The regulation of mitochondrial dynamics in neurite outgrowth by retinoic acid receptor β signaling
ABSTRACT Neuronal regeneration is a highly energy‐demanding process that greatly relies on axonal mitochondrial transport to meet the enhanced metabolic requirements. Mature neurons typically fail to regenerate after injury, partly because of mitochondrial motility and energy deficits in injured axo...
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Neuronal regeneration is a highly energy‐demanding process that greatly relies on axonal mitochondrial transport to meet the enhanced metabolic requirements. Mature neurons typically fail to regenerate after injury, partly because of mitochondrial motility and energy deficits in injured axons. Retinoic acid receptor (RAR)‐β signaling is involved in axonal and neurite regeneration. Here we investigate the effect of RAR‐β signaling on mitochondrial trafficking during neurite outgrowth and find that it enhances their proliferation, speed, and movement toward the growing end of the neuron via hypoxia‐inducible factor 1α signaling. We also show that RAR‐β signaling promotes the binding of the mitochondria to the anchoring protein, glucose‐related protein 75, at the growing tip of neurite, thus allowing them to provide energy and metabolic roles required for neurite outgrowth.—Trigo, D., Goncalves, M. B., Corcoran, J. P. T. The regulation of mitochondrial dynamics in neurite outgrowth by retinoic acid receptor β signaling. FASEB J. 33, 7225–7235 (2019). www.fasebj.org |
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Neuronal regeneration is a highly energy‐demanding process that greatly relies on axonal mitochondrial transport to meet the enhanced metabolic requirements. Mature neurons typically fail to regenerate after injury, partly because of mitochondrial motility and energy deficits in injured axons. Retinoic acid receptor (RAR)‐β signaling is involved in axonal and neurite regeneration. Here we investigate the effect of RAR‐β signaling on mitochondrial trafficking during neurite outgrowth and find that it enhances their proliferation, speed, and movement toward the growing end of the neuron via hypoxia‐inducible factor 1α signaling. We also show that RAR‐β signaling promotes the binding of the mitochondria to the anchoring protein, glucose‐related protein 75, at the growing tip of neurite, thus allowing them to provide energy and metabolic roles required for neurite outgrowth.—Trigo, D., Goncalves, M. B., Corcoran, J. P. T. The regulation of mitochondrial dynamics in neurite outgrowth by retinoic acid receptor β signaling. FASEB J. 33, 7225–7235 (2019). www.fasebj.org</description><identifier>ISSN: 0892-6638</identifier><identifier>EISSN: 1530-6860</identifier><identifier>DOI: 10.1096/fj.201802097R</identifier><identifier>PMID: 30857414</identifier><language>eng</language><publisher>United States: Federation of American Societies for Experimental Biology</publisher><subject>Adenosine Triphosphate - metabolism ; Animals ; Cells, Cultured ; energy metabolism ; growth cone ; HSP70 Heat-Shock Proteins - antagonists & inhibitors ; HSP70 Heat-Shock Proteins - genetics ; HSP70 Heat-Shock Proteins - physiology ; Hypoxia-Inducible Factor 1, alpha Subunit - biosynthesis ; Hypoxia-Inducible Factor 1, alpha Subunit - genetics ; Hypoxia-Inducible Factor 1, alpha Subunit - physiology ; Membrane Proteins - antagonists & inhibitors ; Membrane Proteins - genetics ; Membrane Proteins - physiology ; Mice ; Mitochondrial Dynamics - drug effects ; Mitochondrial Dynamics - physiology ; Naphthalenes - pharmacology ; neuron ; Neuronal Outgrowth - drug effects ; Neuronal Outgrowth - physiology ; Neurons - metabolism ; Receptors, Retinoic Acid - agonists ; Receptors, Retinoic Acid - physiology ; retinoid ; RNA Interference ; RNA, Small Interfering - pharmacology</subject><ispartof>The FASEB journal, 2019-06, Vol.33 (6), p.7225-7235</ispartof><rights>FASEB</rights><rights>The Author(s) 2019 FASEB</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c439R-e95e472474b5f4bc0feaa276046a3c1ea86ae3bd260ea7a118836fc47abf54f33</citedby><cites>FETCH-LOGICAL-c439R-e95e472474b5f4bc0feaa276046a3c1ea86ae3bd260ea7a118836fc47abf54f33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1096%2Ffj.201802097R$$EPDF$$P50$$Gwiley$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1096%2Ffj.201802097R$$EHTML$$P50$$Gwiley$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30857414$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Trigo, Diogo</creatorcontrib><creatorcontrib>Goncalves, Maria B.</creatorcontrib><creatorcontrib>Corcoran, Jonathan P. T.</creatorcontrib><title>The regulation of mitochondrial dynamics in neurite outgrowth by retinoic acid receptor β signaling</title><title>The FASEB journal</title><addtitle>FASEB J</addtitle><description>ABSTRACT
