0.1 to 1 Tesla) to alter the biophysical properties of lipid bilayers and in turn modulate cellular signaling pathways. In particular, previous results from our laboratory (Wang et al., BMC Genomics, 10, 356 (2009)) established that moderate strength static magnetic field (SMF) exposure altered cellular endpoints associated with neuronal function and differentiation. Building on this background, the current paper investigated SMF by focusing on the adenosine A(2A) receptor (A(2A)R) in the PC12 rat adrenal pheochromocytoma cell line that displays metabolic features of Parkinson's disease (PD).SMF reproduced several responses elicited by ZM241385, a selective A(2A)R antagonist, in PC12 cells including altered calcium flux, increased ATP levels, reduced cAMP levels, reduced nitric oxide production, reduced p44/42 MAPK phosphorylation, inhibited proliferation, and reduced iron uptake. SMF also counteracted several PD-relevant endpoints exacerbated by A(2A)R agonist CGS21680 in a manner similar to ZM241385; these include reduction of increased expression of A(2A)R, reversal of altered calcium efflux, dampening of increased adenosine production, reduction of enhanced proliferation and associated p44/42 MAPK phosphorylation, and inhibition of neurite outgrowth.When measured against multiple endpoints, SMF elicited qualitatively similar responses as ZM241385, a PD drug candidate. Provided that the in vitro results presented in this paper apply in vivo, SMF holds promise as an intriguing non-invasive approach to treat PD and potentially other neurological disorders.http://europepmc.org/articles/PMC2975637?pdf=render |
| spellingShingle | Zhiyun Wang Pao-Lin Che Jian Du Barbara Ha Kevin J Yarema Static magnetic field exposure reproduces cellular effects of the Parkinson's disease drug candidate ZM241385. PLoS ONE |
| title | Static magnetic field exposure reproduces cellular effects of the Parkinson's disease drug candidate ZM241385. |
| title_full | Static magnetic field exposure reproduces cellular effects of the Parkinson's disease drug candidate ZM241385. |
| title_fullStr | Static magnetic field exposure reproduces cellular effects of the Parkinson's disease drug candidate ZM241385. |
| title_full_unstemmed | Static magnetic field exposure reproduces cellular effects of the Parkinson's disease drug candidate ZM241385. |
| title_short | Static magnetic field exposure reproduces cellular effects of the Parkinson's disease drug candidate ZM241385. |
| title_sort | static magnetic field exposure reproduces cellular effects of the parkinson s disease drug candidate zm241385 |
| url | http://europepmc.org/articles/PMC2975637?pdf=render |
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