Activity deprivation induces neuronal cell death: mediation by tissue-type plasminogen activator
Spontaneous activity is an essential attribute of neuronal networks and plays a critical role in their development and maintenance. Upon blockade of activity with tetrodotoxin (TTX), neurons degenerate slowly and die in a manner resembling neurodegenerative diseases-induced neuronal cell death. The...
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| Veröffentlicht in: | PloS one 2011-10, Vol.6 (10), p.e25919 |
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| description | Spontaneous activity is an essential attribute of neuronal networks and plays a critical role in their development and maintenance. Upon blockade of activity with tetrodotoxin (TTX), neurons degenerate slowly and die in a manner resembling neurodegenerative diseases-induced neuronal cell death. The molecular cascade leading to this type of slow cell death is not entirely clear. Primary post-natal cortical neurons were exposed to TTX for up to two weeks, followed by molecular, biochemical and immunefluorescence analysis. The expression of the neuronal marker, neuron specific enolase (NSE), was down-regulated, as expected, but surprisingly, there was a concomitant and striking elevation in expression of tissue-type plasminogen activator (tPA). Immunofluorescence analysis indicated that tPA was highly elevated inside affected neurons. Transfection of an endogenous tPA inhibitor, plasminogen activator inhibitor-1 (PAI-1), protected the TTX-exposed neurons from dying. These results indicate that tPA is a pivotal player in slowly progressing activity deprivation-induced neurodegeneration. |
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Upon blockade of activity with tetrodotoxin (TTX), neurons degenerate slowly and die in a manner resembling neurodegenerative diseases-induced neuronal cell death. The molecular cascade leading to this type of slow cell death is not entirely clear. Primary post-natal cortical neurons were exposed to TTX for up to two weeks, followed by molecular, biochemical and immunefluorescence analysis. The expression of the neuronal marker, neuron specific enolase (NSE), was down-regulated, as expected, but surprisingly, there was a concomitant and striking elevation in expression of tissue-type plasminogen activator (tPA). Immunofluorescence analysis indicated that tPA was highly elevated inside affected neurons. Transfection of an endogenous tPA inhibitor, plasminogen activator inhibitor-1 (PAI-1), protected the TTX-exposed neurons from dying. These results indicate that tPA is a pivotal player in slowly progressing activity deprivation-induced neurodegeneration.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0025919</identifier><identifier>PMID: 21998719</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Analysis ; Animals ; Apoptosis ; Biochemistry ; Biology ; Cell death ; Cell Death - drug effects ; Cell Survival - drug effects ; Deprivation ; Down-Regulation - drug effects ; Experiments ; Growth factors ; Immunofluorescence ; Inhibitors ; Ischemia ; Localization ; Mediation ; Medicine ; Mortality ; Nervous system ; Nervous system diseases ; Neural networks ; Neurobiology ; Neurodegeneration ; Neurodegenerative diseases ; Neurological diseases ; Neurons ; Neurons - cytology ; Neurons - drug effects ; Neurons - metabolism ; Neurosciences ; Neurotoxicity ; Neurotoxins - toxicity ; Phosphopyruvate hydratase ; Phosphopyruvate Hydratase - genetics ; Plasminogen activator inhibitors ; Polyamide-imides ; Proteins ; Rats ; Rats, Wistar ; t-Plasminogen activator ; Tetrodotoxin ; Tetrodotoxin - toxicity ; Tissue plasminogen activator ; Tissue Plasminogen Activator - genetics ; Tissue Plasminogen Activator - metabolism ; Transfection ; Tumor necrosis factor-TNF ; Up-Regulation - drug effects</subject><ispartof>PloS one, 2011-10, Vol.6 (10), p.e25919</ispartof><rights>COPYRIGHT 2011 Public Library of Science</rights><rights>2011 Schonfeld-Dado, Segal. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. 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Upon blockade of activity with tetrodotoxin (TTX), neurons degenerate slowly and die in a manner resembling neurodegenerative diseases-induced neuronal cell death. The molecular cascade leading to this type of slow cell death is not entirely clear. Primary post-natal cortical neurons were exposed to TTX for up to two weeks, followed by molecular, biochemical and immunefluorescence analysis. The expression of the neuronal marker, neuron specific enolase (NSE), was down-regulated, as expected, but surprisingly, there was a concomitant and striking elevation in expression of tissue-type plasminogen activator (tPA). Immunofluorescence analysis indicated that tPA was highly elevated inside affected neurons. Transfection of an endogenous tPA inhibitor, plasminogen activator inhibitor-1 (PAI-1), protected the TTX-exposed neurons from dying. 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Upon blockade of activity with tetrodotoxin (TTX), neurons degenerate slowly and die in a manner resembling neurodegenerative diseases-induced neuronal cell death. The molecular cascade leading to this type of slow cell death is not entirely clear. Primary post-natal cortical neurons were exposed to TTX for up to two weeks, followed by molecular, biochemical and immunefluorescence analysis. The expression of the neuronal marker, neuron specific enolase (NSE), was down-regulated, as expected, but surprisingly, there was a concomitant and striking elevation in expression of tissue-type plasminogen activator (tPA). Immunofluorescence analysis indicated that tPA was highly elevated inside affected neurons. Transfection of an endogenous tPA inhibitor, plasminogen activator inhibitor-1 (PAI-1), protected the TTX-exposed neurons from dying. These results indicate that tPA is a pivotal player in slowly progressing activity deprivation-induced neurodegeneration.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>21998719</pmid><doi>10.1371/journal.pone.0025919</doi><tpages>e25919</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Analysis Animals Apoptosis Biochemistry Biology Cell death Cell Death - drug effects Cell Survival - drug effects Deprivation Down-Regulation - drug effects Experiments Growth factors Immunofluorescence Inhibitors Ischemia Localization Mediation Medicine Mortality Nervous system Nervous system diseases Neural networks Neurobiology Neurodegeneration Neurodegenerative diseases Neurological diseases Neurons Neurons - cytology Neurons - drug effects Neurons - metabolism Neurosciences Neurotoxicity Neurotoxins - toxicity Phosphopyruvate hydratase Phosphopyruvate Hydratase - genetics Plasminogen activator inhibitors Polyamide-imides Proteins Rats Rats, Wistar t-Plasminogen activator Tetrodotoxin Tetrodotoxin - toxicity Tissue plasminogen activator Tissue Plasminogen Activator - genetics Tissue Plasminogen Activator - metabolism Transfection Tumor necrosis factor-TNF Up-Regulation - drug effects |
| title | Activity deprivation induces neuronal cell death: mediation by tissue-type plasminogen activator |
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