A role for Piezo2 in EPAC1-dependent mechanical allodynia
Aberrant mechanosensation has an important role in different pain states. Here we show that Epac1 (cyclic AMP sensor) potentiation of Piezo2-mediated mechanotransduction contributes to mechanical allodynia. Dorsal root ganglia Epac1 mRNA levels increase during neuropathic pain, and nerve damage-indu...
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| Veröffentlicht in: | Nature communications 2013-04, Vol.4 (1), p.1682, Article 1682 |
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| creator | Eijkelkamp, N Linley, J.E. Torres, J.M. Bee, L. Dickenson, A.H. Gringhuis, M. Minett, M.S. Hong, G.S. Lee, E. Oh, U. Ishikawa, Y. Zwartkuis, F.J. Cox, J.J. Wood, J.N. |
| description | Aberrant mechanosensation has an important role in different pain states. Here we show that Epac1 (cyclic AMP sensor) potentiation of Piezo2-mediated mechanotransduction contributes to mechanical allodynia. Dorsal root ganglia Epac1 mRNA levels increase during neuropathic pain, and nerve damage-induced allodynia is reduced in Epac1−/− mice. The Epac-selective cAMP analogue 8-pCPT sensitizes mechanically evoked currents in sensory neurons. Human Piezo2 produces large mechanically gated currents that are enhanced by the activation of the cAMP-sensor Epac1 or cytosolic calcium but are unaffected by protein kinase C or protein kinase A and depend on the integrity of the cytoskeleton.
In vivo
, 8-pCPT induces long-lasting allodynia that is prevented by the knockdown of Epac1 and attenuated by mouse Piezo2 knockdown. Piezo2 knockdown also enhanced thresholds for light touch. Finally, 8-pCPT sensitizes responses to innocuous mechanical stimuli without changing the electrical excitability of sensory fibres. These data indicate that the Epac1–Piezo2 axis has a role in the development of mechanical allodynia during neuropathic pain.
Mechanical allodynia describes the process whereby innocuous stimuli is perceived as being noxious and is a common symptom of neuropathic pain. Using mice deficient in the cAMP sensor Epac1, the authors in this study find that Epac1 regulates mechanical allodynia by sensitizing the mechanotransducer Piezo2. |
| doi_str_mv | 10.1038/ncomms2673 |
| format | Article |
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In vivo
, 8-pCPT induces long-lasting allodynia that is prevented by the knockdown of Epac1 and attenuated by mouse Piezo2 knockdown. Piezo2 knockdown also enhanced thresholds for light touch. Finally, 8-pCPT sensitizes responses to innocuous mechanical stimuli without changing the electrical excitability of sensory fibres. These data indicate that the Epac1–Piezo2 axis has a role in the development of mechanical allodynia during neuropathic pain.
Mechanical allodynia describes the process whereby innocuous stimuli is perceived as being noxious and is a common symptom of neuropathic pain. Using mice deficient in the cAMP sensor Epac1, the authors in this study find that Epac1 regulates mechanical allodynia by sensitizing the mechanotransducer Piezo2.</description><identifier>ISSN: 2041-1723</identifier><identifier>EISSN: 2041-1723</identifier><identifier>DOI: 10.1038/ncomms2673</identifier><identifier>PMID: 23575686</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/378/2620/410 ; 631/80/79/2066 ; Animals ; Base Sequence ; Cells, Cultured ; Guanine Nucleotide Exchange Factors - metabolism ; Guanine Nucleotide Exchange Factors - physiology ; Humanities and Social Sciences ; Hyperalgesia - etiology ; Ion Channels - physiology ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; multidisciplinary ; Oligodeoxyribonucleotides ; Science ; Science (multidisciplinary) ; Signal Transduction</subject><ispartof>Nature communications, 2013-04, Vol.4 (1), p.1682, Article 