IRIS publication 73312038
Effect of Interleukin-1b and 6-Hydroxydopamine on MKP-1 Expression in Embryonic Rat Ventral Mesencephalic Precursor Cells.
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TY - CONF - Collins L. M., Toulouse A., Nolan Y. M. - 5th Neuroscience Ireland Annual Conference - Effect of Interleukin-1b and 6-Hydroxydopamine on MKP-1 Expression in Embryonic Rat Ventral Mesencephalic Precursor Cells. - 2010 - September - Validated - 1 - () - 180 - University College Dublin - 02-SEP-10 - 03-SEP-10 - Inflammation is associated with the neuropathology of neurodegenerative disorders such as Parkinson¿s disease (PD). Excessive microglial activation and the increase of pro-inflammatory cytokines, such as interleukin-1b (IL-1b), have been associated with exacerbated cell death in patients and models of PD. Members of the mitogen-activated protein (MAP) kinase pathway, p38 and JNK, mediate the death of dopaminergic (DA) neurons in response to inflammatory stress-signals. This pathway is inhibited by the dual-specificity mitogen-activated protein kinase phosphatase1 (MKP-1) through dephosphorylation of tyrosine and threonine residues of activated kinases. Over-expression of MKP-1 has been shown to protect non-neuronal cells from apoptosis through its ability to dephosphorylate p38 and JNK. 6-hydroxydopamine (6-OHDA) treatment of DA neuronal-enriched cultures causes a decrease in the intensity of fluorescence of MKP-1, accompanied by an increase in p38 activity (Nolan ; Long- Smith, unpublished data). This study assessed the effect of an inflammatory environment (IL-1b) and the DA neurotoxin, 6-OHDA, on ventral mesencephalic neural precursor cell (VMNPC) proliferation and differentiation. Sprague¿Dawley rat ventral mesencephalic tissue was isolated at embryonic (E) day 14 and VMNPCs were proliferated as neurospheres for 7 days in vitro (DIV) with appropriate mitogens. Cells were treated with IL-1b (10 ng/ml) on the day of seeding and every 2¿3 days for 7 days and with 6-OHDA (40 lM) at 7DIV for 30 min. At 7DIV neurospheres were dissociated and allowed to differentiate for a further 7DIV during which time cells were treated with IL-1b (10 ng/ml) on the day of seeding and every 2¿3 days for 7 days and with 6-OHDA (40 lM) at 14DIV for 30 min. Cells were immunocytochemically stained for nestin to label neural progenitor cells, doublecortin (DCX) to label newly-born neurons and glial fibrillary acidic protein (GFAP) to label astrocytes. IL-1b and 6-OHDA alter the expression of MKP-1 + nestin + , GFAP + and DCX + cells both during proliferation and differentiation. MKP-1 is a possible key modulator of DA neuronal survival both in response to DA neurotoxins and exposure to an inflammatory environment and could be a possible therapeutic target for the treatment of PD. - DOI 10.1007/s11845-011-0690-8 DA - 2010/09 ER -
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@inproceedings{V73312038, = {Collins L. M., Toulouse A. and Nolan Y. M. }, = {5th Neuroscience Ireland Annual Conference}, = {{Effect of Interleukin-1b and 6-Hydroxydopamine on MKP-1 Expression in Embryonic Rat Ventral Mesencephalic Precursor Cells.}}, = {2010}, = {September}, = {Validated}, = {1}, = {()}, pages = {180}, = {University College Dublin}, month = {Sep}, = {03-SEP-10}, = {{Inflammation is associated with the neuropathology of neurodegenerative disorders such as Parkinson¿s disease (PD). Excessive microglial activation and the increase of pro-inflammatory cytokines, such as interleukin-1b (IL-1b), have been associated with exacerbated cell death in patients and models of PD. Members of the mitogen-activated protein (MAP) kinase pathway, p38 and JNK, mediate the death of dopaminergic (DA) neurons in response to inflammatory stress-signals. This pathway is inhibited by the dual-specificity mitogen-activated protein kinase phosphatase1 (MKP-1) through dephosphorylation of tyrosine and threonine residues of activated kinases. Over-expression of MKP-1 has been shown to protect non-neuronal cells from apoptosis through its ability to dephosphorylate p38 and JNK. 6-hydroxydopamine (6-OHDA) treatment of DA neuronal-enriched cultures causes a decrease in the intensity of fluorescence of MKP-1, accompanied by an increase in p38 activity (Nolan ; Long- Smith, unpublished data). This study assessed the effect of