Suppression of p140trkA Does Not Abolish Nerve Growth Factor‐Mediated Rescue of Serum‐Free PC12 Cells
: Programmed cell death, the intrinsic form of apoptosis, plays an integral role in those neurodegenerative events associated with age‐related neuropathology. Neurotrophins (NTs), such as nerve growth factor (NGF), brain‐derived neurotrophic factor (BDNF), and NT‐3, are required for survival of cert...
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| Veröffentlicht in: | Journal of neurochemistry 1996-05, Vol.66 (5), p.1826-1835 |
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| container_title | Journal of neurochemistry |
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| creator | Taglialatela, Giulio Hibbert, Chris J. Hutton, Leslie A. Werrbach‐Perez, Karin Perez‐Polo, J. Regino |
| description | : Programmed cell death, the intrinsic form of apoptosis, plays an integral role in those neurodegenerative events associated with age‐related neuropathology. Neurotrophins (NTs), such as nerve growth factor (NGF), brain‐derived neurotrophic factor (BDNF), and NT‐3, are required for survival of certain neurons, and thus their clinical use to counteract age‐ and pathology‐associated neurodegeneration has been suggested, although mechanistic descriptions for NT cell rescue from apoptosis are not definitive. Here we attempted to isolate the individual actions of high‐affinity tyrosine kinase (Trk) receptors and p75NGFR, the common low‐affinity NT receptor, in NT rescue of apoptotic PC12 cells. Our results showed that whereas inhibiting Trk receptor phosphorylation abolishes NGF rescue of serum‐deprived PC12 cells from apoptosis, TrkA suppression with antisense oligonucleotides did not. Also, although BDNF did not rescue naive serumless PC12 cells, which lack the BDNF‐specific TrkB receptor, it significantly increased survival of TrkA‐suppressed serum‐starved PC12 cells. These data confirm the hypothesis that binding of any NT to Trk‐free p75NGFR‐bearing cells blocks apoptosis but also suggest that if Trk receptors are expressed, prohibiting Trk phosphorylation also blocks NT‐mediated rescue from apoptosis. |
| doi_str_mv | 10.1046/j.1471-4159.1996.66051826.x |
| format | Article |
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Regino</creator><creatorcontrib>Taglialatela, Giulio ; Hibbert, Chris J. ; Hutton, Leslie A. ; Werrbach‐Perez, Karin ; Perez‐Polo, J. Regino</creatorcontrib><description>: Programmed cell death, the intrinsic form of apoptosis, plays an integral role in those neurodegenerative events associated with age‐related neuropathology. Neurotrophins (NTs), such as nerve growth factor (NGF), brain‐derived neurotrophic factor (BDNF), and NT‐3, are required for survival of certain neurons, and thus their clinical use to counteract age‐ and pathology‐associated neurodegeneration has been suggested, although mechanistic descriptions for NT cell rescue from apoptosis are not definitive. Here we attempted to isolate the individual actions of high‐affinity tyrosine kinase (Trk) receptors and p75NGFR, the common low‐affinity NT receptor, in NT rescue of apoptotic PC12 cells. Our results showed that whereas inhibiting Trk receptor phosphorylation abolishes NGF rescue of serum‐deprived PC12 cells from apoptosis, TrkA suppression with antisense oligonucleotides did not. Also, although BDNF did not rescue naive serumless PC12 cells, which lack the BDNF‐specific TrkB receptor, it significantly increased survival of TrkA‐suppressed serum‐starved PC12 cells. These data confirm the hypothesis that binding of any NT to Trk‐free p75NGFR‐bearing cells blocks apoptosis but also suggest that if Trk receptors are expressed, prohibiting Trk phosphorylation also blocks NT‐mediated rescue from apoptosis.