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Reduced current density, partially rescued by mexiletine, and depolarizing shift in activation of SCN5A W374G channels as a cause of severe form of Brugada syndrome
Background SCN5A‐related Brugada syndrome (BrS) can be caused by multiple mechanisms including trafficking defects and altered channel gating properties. Most SCN5A mutations at pore region cause trafficking defects, and some of them can be rescued by mexiletine (MEX). Objective We recently encounte...
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| Published in: | Annals of noninvasive electrocardiology 2021-05, Vol.26 (3), p.e12828-n/a |
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| creator | Nakajima, Tadashi Dharmawan, Tommy Kawabata‐Iwakawa, Reika Tamura, Shuntaro Hasegawa, Hiroshi Kobari, Takashi Ota, Masaki Tange, Shoichi Nishiyama, Masahiko Kaneko, Yoshiaki Kurabayashi, Masahiko |
| description | Background
SCN5A‐related Brugada syndrome (BrS) can be caused by multiple mechanisms including trafficking defects and altered channel gating properties. Most SCN5A mutations at pore region cause trafficking defects, and some of them can be rescued by mexiletine (MEX).
Objective
We recently encountered symptomatic siblings with BrS and sought to identify a responsible mutation and reveal its biophysical defects.
Methods
Target panel sequencing was performed. Wild‐type (WT) or identified mutant SCN5A was transfected into tsA201 cells. After incubation of transfected cells with or without 0.1 mM MEX for 24–36 hr, whole‐cell sodium currents (INa) were recorded using patch‐clamp techniques.
Results
The proband was 29‐year‐old male who experienced cardiopulmonary arrest. Later, his 36‐year‐old sister, who had been suffering from recurrent episodes of syncope since 12 years, was diagnosed with BrS. An SCN5A W374G mutation, located at pore region of domain 1 (D1 pore), was identified in both. The peak density of W374G‐INa was markedly reduced (WT: 521 ± 38 pA/pF, W374G: 60 ± 10 pA/pF, p |
| doi_str_mv | 10.1111/anec.12828 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_doaj_</sourceid><recordid>TN_cdi_doaj_primary_oai_doaj_org_article_7f581cf3e4594759af2b0237dd9422a7</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><doaj_id>oai_doaj_org_article_7f581cf3e4594759af2b0237dd9422a7</doaj_id><sourcerecordid>2479038533</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5808-17839218a3da6f1048d1fda64a5e7c4aca54f627dcaec7905aa3e5c09f7110b03</originalsourceid><addsrcrecordid>eNp9kl1rFDEUhgdRbK3e-AMk4I1It-ZzMnNTqEuthVLBD-xdOJuc2c0ym6zJTHX9Pf5Qs91arBeGQE5yHl5Oznmr6jmjR6ysNxDQHjHe8OZBtc-U5BOp5dXDEtOGTzSnV3vVk5yXlHIuuX5c7Qkha9EotV_9-ohutOiIHVPCMBCHIfthc0jWkAYPfb8hCbMdCzLbkBX-8D0OPuAhgeAKvY49JP_ThznJC98NxAcCdvDXMPgYSOzIp-mlOiFfhZZnxC4gBOwzgbKJhTHjFsl4jQlJF9Nqe32bxjk4IHkTXIorfFo96qDP-Oz2PKi-vDv9PH0_ufhwdj49uZhY1dBmwnQjWs4aEA7qjlHZONaVUIJCbSVYULKruXYW0OqWKgCBytK204zRGRUH1flO10VYmnXyK0gbE8Gbm4eY5mbbFNuj0Z1qmO0EStVKrVro-IxyoZ1rJeegi9bxTms9zlbobOltgv6e6P1M8Aszj9emYbVkqi4Cr24FUvw2Yh7MymeLfV_GHcdsuCxfKEMUoqAv_0GXcUyhtMrwkq9rQVtVqNc7yqaYc8LurhhGzdZIZmskc2OkAr_4u_w79I9zCsB2wPdiiM1_pMzJ5el0J_ob6P_U2A</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2533663095</pqid></control><display><type>article</type><title>Reduced