Expression of endogenous Mkp1 in 6-OHDA rat models of Parkinson’s disease.

Typeset version

 

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  - 
@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}
}
AUTHORSCollins L.M., Gavin A.M., Walsh S., Sullivan A.M., Wyatt S.L., O’Keeffe G.W., Nolan Y.M, Toulouse A.
YEAR2014
MONTHMay
JOURNAL_CODESpringerPlus
TITLEExpression of endogenous Mkp1 in 6-OHDA rat models of Parkinson’s disease.
STATUSPublished
TIMES_CITED()
SEARCH_KEYWORD
VOLUME
ISSUE
START_PAGE205
END_PAGE206
ABSTRACTWe 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.
PUBLISHER_LOCATION
ISBN_ISSN
EDITION
URLhttp://www.springerplus.com/content/3/1/205
DOI_LINKdoi:10.1186/2193-1801-3-205
FUNDING_BODY
GRANT_DETAILS