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Cardioprotective role of GABA-B receptor activation on ventricular arrhythmia following myocardial infarction
O papel cardioprotetor da ativação do recetor GABA-B nas arritmias ventriculares após enfarte do miocárdio
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regulation of M2 macrophage polarization after myocardial infarction" "tienePdf" => "en" "tieneTextoCompleto" => "en" "tieneResumen" => array:2 [ 0 => "en" 1 => "pt" ] "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "125" "paginaFinal" => "135" ] ] "titulosAlternativos" => array:1 [ "pt" => array:1 [ "titulo" => "Efeito protetor da ativação do recetor GABA<span class="elsevierStyleInf">B</span> na remodelagem simpática através da regulação da polarização de macrófagos M2 após enfarte do miocárdio" ] ] "contieneResumen" => array:2 [ "en" => true "pt" => true ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0015" "etiqueta" => "Figure 3" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr3.jpeg" "Alto" => 2835 "Ancho" => 2925 "Tamanyo" => 634618 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0060" class="elsevierStyleSimplePara elsevierViewall">GABA<span class="elsevierStyleInf">B</span> receptor activation promoted M2 macrophage polarization in vivo.</p> <p id="spar0065" class="elsevierStyleSimplePara elsevierViewall">A, Representative graphs of CD206 positive cell staining (red, white arrow head) in cardiac tissue slice from MI rats of con, Bac, CGP+Bac and GABA groups. CD68 positive cells were stained green (white arrow). B, MI, Bac and GABA groups increased CD206 positive cell number significantly (‘*’: p<0.05, compared with MI group). Baclofen and GABA induced a higher CD206 positive cell percentage comparing with MI group (con in figure) (‘#’: p<0.05). CGP52432 decreased CD206 positive cell percentage comparing with Bac group (‘&’: p<0.05). C and D, Serum IL-10 and TGF-β1 levels were increased in all MI surgery groups (‘*’: p<0.05, compared with Sham group). CGP52432 decreased IL-10 and TGF-β1 level significantly comparing with Bac group (‘&’: p<0.05). Baclofen decreased TGF-β1 level comparing Con group (‘#’: p<0.05). E, Serum IL-12 level were increased in MI groups comparing sham group (‘*’: p<0.05). Baclofen inhibited IL-12 secretion significantly comparing Con group (‘#’: p<0.05). Sham: surgery without ligating LAD; MI: myocardial infarction group; Bac: baclofen group; CGP+Bac: CGP52432+baclofen group.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Qian Liu, Yan Li, Yugen Shi, Jiayu Tan, Wenju Yan, Junyi Zhang, Peng Gao, Suhua Yan" "autores" => array:8 [ 0 => array:2 [ "nombre" => "Qian" "apellidos" => "Liu" ] 1 => array:2 [ "nombre" => "Yan" "apellidos" => "Li" ] 2 => array:2 [ "nombre" => "Yugen" "apellidos" => "Shi" ] 3 => array:2 [ "nombre" => "Jiayu" "apellidos" => "Tan" ] 4 => array:2 [ "nombre" => "Wenju" "apellidos" => "Yan" ] 5 => array:2 [ "nombre" => "Junyi" "apellidos" => "Zhang" ] 6 => array:2 [ "nombre" => "Peng" "apellidos" => "Gao" ] 7 => array:2 [ "nombre" => "Suhua" "apellidos" => "Yan" ] ] ] ] ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0870255122002827?idApp=UINPBA00004E" "url" => "/08702551/0000004200000002/v1_202302081302/S0870255122002827/v1_202302081302/en/main.assets" ] "asociados" => array:1 [ 0 => array:19 [ "pii" => "S0870255122002827" "issn" => "08702551" "doi" => "10.1016/j.repc.2021.10.011" "estado" => "S300" "fechaPublicacion" => "2023-02-01" "aid" => "2002" "copyright" => "Sociedade Portuguesa de Cardiologia" "documento" => "article" "crossmark" => 1 "licencia" => "http://creativecommons.org/licenses/by-nc-nd/4.0/" "subdocumento" => "fla" "cita" => "Rev Port Cardiol. 2023;42:125-35" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:1 [ "total" => 0 ] "en" => array:13 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Original Article</span>" "titulo" => "The protective effect of gamma aminobutyric acid B receptor activation on sympathetic nerve remodeling via the regulation of M2 macrophage polarization after myocardial infarction" "tienePdf" => "en" "tieneTextoCompleto" => "en" "tieneResumen" => array:2 [ 0 => "en" 1 => "pt" ] "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "125" "paginaFinal" => "135" ] ] "titulosAlternativos" => array:1 [ "pt" => array:1 [ "titulo" => "Efeito protetor da ativação do recetor GABA<span class="elsevierStyleInf">B</span> na remodelagem simpática através da regulação da polarização de macrófagos M2 após enfarte do miocárdio" ] ] "contieneResumen" => array:2 [ "en" => true "pt" => true ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0015" "etiqueta" => "Figure 3" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr3.jpeg" "Alto" => 2835 "Ancho" => 2925 "Tamanyo" => 634618 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0060" class="elsevierStyleSimplePara elsevierViewall">GABA<span class="elsevierStyleInf">B</span> receptor activation promoted M2 macrophage polarization in vivo.