</description><identifier>ISSN: 0022-3042</identifier><identifier>EISSN: 1471-4159</identifier><identifier>DOI: 10.1046/j.1471-4159.1996.66051826.x</identifier><identifier>PMID: 8780007</identifier><identifier>CODEN: JONRA9</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Aging ; Animals ; Antisense oligonucleotide ; Apoptosis ; Apoptosis - physiology ; Base Sequence ; Biological and medical sciences ; Brain-Derived Neurotrophic Factor - pharmacology ; Carbazoles - pharmacology ; Cell Survival - drug effects ; Culture Media, Serum-Free ; Development. Senescence. Regeneration. Transplantation ; Fundamental and applied biological sciences. Psychology ; Indole Alkaloids ; Molecular Sequence Data ; Nerve Growth Factors - pharmacology ; Nerve Growth Factors - physiology ; Neurotrophin ; Neurotrophin 3 ; Oligonucleotides, Antisense - genetics ; Oligonucleotides, Antisense - pharmacology ; p75NGFR ; PC12 Cells - drug effects ; PC12 Cells - physiology ; Proto-Oncogene Proteins - antagonists & inhibitors ; Rats ; Receptor Protein-Tyrosine Kinases - antagonists & inhibitors ; Receptor, trkA ; Receptors, Nerve Growth Factor - antagonists & inhibitors ; Tyrosine kinase ; Vertebrates: nervous system and sense organs</subject><ispartof>Journal of neurochemistry, 1996-05, Vol.66 (5), p.1826-1835</ispartof><rights>1996 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1046%2Fj.1471-4159.1996.66051826.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1046%2Fj.1471-4159.1996.66051826.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3046794$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8780007$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Taglialatela, Giulio</creatorcontrib><creatorcontrib>Hibbert, Chris J.</creatorcontrib><creatorcontrib>Hutton, Leslie A.</creatorcontrib><creatorcontrib>Werrbach‐Perez, Karin</creatorcontrib><creatorcontrib>Perez‐Polo, J. Regino</creatorcontrib><title>Suppression of p140trkA Does Not Abolish Nerve Growth Factor‐Mediated Rescue of Serum‐Free PC12 Cells</title><title>Journal of neurochemistry</title><addtitle>J Neurochem</addtitle><description>: Programmed cell death, the intrinsic form of apoptosis, plays an integral role in those neurodegenerative events associated with age‐related neuropathology. Neurotrophins (NTs), such as nerve growth factor (NGF), brain‐derived neurotrophic factor (BDNF), and NT‐3, are required for survival of certain neurons, and thus their clinical use to counteract age‐ and pathology‐associated neurodegeneration has been suggested, although mechanistic descriptions for NT cell rescue from apoptosis are not definitive. Here we attempted to isolate the individual actions of high‐affinity tyrosine kinase (Trk) receptors and p75NGFR, the common low‐affinity NT receptor, in NT rescue of apoptotic PC12 cells. Our results showed that whereas inhibiting Trk receptor phosphorylation abolishes NGF rescue of serum‐deprived PC12 cells from apoptosis, TrkA suppression with antisense oligonucleotides did not. Also, although BDNF did not rescue naive serumless PC12 cells, which lack the BDNF‐specific TrkB receptor, it significantly increased survival of TrkA‐suppressed serum‐starved PC12 cells. These data confirm the hypothesis that binding of any NT to Trk‐free p75NGFR‐bearing cells blocks apoptosis but also suggest that if Trk receptors are expressed, prohibiting Trk phosphorylation also blocks NT‐mediated rescue from apoptosis.