Neuronal regeneration is a highly energy‐demanding process that greatly relies on axonal mitochondrial transport to meet the enhanced metabolic requirements. Mature neurons typically fail to regenerate after injury, partly because of mitochondrial motility and energy deficits in injured axons. Retinoic acid receptor (RAR)‐β signaling is involved in axonal and neurite regeneration. Here we investigate the effect of RAR‐β signaling on mitochondrial trafficking during neurite outgrowth and find that it enhances their proliferation, speed, and movement toward the growing end of the neuron via hypoxia‐inducible factor 1α signaling. We also show that RAR‐β signaling promotes the binding of the mitochondria to the anchoring protein, glucose‐related protein 75, at the growing tip of neurite, thus allowing them to provide energy and metabolic roles required for neurite outgrowth.—Trigo, D., Goncalves, M. B., Corcoran, J. P. T. The regulation of mitochondrial dynamics in neurite outgrowth by retinoic acid receptor β signaling. FASEB J. 33, 7225–7235 (2019). www.fasebj.org</description><subject>Adenosine Triphosphate - metabolism</subject><subject>Animals</subject><subject>Cells, Cultured</subject><subject>energy metabolism</subject><subject>growth cone</subject><subject>HSP70 Heat-Shock Proteins - antagonists & inhibitors</subject><subject>HSP70 Heat-Shock Proteins - genetics</subject><subject>HSP70 Heat-Shock Proteins - physiology</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit - biosynthesis</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit - genetics</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit - physiology</subject><subject>Membrane Proteins - antagonists & inhibitors</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - physiology</subject><subject>Mice</subject><subject>Mitochondrial Dynamics - drug effects</subject><subject>Mitochondrial Dynamics - physiology</subject><subject>Naphthalenes - pharmacology</subject><subject>neuron</subject><subject>Neuronal Outgrowth - drug effects</subject><subject>Neuronal Outgrowth - physiology</subject><subject>Neurons - metabolism</subject><subject>Receptors, Retinoic Acid - agonists</subject><subject>Receptors, Retinoic Acid - physiology</subject><subject>retinoid</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering - pharmacology</subject><issn>0892-6638</issn><issn>1530-6860</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><recordid>eNp9kU1v1DAQhi1ERZfCkSvykUuKv-I4QkKiFcuHKiGVcrYcZ5z1KrEX26Hav8UP4TeRaktpLz2NRvPMMyO9CL2i5JSSVr5121NGqCKMtM3lE7SiNSeVVJI8RSuiWlZJydUxep7zlhBCCZXP0DEnqm4EFSvUX20AJxjm0RQfA44OT75Eu4mhT96MuN8HM3mbsQ84wJx8ARznMqR4XTa42y_LxYfoLTbW90tnYVdiwn9-4-yHYEYfhhfoyJkxw8vbeoJ-rD9enX-uLr59-nL-4aKygreXFbQ1iIaJRnS1E50lDoxhjSRCGm4pGCUN8K5nkoBpDKVKcemsaEznauE4P0HvD97d3E3QWwglmVHvkp9M2utovH44CX6jh_hLy5q1nMtF8OZWkOLPGXLRk88WxtEEiHPWjLZEKN5KuqDVAbUp5pzA3Z2hRN8ko91W_09m4V_f_-2O_hfFArw7ANd-hP3jNr3-fsbWX-_p_wL5P57K</recordid><startdate>201906</startdate><enddate>201906</enddate><creator>Trigo, Diogo</creator><creator>Goncalves, Maria B.</creator><creator>Corcoran, Jonathan P. T.