In vitro optimization of retinoic acid–induced neuritogenesis and TH endogenous expression in human SH-SY5Y neuroblastoma cells by the antioxidant Trolox
Though, it is quite well-known how retinoic acid (RA) is able to induce neuritogenesis in different in vitro models, the putative role exerted by reactive oxygen species (ROS) during this process still need to be further studied. For such purpose, we used a neuronal-like cell line (SH-SY5Y cells) in...
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creator | Frota Junior, Mario Luiz Conte da Pires, André Simões Zeidán-Chuliá, Fares Bristot, Ivi Juliana Lopes, Fernanda M. de Bittencourt Pasquali, Matheus Augusto Zanotto-Filho, Alfeu Behr, Guilherme Antônio Klamt, Fabio Gelain, Daniel Pens Moreira, José Cláudio Fonseca |
description | Though, it is quite well-known how retinoic acid (RA) is able to induce neuritogenesis in different in vitro models, the putative role exerted by reactive oxygen species (ROS) during this process still need to be further studied. For such purpose, we used a neuronal-like cell line (SH-SY5Y cells) in order to investigate whether the antioxidant Trolox (a hydrophilic analog of alpha-tocopherol) could have any effect on the number of RA-induced neurites, and how significant changes in cellular redox homeostasis may affect the cellular endogenous expression of tyrosine hydroxylase (TH). Our results show a significant enhancement of RA (10 μM)-induced neuritogenesis and TH endogenous expression, when cells were co-treated with Trolox (100 μM) for 7 days. Moreover, this effect was associated with an improvement in cellular viability. The mechanism seems to mainly involve PI3 K/Akt rather than MEK signaling pathway. Therefore, our data demonstrate that concomitant decreases in basal reactive oxygen species (ROS) production could exert a positive effect on the neuritogenic process of RA-treated SH-SY5Y cells. |
doi_str_mv | 10.1007/s11010-011-0983-2 |
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For such purpose, we used a neuronal-like cell line (SH-SY5Y cells) in order to investigate whether the antioxidant Trolox (a hydrophilic analog of alpha-tocopherol) could have any effect on the number of RA-induced neurites, and how significant changes in cellular redox homeostasis may affect the cellular endogenous expression of tyrosine hydroxylase (TH). Our results show a significant enhancement of RA (10 μM)-induced neuritogenesis and TH endogenous expression, when cells were co-treated with Trolox (100 μM) for 7 days. Moreover, this effect was associated with an improvement in cellular viability. The mechanism seems to mainly involve PI3 K/Akt rather than MEK signaling pathway. Therefore, our data demonstrate that concomitant decreases in basal reactive oxygen species (ROS) production could exert a positive effect on the neuritogenic process of RA-treated SH-SY5Y cells.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-011-0983-2</identifier><identifier>PMID: 21735090</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Analysis ; Antioxidants ; Antioxidants - pharmacology ; Biochemistry ; Biomedical and Life Sciences ; Cardiology ; Cell Line, Tumor ; Cell Survival - drug effects ; Cellular biology ; Chromans - pharmacology ; Homeostasis ; Humans ; Indexing in process ; Life Sciences ; Lipid Peroxidation - drug effects ; Medical Biochemistry ; Microscopy, Phase-Contrast ; Neurites - drug effects ; Neurites - metabolism ; Neuroblastoma - enzymology ; Neuroblastoma - pathology ; Neurogenesis - drug effects ; Oncology ; Oxidative Stress - drug effects ; Parkinson's disease ; Phosphatidylinositol 3-Kinases - antagonists & inhibitors ; Phosphatidylinositol 3-Kinases - metabolism ; Protein Kinase Inhibitors - pharmacology ; Proto-Oncogene Proteins c-akt - antagonists & inhibitors ; Proto-Oncogene Proteins c-akt - metabolism ; Reactive Oxygen Species - metabolism ; Tocopherols ; Toy industry ; Tretinoin ; Tretinoin - pharmacology ; Tyrosine 3-Monooxygenase - metabolism</subject><ispartof>Molecular and cellular biochemistry, 2011-12, Vol.358 (1-2), p.325-334</ispartof><rights>Springer Science+Business Media, LLC. 2011</rights><rights>COPYRIGHT 2011 Springer</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-3fba000c79c3a4d8f0575a26e113b2885f067721866cf5908393faf85e3bc1783</citedby><cites>FETCH-LOGICAL-c470t-3fba000c79c3a4d8f0575a26e113b2885f067721866cf5908393faf85e3bc1783</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11010-011-0983-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11010-011-0983-2$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21735090$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Frota Junior, Mario Luiz Conte da</creatorcontrib><creatorcontrib>Pires, André Simões</creatorcontrib><creatorcontrib>Zeidán-Chuliá, Fares</creatorcontrib><creatorcontrib>Bristot, Ivi Juliana</creatorcontrib><creatorcontrib>Lopes, Fernanda M.