</description><subject>Aging</subject><subject>Animals</subject><subject>Antisense oligonucleotide</subject><subject>Apoptosis</subject><subject>Apoptosis - physiology</subject><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>Brain-Derived Neurotrophic Factor - pharmacology</subject><subject>Carbazoles - pharmacology</subject><subject>Cell Survival - drug effects</subject><subject>Culture Media, Serum-Free</subject><subject>Development. Senescence. Regeneration. Transplantation</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Indole Alkaloids</subject><subject>Molecular Sequence Data</subject><subject>Nerve Growth Factors - pharmacology</subject><subject>Nerve Growth Factors - physiology</subject><subject>Neurotrophin</subject><subject>Neurotrophin 3</subject><subject>Oligonucleotides, Antisense - genetics</subject><subject>Oligonucleotides, Antisense - pharmacology</subject><subject>p75NGFR</subject><subject>PC12 Cells - drug effects</subject><subject>PC12 Cells - physiology</subject><subject>Proto-Oncogene Proteins - antagonists & inhibitors</subject><subject>Rats</subject><subject>Receptor Protein-Tyrosine Kinases - antagonists & inhibitors</subject><subject>Receptor, trkA</subject><subject>Receptors, Nerve Growth Factor - antagonists & inhibitors</subject><subject>Tyrosine kinase</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0022-3042</issn><issn>1471-4159</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kd1O2zAUgK1piBW2R5hkadPuEnwc13Yuq7Dyo1LQ2K4tJzkR6dI62Ak_dzwCz8iTkIi2V5b1fTq2zkfID2AxMCFPVjEIBZGAaRpDmspYSjYFzWX89IlM9uwzmTDGeZQwwb-QoxBWjIEUEg7JoVaaMaYmpL7t29ZjCLXbUFfRFgTr_P8ZPXUY6NJ1dJa7pg53dIn-AemZd4_dHZ3bonP-7eX1CsvadljSPxiKHscRt-j79YDmHpHeZMBphk0TvpKDyjYBv23PY_Jv_vtvdh4trs8ustkiGp5OZJRIJbjQUiNWVSkgSXVh0zK3vFSlEjIXCQhgKuWYFKitBZtLRC4EMl1AlRyTXx9zW-_uewydWdehGH5gN-j6YJTmGlI9HcTvW7HP11ia1tdr65_NdjcD_7nlNhS2qbzdFHXYa8NapUrFoJ1-aI91g897DMyMsczKjEHMGMSMscwulnkyl8tsd0veAW8niXo</recordid><startdate>199605</startdate><enddate>199605</enddate><creator>Taglialatela, Giulio</creator><creator>Hibbert, Chris J.</creator><creator>Hutton, Leslie A.</creator><creator>Werrbach‐Perez, Karin</creator><creator>Perez‐Polo, J. Regino</creator><general>Blackwell Science Ltd</general><general>Blackwell</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>199605</creationdate><title>Suppression of p140trkA Does Not Abolish Nerve Growth Factor‐Mediated Rescue of Serum‐Free PC12 Cells</title><author>Taglialatela, Giulio ; Hibbert, Chris J. ; Hutton, Leslie A. ; Werrbach‐Perez, Karin ; Perez‐Polo, J. Regino</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p1436-367424868eeffd41398ca9dba2d7d746b431410792e3ce8aa1ab6ee244e08c1f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Aging</topic><topic>Animals</topic><topic>Antisense oligonucleotide</topic><topic>Apoptosis</topic><topic>Apoptosis - physiology</topic><topic>Base Sequence</topic><topic>Biological and medical sciences</topic><topic>Brain-Derived Neurotrophic Factor - pharmacology</topic><topic>Carbazoles - pharmacology</topic><topic>Cell Survival - drug effects</topic><topic>Culture Media, Serum-Free</topic><topic>Development. Senescence. Regeneration. Transplantation</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Indole Alkaloids</topic><topic>Molecular Sequence Data</topic><topic>Nerve Growth Factors - pharmacology</topic><topic>Nerve Growth Factors - physiology</topic><topic>Neurotrophin</topic><topic>Neurotrophin 3</topic><topic>Oligonucleotides, Antisense - genetics</topic><topic>Oligonucleotides, Antisense - pharmacology</topic><topic>p75NGFR</topic><topic>PC12 Cells - drug effects</topic><topic>PC12 Cells - physiology</topic><topic>Proto-Oncogene Proteins - antagonists & inhibitors</topic><topic>Rats</topic><topic>Receptor Protein-Tyrosine Kinases - antagonists & inhibitors</topic><topic>Receptor, trkA</topic><topic>Receptors, Nerve Growth Factor - antagonists & inhibitors</topic><topic>Tyrosine kinase</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Taglialatela, Giulio</creatorcontrib><creatorcontrib>Hibbert, Chris J.