IRIS publication 253781800
Expression of endogenous Mkp1 in 6-OHDA rat models of Parkinson’s disease.
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TY - JOUR - Collins L.M., Gavin A.M., Walsh S., Sullivan A.M., Wyatt S.L., O’Keeffe G.W., Nolan Y.M, Toulouse A. - 2014 - May - SpringerPlus - Expression of endogenous Mkp1 in 6-OHDA rat models of Parkinson’s disease. - Published - () - 205 - 206 - We have previously demonstrated that mitogen-activated protein kinase phosphatase 1, Mkp1, is expressed in the developing and rat adult substantia nigra and striatum, where it promotes the growth of nigral dopaminergic neurons. Mkp1 may therefore have therapeutic potential for Parkinson’s disease. In the present study, we have assessed the expression of Mkp1 and TH in the substantia nigra and striatum of parkinsonian rat models. Expression was measured at 4 and 10 days post-lesion in the 6-hydroxydopamine (6-OHDA) medial forebrain bundle lesion model and after 4, 10 and 28 days in the 6-OHDA striatal lesion model. Our results show that Mkp1 expression was transiently up-regulated in the substantia nigra at 4 days post-6-OHDA administration in the two models while TH expression was decreased at the later time-points examined. These data suggest that Mkp1 may play a role in counteracting the neurotoxic effects of 6-OHDA in nigral dopaminergic neurons. - http://www.springerplus.com/content/3/1/205 - doi:10.1186/2193-1801-3-205 DA - 2014/05 ER -
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@article{V253781800, = {Collins L.M., Gavin A.M. and Walsh S., Sullivan A.M. and Wyatt S.L., O’Keeffe G.W. and Nolan Y.M, Toulouse A. }, = {2014}, = {May}, = {SpringerPlus}, = {Expression of endogenous Mkp1 in 6-OHDA rat models of Parkinson’s disease.}, = {Published}, = {()}, pages = {205--206}, = {{We have previously demonstrated that mitogen-activated protein kinase phosphatase 1, Mkp1, is expressed in the developing and rat adult substantia nigra and striatum, where it promotes the growth of nigral dopaminergic neurons. Mkp1 may therefore have therapeutic potential for Parkinson’s disease. In the present study, we have assessed the expression of Mkp1 and TH in the substantia nigra and striatum of parkinsonian rat models. Expression was measured at 4 and 10 days post-lesion in the 6-hydroxydopamine (6-OHDA) medial forebrain bundle lesion model and after 4, 10 and 28 days in the 6-OHDA striatal lesion model. Our results show that Mkp1 expression was transiently up-regulated in the substantia nigra at 4 days post-6-OHDA administration in the two models while TH expression was decreased at the later time-points examined. These data suggest that Mkp1 may play a role in counteracting the neurotoxic effects of 6-OHDA in nigral dopaminergic neurons.}}, = {http://www.springerplus.com/content/3/1/205}, = {doi:10.1186/2193-1801-3-205}, source = {IRIS} }
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AUTHORS | Collins L.M., Gavin A.M., Walsh S., Sullivan A.M., Wyatt S.L., O’Keeffe G.W., Nolan Y.M, Toulouse A. | ||
YEAR | 2014 | ||
MONTH | May | ||
JOURNAL_CODE | SpringerPlus | ||
TITLE | Expression of endogenous Mkp1 in 6-OHDA rat models of Parkinson’s disease. | ||
STATUS | Published | ||
TIMES_CITED | () | ||
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START_PAGE | 205 | ||
END_PAGE | 206 | ||
ABSTRACT | We have previously demonstrated that mitogen-activated protein kinase phosphatase 1, Mkp1, is expressed in the developing and rat adult substantia nigra and striatum, where it promotes the growth of nigral dopaminergic neurons. Mkp1 may therefore have therapeutic potential for Parkinson’s disease. In the present study, we have assessed the expression of Mkp1 and TH in the substantia nigra and striatum of parkinsonian rat models. Expression was measured at 4 and 10 days post-lesion in the 6-hydroxydopamine (6-OHDA) medial forebrain bundle lesion model and after 4, 10 and 28 days in the 6-OHDA striatal lesion model. Our results show that Mkp1 expression was transiently up-regulated in the substantia nigra at 4 days post-6-OHDA administration in the two models while TH expression was decreased at the later time-points examined. These data suggest that Mkp1 may play a role in counteracting the neurotoxic effects of 6-OHDA in nigral dopaminergic neurons. | ||
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URL | http://www.springerplus.com/content/3/1/205 | ||
DOI_LINK | doi:10.1186/2193-1801-3-205 | ||
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