current density, partially rescued by mexiletine, and depolarizing shift in activation of SCN5A W374G channels as a cause of severe form of Brugada syndrome</title><source>Publicly Available Content Database</source><source>Wiley_OA刊</source><source>PubMed</source><creator>Nakajima, Tadashi ; Dharmawan, Tommy ; Kawabata‐Iwakawa, Reika ; Tamura, Shuntaro ; Hasegawa, Hiroshi ; Kobari, Takashi ; Ota, Masaki ; Tange, Shoichi ; Nishiyama, Masahiko ; Kaneko, Yoshiaki ; Kurabayashi, Masahiko</creator><creatorcontrib>Nakajima, Tadashi ; Dharmawan, Tommy ; Kawabata‐Iwakawa, Reika ; Tamura, Shuntaro ; Hasegawa, Hiroshi ; Kobari, Takashi ; Ota, Masaki ; Tange, Shoichi ; Nishiyama, Masahiko ; Kaneko, Yoshiaki ; Kurabayashi, Masahiko</creatorcontrib><description>Background
SCN5A‐related Brugada syndrome (BrS) can be caused by multiple mechanisms including trafficking defects and altered channel gating properties. Most SCN5A mutations at pore region cause trafficking defects, and some of them can be rescued by mexiletine (MEX).
Objective
We recently encountered symptomatic siblings with BrS and sought to identify a responsible mutation and reveal its biophysical defects.
Methods
Target panel sequencing was performed. Wild‐type (WT) or identified mutant SCN5A was transfected into tsA201 cells. After incubation of transfected cells with or without 0.1 mM MEX for 24–36 hr, whole‐cell sodium currents (INa) were recorded using patch‐clamp techniques.
Results
The proband was 29‐year‐old male who experienced cardiopulmonary arrest. Later, his 36‐year‐old sister, who had been suffering from recurrent episodes of syncope since 12 years, was diagnosed with BrS. An SCN5A W374G mutation, located at pore region of domain 1 (D1 pore), was identified in both. The peak density of W374G‐INa was markedly reduced (WT: 521 ± 38 pA/pF, W374G: 60 ± 10 pA/pF, p < .01), and steady‐state activation (SSA) was shifted to depolarizing potentials compared with WT‐INa (V1/2‐WT: −39.1 ± 0.8 mV, W374G: −30.9 ± 1.1 mV, p < .01). Incubation of W374G‐transfected cells with MEX (W374G‐MEX) increased INa density, but it was still reduced compared with WT‐INa (W374G‐MEX: 174 ± 19 pA/pF, p < .01 versus W374G, p < .01 versus WT). The SSA of W374G‐MEX‐INa was comparable to W374G‐INa (V1/2‐W374G‐MEX: −31.6 ± 0.7 mV, P = NS).
Conclusions
Reduced current density, possibly due to a trafficking defect, and depolarizing shift in activation of SCN5A W374G are underlying biophysical defects in this severe form of BrS. Trafficking defects of SCN5A mutations at D1 pore may be commonly rescued by MEX.</description><identifier>ISSN: 1082-720X</identifier><identifier>EISSN: 1542-474X</identifier><identifier>DOI: 10.1111/anec.12828</identifier><identifier>PMID: 33463855</identifier><language>eng</language><publisher>United States: John Wiley & Sons, Inc</publisher><subject>Brugada syndrome ; Channel gating ; Current density ; Defects ; Depolarization ; mexiletine ; Mutation ; Original ; rescue ; SCN5A ; Sodium currents ; Syncope ; trafficking defect</subject><ispartof>Annals of noninvasive electrocardiology, 2021-05, Vol.26 (3), p.e12828-n/a</ispartof><rights>2021 published by Wiley Periodicals LLC</rights><rights>2021 The Authors. Annals of Noninvasive Electrocardiology published by Wiley Periodicals LLC.