1682</ispartof><rights>The Author(s) 2013</rights><rights>Copyright Nature Publishing Group Apr 2013</rights><rights>Copyright © 2013, Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved. 2013 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c442t-25e55da004b078b63bcba361eae1090404597a43b2aeb13ef15569a45d21c39f3</citedby><cites>FETCH-LOGICAL-c442t-25e55da004b078b63bcba361eae1090404597a43b2aeb13ef15569a45d21c39f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3644070/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3644070/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23575686$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Eijkelkamp, N</creatorcontrib><creatorcontrib>Linley, J.E.</creatorcontrib><creatorcontrib>Torres, J.M.</creatorcontrib><creatorcontrib>Bee, L.</creatorcontrib><creatorcontrib>Dickenson, A.H.</creatorcontrib><creatorcontrib>Gringhuis, M.</creatorcontrib><creatorcontrib>Minett, M.S.</creatorcontrib><creatorcontrib>Hong, G.S.</creatorcontrib><creatorcontrib>Lee, E.</creatorcontrib><creatorcontrib>Oh, U.</creatorcontrib><creatorcontrib>Ishikawa, Y.</creatorcontrib><creatorcontrib>Zwartkuis, F.J.</creatorcontrib><creatorcontrib>Cox, J.J.</creatorcontrib><creatorcontrib>Wood, J.N.</creatorcontrib><title>A role for Piezo2 in EPAC1-dependent mechanical allodynia</title><title>Nature communications</title><addtitle>Nat Commun</addtitle><addtitle>Nat Commun</addtitle><description>Aberrant mechanosensation has an important role in different pain states. Here we show that Epac1 (cyclic AMP sensor) potentiation of Piezo2-mediated mechanotransduction contributes to mechanical allodynia. Dorsal root ganglia Epac1 mRNA levels increase during neuropathic pain, and nerve damage-induced allodynia is reduced in Epac1−/− mice. The Epac-selective cAMP analogue 8-pCPT sensitizes mechanically evoked currents in sensory neurons. Human Piezo2 produces large mechanically gated currents that are enhanced by the activation of the cAMP-sensor Epac1 or cytosolic calcium but are unaffected by protein kinase C or protein kinase A and depend on the integrity of the cytoskeleton.
In vivo
, 8-pCPT induces long-lasting allodynia that is prevented by the knockdown of Epac1 and attenuated by mouse Piezo2 knockdown. Piezo2 knockdown also enhanced thresholds for light touch. Finally, 8-pCPT sensitizes responses to innocuous mechanical stimuli without changing the electrical excitability of sensory fibres. These data indicate that the Epac1–Piezo2 axis has a role in the development of mechanical allodynia during neuropathic pain.
Mechanical allodynia describes the process whereby innocuous stimuli is perceived as being noxious and is a common symptom of neuropathic pain. Using mice deficient in the cAMP sensor Epac1, the authors in this study find that Epac1 regulates mechanical allodynia by sensitizing the mechanotransducer Piezo2.</description><subject>631/378/2620/410</subject><subject>631/80/79/2066</subject><subject>Animals</subject><subject>Base Sequence</subject><subject>Cells, Cultured</subject><subject>Guanine Nucleotide Exchange Factors - metabolism</subject><subject>Guanine Nucleotide Exchange Factors - physiology</subject><subject>Humanities and Social Sciences</subject><subject>Hyperalgesia - etiology</subject><subject>Ion Channels - physiology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Inbred CBA</subject><subject>multidisciplinary</subject><subject>Oligodeoxyribonucleotides</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Signal Transduction</subject><issn>2041-1723</issn><issn>2041-1723</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNplkVtLAzEQhYMottS--ANkwRdRVnPdy4tQSr2AYB_0OWSzs-2W3aQmXaH-eiOttWpeJjAfZ87MQeiU4GuCWXZjtG1bT5OUHaA-xZzEJKXscO_fQ0PvFzg8lpOM82PUo0ykIsmSPspHkbMNRJV10bSGD0uj2kST6WhM4hKWYEowq6gFPVem1qqJVNPYcm1qdYKOKtV4GG7rAL3eTV7GD_HT8_3jePQUa87pKqYChCgVxrzAaVYkrNCFYgkBBQTnmGMu8lRxVlAFBWFQESGSXHFRUqJZXrEBut3oLruihVIHP041cunqVrm1tKqWvzumnsuZfZcs4RynOAhcbAWcfevAr2Rbew1NowzYzkvCwvWooDkN6PkfdGE7Z8J6geJ5xsIFWaAuN5R21nsH1c4MwfIrFPkTSoDP9u3v0O8IAnC1AXxomRm4vZn_5T4BKd6VSw</recordid><startdate>20130409</startdate><enddate>20130409</enddate><creator>Eijkelkamp, N</creator><creator>Linley, J.E.