</p> <p id="spar0065" class="elsevierStyleSimplePara elsevierViewall">A, Representative graphs of CD206 positive cell staining (red, white arrow head) in cardiac tissue slice from MI rats of con, Bac, CGP+Bac and GABA groups. CD68 positive cells were stained green (white arrow). B, MI, Bac and GABA groups increased CD206 positive cell number significantly (‘*’: p<0.05, compared with MI group). Baclofen and GABA induced a higher CD206 positive cell percentage comparing with MI group (con in figure) (‘#’: p<0.05). CGP52432 decreased CD206 positive cell percentage comparing with Bac group (‘&’: p<0.05). C and D, Serum IL-10 and TGF-β1 levels were increased in all MI surgery groups (‘*’: p<0.05, compared with Sham group). CGP52432 decreased IL-10 and TGF-β1 level significantly comparing with Bac group (‘&’: p<0.05). Baclofen decreased TGF-β1 level comparing Con group (‘#’: p<0.05). E, Serum IL-12 level were increased in MI groups comparing sham group (‘*’: p<0.05). Baclofen inhibited IL-12 secretion significantly comparing Con group (‘#’: p<0.05). Sham: surgery without ligating LAD; MI: myocardial infarction group; Bac: baclofen group; CGP+Bac: CGP52432+baclofen group.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Qian Liu, Yan Li, Yugen Shi, Jiayu Tan, Wenju Yan, Junyi Zhang, Peng Gao, Suhua Yan" "autores" => array:8 [ 0 => array:2 [ "nombre" => "Qian" "apellidos" => "Liu" ] 1 => array:2 [ "nombre" => "Yan" "apellidos" => "Li" ] 2 => array:2 [ "nombre" => "Yugen" "apellidos" => "Shi" ] 3 => array:2 [ "nombre" => "Jiayu" "apellidos" => "Tan" ] 4 => array:2 [ "nombre" => "Wenju" "apellidos" => "Yan" ] 5 => array:2 [ "nombre" => "Junyi" "apellidos" => "Zhang" ] 6 => array:2 [ "nombre" => "Peng" "apellidos" => "Gao" ] 7 => array:2 [ "nombre" => "Suhua" "apellidos" => "Yan" ] ] ] ] ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0870255122002827?idApp=UINPBA00004E" "url" => "/08702551/0000004200000002/v1_202302081302/S0870255122002827/v1_202302081302/en/main.assets" ] ] "en" => array:12 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Editorial comment</span>" "titulo" => "Cardioprotective role of GABA-B receptor activation on ventricular arrhythmia following myocardial infarction" "tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "137" "paginaFinal" => "138" ] ] "autores" => array:1 [ 0 => array:3 [ "autoresLista" => "Tânia Martins-Marques" "autores" => array:1 [ 0 => array:4 [ "nombre" => "Tânia" "apellidos" => "Martins-Marques" "email" => array:1 [ 0 => "taniamarques241@gmail.com" ] "referencia" => array:3 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] 2 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">c</span>" "identificador" => "aff0015" ] ] ] ] "afiliaciones" => array:3 [ 0 => array:3 [ "entidad" => "Univ Coimbra, Coimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, Coimbra, Portugal" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Univ Coimbra, Center for Innovative Biomedicine and Biotechnology (CIBB), Coimbra, Portugal" "etiqueta" => "b" "identificador" => "aff0010" ] 2 => array:3 [ "entidad" => "Clinical Academic Centre of Coimbra (CACC), Coimbra, Portugal" "etiqueta" => "c" "identificador" => "aff0015" ] ] ] ] "titulosAlternativos" => array:1 [ "pt" => array:1 [ "titulo" => "O papel cardioprotetor da ativação do recetor GABA-B nas arritmias ventriculares após enfarte do miocárdio" ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Fatal ventricular arrhythmias (VAs) are the leading cause of sudden cardiac death among patients surviving a myocardial infarction (MI).<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> Multiple mechanisms are involved in the development of VAs after MI, including remodeling of ion channels, gap junctions, and histological changes. Sympathetic nerve hyperactivity has also been proposed as a major contributing factor.<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">2,3</span></a> In fact, although rapid activation of the sympathetic nervous system after MI is an important compensatory mechanism for impaired myocardial function, it has been also implicated in increased local norepinephrine (NE) release, triggering malignant arrhythmias.<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">3</span></a> Furthermore, resident and recruited immune cells following MI were shown to elicit a massive inflammatory response that can induce sympathetic remodeling.<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">4</span></a> Hence, it is proposed that macrophages play a key role in this mechanism, arising as a valuable therapeutic target against VAs.</p><p id="par0010" class="elsevierStylePara elsevierViewall">Multiple neurotransmitters are known to control sympathetic nerve activity, and consequently, cardiovascular function. Interestingly, both glutamate (excitatory) and gamma-aminobutyric acid (GABA; inhibitory) were reported to regulate susceptibility to arrhythmia in hypertensive rats.