an inflammatory environment (IL-1b) and the DA neurotoxin, 6-OHDA, on ventral mesencephalic neural precursor cell (VMNPC) proliferation and differentiation. Sprague¿Dawley rat ventral mesencephalic tissue was isolated at embryonic (E) day 14 and VMNPCs were proliferated as neurospheres for 7 days in vitro (DIV) with appropriate mitogens. Cells were treated with IL-1b (10 ng/ml) on the day of seeding and every 2¿3 days for 7 days and with 6-OHDA (40 lM) at 7DIV for 30 min. At 7DIV neurospheres were dissociated and allowed to differentiate for a further 7DIV during which time cells were treated with IL-1b (10 ng/ml) on the day of seeding and every 2¿3 days for 7 days and with 6-OHDA (40 lM) at 14DIV for 30 min. Cells were immunocytochemically stained for nestin to label neural progenitor cells, doublecortin (DCX) to label newly-born neurons and glial fibrillary acidic protein (GFAP) to label astrocytes. IL-1b and 6-OHDA alter the expression of MKP-1 + nestin + , GFAP + and DCX + cells both during proliferation and differentiation. MKP-1 is a possible key modulator of DA neuronal survival both in response to DA neurotoxins and exposure to an inflammatory environment and could be a possible therapeutic target for the treatment of PD.}}, = {DOI 10.1007/s11845-011-0690-8}, source = {IRIS} }
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AUTHORS | Collins L. M., Toulouse A., Nolan Y. M. | ||
TITLE | 5th Neuroscience Ireland Annual Conference | ||
PUBLICATION_NAME | Effect of Interleukin-1b and 6-Hydroxydopamine on MKP-1 Expression in Embryonic Rat Ventral Mesencephalic Precursor Cells. | ||
YEAR | 2010 | ||
MONTH | September | ||
STATUS | Validated | ||
PEER_REVIEW | 1 | ||
TIMES_CITED | () | ||
SEARCH_KEYWORD | |||
EDITORS | |||
START_PAGE | 180 | ||
END_PAGE | |||
LOCATION | University College Dublin | ||
START_DATE | 02-SEP-10 | ||
END_DATE | 03-SEP-10 | ||
ABSTRACT | Inflammation is associated with the neuropathology of neurodegenerative disorders such as Parkinson¿s disease (PD). Excessive microglial activation and the increase of pro-inflammatory cytokines, such as interleukin-1b (IL-1b), have been associated with exacerbated cell death in patients and models of PD. Members of the mitogen-activated protein (MAP) kinase pathway, p38 and JNK, mediate the death of dopaminergic (DA) neurons in response to inflammatory stress-signals. This pathway is inhibited by the dual-specificity mitogen-activated protein kinase phosphatase1 (MKP-1) through dephosphorylation of tyrosine and threonine residues of activated kinases. Over-expression of MKP-1 has been shown to protect non-neuronal cells from apoptosis through its ability to dephosphorylate p38 and JNK. 6-hydroxydopamine (6-OHDA) treatment of DA neuronal-enriched cultures causes a decrease in the intensity of fluorescence of MKP-1, accompanied by an increase in p38 activity (Nolan ; Long- Smith, unpublished data). This study assessed the effect of an inflammatory environment (IL-1b) and the DA neurotoxin, 6-OHDA, on ventral mesencephalic neural precursor cell (VMNPC) proliferation and differentiation. Sprague¿Dawley rat ventral mesencephalic tissue was isolated at embryonic (E) day 14 and VMNPCs were proliferated as neurospheres for 7 days in vitro (DIV) with appropriate mitogens. Cells were treated with IL-1b (10 ng/ml) on the day of seeding and every 2¿3 days for 7 days and with 6-OHDA (40 lM) at 7DIV for 30 min. At 7DIV neurospheres were dissociated and allowed to differentiate for a further 7DIV during which time cells were treated with IL-1b (10 ng/ml) on the day of seeding and every 2¿3 days for 7 days and with 6-OHDA (40 lM) at 14DIV for 30 min. Cells were immunocytochemically stained for nestin to label neural progenitor cells, doublecortin (DCX) to label newly-born neurons and glial fibrillary acidic protein (GFAP) to label astrocytes. IL-1b and 6-OHDA alter the expression of MKP-1 + nestin + , GFAP + and DCX + cells both during proliferation and differentiation. MKP-1 is a possible key modulator of DA neuronal survival both in response to DA neurotoxins and exposure to an inflammatory environment and could be a possible therapeutic target for the treatment of PD. | ||
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DOI_LINK | DOI 10.1007/s11845-011-0690-8 | ||
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