</rights><rights>2021. This article is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5808-17839218a3da6f1048d1fda64a5e7c4aca54f627dcaec7905aa3e5c09f7110b03</citedby><cites>FETCH-LOGICAL-c5808-17839218a3da6f1048d1fda64a5e7c4aca54f627dcaec7905aa3e5c09f7110b03</cites><orcidid>0000-0002-3504-1393 ; 0000-0001-9611-2303 ; 0000-0002-9635-2769 ; 0000-0001-9731-7183 ; 0000-0002-9445-6759</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8164156/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8164156/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,11560,27922,27923,37010,37011,46050,46474,53789,53791</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33463855$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nakajima, Tadashi</creatorcontrib><creatorcontrib>Dharmawan, Tommy</creatorcontrib><creatorcontrib>Kawabata‐Iwakawa, Reika</creatorcontrib><creatorcontrib>Tamura, Shuntaro</creatorcontrib><creatorcontrib>Hasegawa, Hiroshi</creatorcontrib><creatorcontrib>Kobari, Takashi</creatorcontrib><creatorcontrib>Ota, Masaki</creatorcontrib><creatorcontrib>Tange, Shoichi</creatorcontrib><creatorcontrib>Nishiyama, Masahiko</creatorcontrib><creatorcontrib>Kaneko, Yoshiaki</creatorcontrib><creatorcontrib>Kurabayashi, Masahiko</creatorcontrib><title>Reduced current density, partially rescued by mexiletine, and depolarizing shift in activation of SCN5A W374G channels as a cause of severe form of Brugada syndrome</title><title>Annals of noninvasive electrocardiology</title><addtitle>Ann Noninvasive Electrocardiol</addtitle><description>Background
SCN5A‐related Brugada syndrome (BrS) can be caused by multiple mechanisms including trafficking defects and altered channel gating properties. Most SCN5A mutations at pore region cause trafficking defects, and some of them can be rescued by mexiletine (MEX).
Objective
We recently encountered symptomatic siblings with BrS and sought to identify a responsible mutation and reveal its biophysical defects.
Methods
Target panel sequencing was performed. Wild‐type (WT) or identified mutant SCN5A was transfected into tsA201 cells. After incubation of transfected cells with or without 0.1 mM MEX for 24–36 hr, whole‐cell sodium currents (INa) were recorded using patch‐clamp techniques.
Results
The proband was 29‐year‐old male who experienced cardiopulmonary arrest. Later, his 36‐year‐old sister, who had been suffering from recurrent episodes of syncope since 12 years, was diagnosed with BrS. An SCN5A W374G mutation, located at pore region of domain 1 (D1 pore), was identified in both. The peak density of W374G‐INa was markedly reduced (WT: 521 ± 38 pA/pF, W374G: 60 ± 10 pA/pF, p < .01), and steady‐state activation (SSA) was shifted to depolarizing potentials compared with WT‐INa (V1/2‐WT: −39.1 ± 0.8 mV, W374G: −30.9 ± 1.1 mV, p < .01). Incubation of W374G‐transfected cells with MEX (W374G‐MEX) increased INa density, but it was still reduced compared with WT‐INa (W374G‐MEX: 174 ± 19 pA/pF, p < .01 versus W374G, p < .01 versus WT). The SSA of W374G‐MEX‐INa was comparable to W374G‐INa (V1/2‐W374G‐MEX: −31.6 ± 0.7 mV, P = NS).