</creator><creator>Torres, J.M.</creator><creator>Bee, L.</creator><creator>Dickenson, A.H.</creator><creator>Gringhuis, M.</creator><creator>Minett, M.S.</creator><creator>Hong, G.S.</creator><creator>Lee, E.</creator><creator>Oh, U.</creator><creator>Ishikawa, Y.</creator><creator>Zwartkuis, F.J.</creator><creator>Cox, J.J.</creator><creator>Wood, J.N.</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><general>Nature Pub. 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Nature communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Eijkelkamp, N</au><au>Linley, J.E.</au><au>Torres, J.M.</au><au>Bee, L.</au><au>Dickenson, A.H.</au><au>Gringhuis, M.</au><au>Minett, M.S.</au><au>Hong, G.S.</au><au>Lee, E.</au><au>Oh, U.</au><au>Ishikawa, Y.</au><au>Zwartkuis, F.J.</au><au>Cox, J.J.</au><au>Wood, J.N.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A role for Piezo2 in EPAC1-dependent mechanical allodynia</atitle><jtitle>Nature communications</jtitle><stitle>Nat Commun</stitle><addtitle>Nat Commun</addtitle><date>2013-04-09</date><risdate>2013</risdate><volume>4</volume><issue>1</issue><spage>1682</spage><pages>1682-</pages><artnum>1682</artnum><issn>2041-1723</issn><eissn>2041-1723</eissn><abstract>Aberrant mechanosensation has an important role in different pain states. Here we show that Epac1 (cyclic AMP sensor) potentiation of Piezo2-mediated mechanotransduction contributes to mechanical allodynia. Dorsal root ganglia Epac1 mRNA levels increase during neuropathic pain, and nerve damage-induced allodynia is reduced in Epac1−/− mice. The Epac-selective cAMP analogue 8-pCPT sensitizes mechanically evoked currents in sensory neurons. Human Piezo2 produces large mechanically gated currents that are enhanced by the activation of the cAMP-sensor Epac1 or cytosolic calcium but are unaffected by protein kinase C or protein kinase A and depend on the integrity of the cytoskeleton.
In vivo
, 8-pCPT induces long-lasting allodynia that is prevented by the knockdown of Epac1 and attenuated by mouse Piezo2 knockdown. Piezo2 knockdown also enhanced thresholds for light touch. Finally, 8-pCPT sensitizes responses to innocuous mechanical stimuli without changing the electrical excitability of sensory fibres. These data indicate that the Epac1–Piezo2 axis has a role in the development of mechanical allodynia during neuropathic pain.
Mechanical allodynia describes the process whereby innocuous stimuli is perceived as being noxious and is a common symptom of neuropathic pain. Using mice deficient in the cAMP sensor Epac1, the authors in this study find that Epac1 regulates mechanical allodynia by sensitizing the mechanotransducer Piezo2.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>23575686</pmid><doi>10.1038/ncomms2673</doi><oa>free_for_read</oa></addata></record> |
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| subjects | 631/378/2620/410 631/80/79/2066 Animals Base Sequence Cells, Cultured Guanine Nucleotide Exchange Factors - metabolism Guanine Nucleotide Exchange Factors - physiology Humanities and Social Sciences Hyperalgesia - etiology Ion Channels - physiology Mice Mice, Inbred C57BL Mice, Inbred CBA multidisciplinary Oligodeoxyribonucleotides Science Science (multidisciplinary) Signal Transduction |
| title | A role for Piezo2 in EPAC1-dependent mechanical allodynia |
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