</creator><general>Federation of American Societies for Experimental Biology</general><scope>24P</scope><scope>WIN</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201906</creationdate><title>The regulation of mitochondrial dynamics in neurite outgrowth by retinoic acid receptor β signaling</title><author>Trigo, Diogo ; Goncalves, Maria B. ; Corcoran, Jonathan P. T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c439R-e95e472474b5f4bc0feaa276046a3c1ea86ae3bd260ea7a118836fc47abf54f33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adenosine Triphosphate - metabolism</topic><topic>Animals</topic><topic>Cells, Cultured</topic><topic>energy metabolism</topic><topic>growth cone</topic><topic>HSP70 Heat-Shock Proteins - antagonists & inhibitors</topic><topic>HSP70 Heat-Shock Proteins - genetics</topic><topic>HSP70 Heat-Shock Proteins - physiology</topic><topic>Hypoxia-Inducible Factor 1, alpha Subunit - biosynthesis</topic><topic>Hypoxia-Inducible Factor 1, alpha Subunit - genetics</topic><topic>Hypoxia-Inducible Factor 1, alpha Subunit - physiology</topic><topic>Membrane Proteins - antagonists & inhibitors</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - physiology</topic><topic>Mice</topic><topic>Mitochondrial Dynamics - drug effects</topic><topic>Mitochondrial Dynamics - physiology</topic><topic>Naphthalenes - pharmacology</topic><topic>neuron</topic><topic>Neuronal Outgrowth - drug effects</topic><topic>Neuronal Outgrowth - physiology</topic><topic>Neurons - metabolism</topic><topic>Receptors, Retinoic Acid - agonists</topic><topic>Receptors, Retinoic Acid - physiology</topic><topic>retinoid</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Trigo, Diogo</creatorcontrib><creatorcontrib>Goncalves, Maria B.</creatorcontrib><creatorcontrib>Corcoran, Jonathan P. T.</creatorcontrib><collection>Wiley Online Library (Open Access Collection)</collection><collection>Wiley Online Library (Open Access Collection)</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The FASEB journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Trigo, Diogo</au><au>Goncalves, Maria B.</au><au>Corcoran, Jonathan P. T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The regulation of mitochondrial dynamics in neurite outgrowth by retinoic acid receptor β signaling</atitle><jtitle>The FASEB journal</jtitle><addtitle>FASEB J</addtitle><date>2019-06</date><risdate>2019</risdate><volume>33</volume><issue>6</issue><spage>7225</spage><epage>7235</epage><pages>7225-7235</pages><issn>0892-6638</issn><eissn>1530-6860</eissn><abstract>ABSTRACT
Neuronal regeneration is a highly energy‐demanding process that greatly relies on axonal mitochondrial transport to meet the enhanced metabolic requirements. Mature neurons typically fail to regenerate after injury, partly because of mitochondrial motility and energy deficits in injured axons. Retinoic acid receptor (RAR)‐β signaling is involved in axonal and neurite regeneration. Here we investigate the effect of RAR‐β signaling on mitochondrial trafficking during neurite outgrowth and find that it enhances their proliferation, speed, and movement toward the growing end of the neuron via hypoxia‐inducible factor 1α signaling. We also show that RAR‐β signaling promotes the binding of the mitochondria to the anchoring protein, glucose‐related protein 75, at the growing tip of neurite, thus allowing them to provide energy and metabolic roles required for neurite outgrowth.—Trigo, D., Goncalves, M. B., Corcoran, J. P. T. The regulation of mitochondrial dynamics in neurite outgrowth by retinoic acid receptor β signaling. FASEB J. 33, 7225–7235 (2019). www.fasebj.org</abstract><cop>United States</cop><pub>Federation of American Societies for Experimental Biology</pub><pmid>30857414</pmid><doi>10.1096/fj.201802097R</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adenosine Triphosphate - metabolism Animals Cells, Cultured energy metabolism growth cone HSP70 Heat-Shock Proteins - antagonists & inhibitors HSP70 Heat-Shock Proteins - genetics HSP70 Heat-Shock Proteins - physiology Hypoxia-Inducible Factor 1, alpha Subunit - biosynthesis Hypoxia-Inducible Factor 1, alpha Subunit - genetics Hypoxia-Inducible Factor 1, alpha Subunit - physiology Membrane Proteins - antagonists & inhibitors Membrane Proteins - genetics Membrane Proteins - physiology Mice Mitochondrial Dynamics - drug effects Mitochondrial Dynamics - physiology Naphthalenes - pharmacology neuron Neuronal Outgrowth - drug effects Neuronal Outgrowth - physiology Neurons - metabolism Receptors, Retinoic Acid - agonists Receptors, Retinoic Acid - physiology retinoid RNA Interference RNA, Small Interfering - pharmacology |
title | The regulation of mitochondrial dynamics in neurite outgrowth by retinoic acid receptor β signaling |
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