<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">5</span></a> Nonetheless, the mechanisms underlying such responses remain largely unexplored. In recent years, it was uncovered that peripheral immune cells and microglia express GABA receptors subtypes A and B (GABA-A and GABA-B).<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">6</span></a> Therefore, it is conceivable that GABAergic signaling in cardiac resident immune cells modulate sympathetic activity, including under pathological conditions.</p><p id="par0015" class="elsevierStylePara elsevierViewall">This is the question addressed by Qian Liu et al.<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">7</span></a> in the manuscript “The protective effect of GABAB receptor activation on sympathetic nerve remodeling via regulating M2 macrophage polarization after myocardial infarction”. In this article, the authors report the expression of the GABA-B receptor in cultured macrophages, as well as in CD206-positive cells in rat hearts. Moreover, the authors demonstrate GABA-B activation in vitro, either by GABA or with the selective agonist baclofen, promotes the expression of CD206, suggesting a role for GABA-B in mediating transition into alternatively activated macrophages (also termed M2 macrophages). Importantly, they show a similar increased number of alternatively activated macrophages following baclofen treatment in an animal model of MI, with a concomitant decrease in serum-circulating pro-inflammatory cytokines.</p><p id="par0020" class="elsevierStylePara elsevierViewall">Modulation of GABAergic signaling at the onset of MI is not without precedents. In fact, the GABA-A agonist topiramate was previously demonstrated to modulate macrophage phenotype conversion towards the M2/Ly-6C<span class="elsevierStyleSup">low</span> phenotype, being associated with decreased inflammation, reduced infarct size and improved cardiac function after MI.<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">8</span></a> In contrast, data gathered here show that treatment with baclofen did not significantly reduce infarct size, nor increased survival of mice post-MI. Nonetheless, a protective effect was observed by in vivo administration of GABA, suggesting that the role of GABA-A receptors prevail over GABA-B in controlling post-infarction ventricular remodeling. Besides their immunomodulatory roles, molecules secreted by macrophages can directly impact cardiac electric impulse propagation and modulate arrhythmogenesis. Indeed, it was recently demonstrated that amphiregulin produced by cardiac macrophages prevents the lateralization of the gap junctional protein Connexin43 (Cx43) in cardiomyocytes, which may be relevant in suppressing arrhythmia following MI.<a class="elsevierStyleCrossRefs" href="#bib0095"><span class="elsevierStyleSup">9,10</span></a> Therefore, further investigation should aim at a better understanding of the contribution of macrophage polarization and secretome to arrhythmogenesis and structural remodeling of the heart.</p><p id="par0025" class="elsevierStylePara elsevierViewall">Qian Liu et al. also addressed the impact of GABA-B activation in sympathetic nerve remodeling and demonstrate that baclofen counteracted the accumulation of tyrosine hydroxylase (TH) and growth-associated protein 43 (GAP 43) in infarcted hearts. This was accompanied by decreased serum levels of NE, suggesting that baclofen can prevent sympathetic nerve sprouting and activity in vivo. Although arrhythmogenesis after MI was still observed in animals treated with GABA, it is still conceivable that the frequency and/or duration of those arrhythmic phenomena would be decreased, thereby explaining the higher survival rates of treated animals.</p><p id="par0030" class="elsevierStylePara elsevierViewall">Nonetheless, future studies are required to characterize, in-depth, the role of GABAergic signaling in the development of fatal VAs, as well as to establish novel therapies. Comprehensive strategies targeting not only GABA receptors, but also macrophage polarization and communication networks comprising cardiomyocytes and sympathetic neurons, will be key to the prevention of sudden death following MI.<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a></p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0035" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:2 [ 0 => array:2 [ "identificador" => "sec0005" "titulo" => "Conflicts of interest" ] 1 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0015" "bibliografiaReferencia" => array:10 [ 0 => array:3 [ "identificador" => "bib0055" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Ventricular arrhythmias are associated with increased QT interval and QRS dispersion in patients with ST-elevation myocardial infarction" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:3 [ 0 => "E. 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