Conclusions
Reduced current density, possibly due to a trafficking defect, and depolarizing shift in activation of SCN5A W374G are underlying biophysical defects in this severe form of BrS. Trafficking defects of SCN5A mutations at D1 pore may be commonly rescued by MEX.</description><subject>Brugada syndrome</subject><subject>Channel gating</subject><subject>Current density</subject><subject>Defects</subject><subject>Depolarization</subject><subject>mexiletine</subject><subject>Mutation</subject><subject>Original</subject><subject>rescue</subject><subject>SCN5A</subject><subject>Sodium currents</subject><subject>Syncope</subject><subject>trafficking defect</subject><issn>1082-720X</issn><issn>1542-474X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>DOA</sourceid><recordid>eNp9kl1rFDEUhgdRbK3e-AMk4I1It-ZzMnNTqEuthVLBD-xdOJuc2c0ym6zJTHX9Pf5Qs91arBeGQE5yHl5Oznmr6jmjR6ysNxDQHjHe8OZBtc-U5BOp5dXDEtOGTzSnV3vVk5yXlHIuuX5c7Qkha9EotV_9-ohutOiIHVPCMBCHIfthc0jWkAYPfb8hCbMdCzLbkBX-8D0OPuAhgeAKvY49JP_ThznJC98NxAcCdvDXMPgYSOzIp-mlOiFfhZZnxC4gBOwzgbKJhTHjFsl4jQlJF9Nqe32bxjk4IHkTXIorfFo96qDP-Oz2PKi-vDv9PH0_ufhwdj49uZhY1dBmwnQjWs4aEA7qjlHZONaVUIJCbSVYULKruXYW0OqWKgCBytK204zRGRUH1flO10VYmnXyK0gbE8Gbm4eY5mbbFNuj0Z1qmO0EStVKrVro-IxyoZ1rJeegi9bxTms9zlbobOltgv6e6P1M8Aszj9emYbVkqi4Cr24FUvw2Yh7MymeLfV_GHcdsuCxfKEMUoqAv_0GXcUyhtMrwkq9rQVtVqNc7yqaYc8LurhhGzdZIZmskc2OkAr_4u_w79I9zCsB2wPdiiM1_pMzJ5el0J_ob6P_U2A</recordid><startdate>202105</startdate><enddate>202105</enddate><creator>Nakajima, Tadashi</creator><creator>Dharmawan, Tommy</creator><creator>Kawabata‐Iwakawa, Reika</creator><creator>Tamura, Shuntaro</creator><creator>Hasegawa, Hiroshi</creator><creator>Kobari, Takashi</creator><creator>Ota, Masaki</creator><creator>Tange, Shoichi</creator><creator>Nishiyama, Masahiko</creator><creator>Kaneko, Yoshiaki</creator><creator>Kurabayashi, Masahiko</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><general>Wiley</general><scope>24P</scope><scope>WIN</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-3504-1393</orcidid><orcidid>https://orcid.org/0000-0001-9611-2303</orcidid><orcidid>https://orcid.org/0000-0002-9635-2769</orcidid><orcidid>https://orcid.org/0000-0001-9731-7183</orcidid><orcidid>https://orcid.org/0000-0002-9445-6759</orcidid></search><sort><creationdate>202105</creationdate><title>Reduced current density, partially rescued by mexiletine, and depolarizing shift in activation of SCN5A W374G channels as a cause of severe form of Brugada syndrome</title><author>Nakajima, Tadashi ; Dharmawan, Tommy ; Kawabata‐Iwakawa, Reika ; Tamura, Shuntaro ; Hasegawa, Hiroshi ; Kobari, Takashi ; Ota, Masaki ; Tange, Shoichi ; Nishiyama, Masahiko ; Kaneko, Yoshiaki ; Kurabayashi, Masahiko</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5808-17839218a3da6f1048d1fda64a5e7c4aca54f627dcaec7905aa3e5c09f7110b03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Brugada syndrome</topic><topic>Channel gating</topic><topic>Current density</topic><topic>Defects</topic><topic>Depolarization</topic><topic>mexiletine</topic><topic>Mutation</topic><topic>Original</topic><topic>rescue</topic><topic>SCN5A</topic><topic>Sodium currents</topic><topic>Syncope</topic><topic>trafficking defect</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nakajima, Tadashi</creatorcontrib><creatorcontrib>Dharmawan, Tommy</creatorcontrib><creatorcontrib>Kawabata‐Iwakawa, Reika</creatorcontrib><creatorcontrib>Tamura, Shuntaro</creatorcontrib><creatorcontrib>Hasegawa, Hiroshi</creatorcontrib><creatorcontrib>Kobari, Takashi</creatorcontrib><creatorcontrib>Ota, Masaki</creatorcontrib><creatorcontrib>Tange, Shoichi</creatorcontrib><creatorcontrib>Nishiyama, Masahiko</creatorcontrib><creatorcontrib>Kaneko, Yoshiaki</creatorcontrib><creatorcontrib>Kurabayashi, Masahiko</creatorcontrib><collection>Wiley_OA刊</collection><collection>Wiley-Blackwell