</creatorcontrib><creatorcontrib>Hutton, Leslie A.</creatorcontrib><creatorcontrib>Werrbach‐Perez, Karin</creatorcontrib><creatorcontrib>Perez‐Polo, J. Regino</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of neurochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Taglialatela, Giulio</au><au>Hibbert, Chris J.</au><au>Hutton, Leslie A.</au><au>Werrbach‐Perez, Karin</au><au>Perez‐Polo, J. Regino</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Suppression of p140trkA Does Not Abolish Nerve Growth Factor‐Mediated Rescue of Serum‐Free PC12 Cells</atitle><jtitle>Journal of neurochemistry</jtitle><addtitle>J Neurochem</addtitle><date>1996-05</date><risdate>1996</risdate><volume>66</volume><issue>5</issue><spage>1826</spage><epage>1835</epage><pages>1826-1835</pages><issn>0022-3042</issn><eissn>1471-4159</eissn><coden>JONRA9</coden><abstract>: Programmed cell death, the intrinsic form of apoptosis, plays an integral role in those neurodegenerative events associated with age‐related neuropathology. Neurotrophins (NTs), such as nerve growth factor (NGF), brain‐derived neurotrophic factor (BDNF), and NT‐3, are required for survival of certain neurons, and thus their clinical use to counteract age‐ and pathology‐associated neurodegeneration has been suggested, although mechanistic descriptions for NT cell rescue from apoptosis are not definitive. Here we attempted to isolate the individual actions of high‐affinity tyrosine kinase (Trk) receptors and p75NGFR, the common low‐affinity NT receptor, in NT rescue of apoptotic PC12 cells. Our results showed that whereas inhibiting Trk receptor phosphorylation abolishes NGF rescue of serum‐deprived PC12 cells from apoptosis, TrkA suppression with antisense oligonucleotides did not. Also, although BDNF did not rescue naive serumless PC12 cells, which lack the BDNF‐specific TrkB receptor, it significantly increased survival of TrkA‐suppressed serum‐starved PC12 cells. These data confirm the hypothesis that binding of any NT to Trk‐free p75NGFR‐bearing cells blocks apoptosis but also suggest that if Trk receptors are expressed, prohibiting Trk phosphorylation also blocks NT‐mediated rescue from apoptosis.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>8780007</pmid><doi>10.1046/j.1471-4159.1996.66051826.x</doi><tpages>10</tpages></addata></record> |
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| ispartof | Journal of neurochemistry, 1996-05, Vol.66 (5), p.1826-1835 |
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| source | MEDLINE; Access via Wiley Online Library |
| subjects | Aging Animals Antisense oligonucleotide Apoptosis Apoptosis - physiology Base Sequence Biological and medical sciences Brain-Derived Neurotrophic Factor - pharmacology Carbazoles - pharmacology Cell Survival - drug effects Culture Media, Serum-Free Development. Senescence. Regeneration. Transplantation Fundamental and applied biological sciences. Psychology Indole Alkaloids Molecular Sequence Data Nerve Growth Factors - pharmacology Nerve Growth Factors - physiology Neurotrophin Neurotrophin 3 Oligonucleotides, Antisense - genetics Oligonucleotides, Antisense - pharmacology p75NGFR PC12 Cells - drug effects PC12 Cells - physiology Proto-Oncogene Proteins - antagonists & inhibitors Rats Receptor Protein-Tyrosine Kinases - antagonists & inhibitors Receptor, trkA Receptors, Nerve Growth Factor - antagonists & inhibitors Tyrosine kinase Vertebrates: nervous system and sense organs |
| title | Suppression of p140trkA Does Not Abolish Nerve Growth Factor‐Mediated Rescue of Serum‐Free PC12 Cells |
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