</creatorcontrib><creatorcontrib>de Bittencourt Pasquali, Matheus Augusto</creatorcontrib><creatorcontrib>Zanotto-Filho, Alfeu</creatorcontrib><creatorcontrib>Behr, Guilherme Antônio</creatorcontrib><creatorcontrib>Klamt, Fabio</creatorcontrib><creatorcontrib>Gelain, Daniel Pens</creatorcontrib><creatorcontrib>Moreira, José Cláudio Fonseca</creatorcontrib><title>In vitro optimization of retinoic acid–induced neuritogenesis and TH endogenous expression in human SH-SY5Y neuroblastoma cells by the antioxidant Trolox</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><addtitle>Mol Cell Biochem</addtitle><description>Though, it is quite well-known how retinoic acid (RA) is able to induce neuritogenesis in different in vitro models, the putative role exerted by reactive oxygen species (ROS) during this process still need to be further studied. 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Therefore, our data demonstrate that concomitant decreases in basal reactive oxygen species (ROS) production could exert a positive effect on the neuritogenic process of RA-treated SH-SY5Y cells.</description><subject>Analysis</subject><subject>Antioxidants</subject><subject>Antioxidants - pharmacology</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cardiology</subject><subject>Cell Line, Tumor</subject><subject>Cell Survival - drug effects</subject><subject>Cellular biology</subject><subject>Chromans - pharmacology</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Indexing in process</subject><subject>Life Sciences</subject><subject>Lipid Peroxidation - drug effects</subject><subject>Medical Biochemistry</subject><subject>Microscopy, Phase-Contrast</subject><subject>Neurites - drug effects</subject><subject>Neurites - metabolism</subject><subject>Neuroblastoma - enzymology</subject><subject>Neuroblastoma - 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Biochem</addtitle><date>2011-12-01</date><risdate>2011</risdate><volume>358</volume><issue>1-2</issue><spage>325</spage><epage>334</epage><pages>325-334</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>Though, it is quite well-known how retinoic acid (RA) is able to induce neuritogenesis in different in vitro models, the putative role exerted by reactive oxygen species (ROS) during this process still need to be further studied. For such purpose, we used a neuronal-like cell line (SH-SY5Y cells) in order to investigate whether the antioxidant Trolox (a hydrophilic analog of alpha-tocopherol) could have any effect on the number of RA-induced neurites, and how significant changes in cellular redox homeostasis may affect the cellular endogenous expression of tyrosine hydroxylase (TH). Our results show a significant enhancement of RA (10 μM)-induced neuritogenesis and TH endogenous expression, when cells were co-treated with Trolox (100 μM) for 7 days. Moreover, this effect was associated with an improvement in cellular viability. The mechanism seems to mainly involve PI3 K/Akt rather than MEK signaling pathway. Therefore, our data demonstrate that concomitant decreases in basal reactive oxygen species (ROS) production could exert a positive effect on the neuritogenic process of RA-treated SH-SY5Y cells.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>21735090</pmid><doi>10.1007/s11010-011-0983-2</doi><tpages>10</tpages></addata></record> |
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subjects | Analysis Antioxidants Antioxidants - pharmacology Biochemistry Biomedical and Life Sciences Cardiology Cell Line, Tumor Cell Survival - drug effects Cellular biology Chromans - pharmacology Homeostasis Humans Indexing in process Life Sciences Lipid Peroxidation - drug effects Medical Biochemistry Microscopy, Phase-Contrast Neurites - drug effects Neurites - metabolism Neuroblastoma - enzymology Neuroblastoma - pathology Neurogenesis - drug effects Oncology Oxidative Stress - drug effects Parkinson's disease Phosphatidylinositol 3-Kinases - antagonists & inhibitors Phosphatidylinositol 3-Kinases - metabolism Protein Kinase Inhibitors - pharmacology Proto-Oncogene Proteins c-akt - antagonists & inhibitors Proto-Oncogene Proteins c-akt - metabolism Reactive Oxygen Species - metabolism Tocopherols Toy industry Tretinoin Tretinoin - pharmacology Tyrosine 3-Monooxygenase - metabolism |
title | In vitro optimization of retinoic acid–induced neuritogenesis and TH endogenous expression in human SH-SY5Y neuroblastoma cells by the antioxidant Trolox |
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