Backfiles (Open access)</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Annals of noninvasive electrocardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nakajima, Tadashi</au><au>Dharmawan, Tommy</au><au>Kawabata‐Iwakawa, Reika</au><au>Tamura, Shuntaro</au><au>Hasegawa, Hiroshi</au><au>Kobari, Takashi</au><au>Ota, Masaki</au><au>Tange, Shoichi</au><au>Nishiyama, Masahiko</au><au>Kaneko, Yoshiaki</au><au>Kurabayashi, Masahiko</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reduced current density, partially rescued by mexiletine, and depolarizing shift in activation of SCN5A W374G channels as a cause of severe form of Brugada syndrome</atitle><jtitle>Annals of noninvasive electrocardiology</jtitle><addtitle>Ann Noninvasive Electrocardiol</addtitle><date>2021-05</date><risdate>2021</risdate><volume>26</volume><issue>3</issue><spage>e12828</spage><epage>n/a</epage><pages>e12828-n/a</pages><issn>1082-720X</issn><eissn>1542-474X</eissn><abstract>Background
SCN5A‐related Brugada syndrome (BrS) can be caused by multiple mechanisms including trafficking defects and altered channel gating properties. Most SCN5A mutations at pore region cause trafficking defects, and some of them can be rescued by mexiletine (MEX).
Objective
We recently encountered symptomatic siblings with BrS and sought to identify a responsible mutation and reveal its biophysical defects.
Methods
Target panel sequencing was performed. Wild‐type (WT) or identified mutant SCN5A was transfected into tsA201 cells. After incubation of transfected cells with or without 0.1 mM MEX for 24–36 hr, whole‐cell sodium currents (INa) were recorded using patch‐clamp techniques.
Results
The proband was 29‐year‐old male who experienced cardiopulmonary arrest. Later, his 36‐year‐old sister, who had been suffering from recurrent episodes of syncope since 12 years, was diagnosed with BrS. An SCN5A W374G mutation, located at pore region of domain 1 (D1 pore), was identified in both. The peak density of W374G‐INa was markedly reduced (WT: 521 ± 38 pA/pF, W374G: 60 ± 10 pA/pF, p < .01), and steady‐state activation (SSA) was shifted to depolarizing potentials compared with WT‐INa (V1/2‐WT: −39.1 ± 0.8 mV, W374G: −30.9 ± 1.1 mV, p < .01). Incubation of W374G‐transfected cells with MEX (W374G‐MEX) increased INa density, but it was still reduced compared with WT‐INa (W374G‐MEX: 174 ± 19 pA/pF, p < .01 versus W374G, p < .01 versus WT). The SSA of W374G‐MEX‐INa was comparable to W374G‐INa (V1/2‐W374G‐MEX: −31.6 ± 0.7 mV, P = NS).
Conclusions
Reduced current density, possibly due to a trafficking defect, and depolarizing shift in activation of SCN5A W374G are underlying biophysical defects in this severe form of BrS. Trafficking defects of SCN5A mutations at D1 pore may be commonly rescued by MEX.</abstract><cop>United States</cop><pub>John Wiley & Sons, Inc</pub><pmid>33463855</pmid><doi>10.1111/anec.12828</doi><tpages>7</tpages><orcidid>https://orcid.org/0000-0002-3504-1393</orcidid><orcidid>https://orcid.org/0000-0001-9611-2303</orcidid><orcidid>https://orcid.org/0000-0002-9635-2769</orcidid><orcidid>https://orcid.org/0000-0001-9731-7183</orcidid><orcidid>https://orcid.org/0000-0002-9445-6759</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Annals of noninvasive electrocardiology, 2021-05, Vol.26 (3), p.e12828-n/a |
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| source | Publicly Available Content Database; Wiley_OA刊; PubMed |
| subjects | Brugada syndrome Channel gating Current density Defects Depolarization mexiletine Mutation Original rescue SCN5A Sodium currents Syncope trafficking defect |
| title | Reduced current density, partially rescued by mexiletine, and depolarizing shift in activation of SCN5A W374G channels as a cause of severe form of Brugada syndrome |
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