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1.
Chinese Pharmacological Bulletin ; (12): 1481-1484, 2017.
Artículo en Chino | WPRIM (Pacífico Occidental) | ID: wpr-667682

RESUMEN

Neuregulin-1 (NRG-1) and the ErbBs family of receptor tyrosine kinases are widely expressed in the cardiovascular system.NRG-1/ErbBs signaling plays an essential role in physiology and pathophysiology of the heart,including stabilization of cardiac myocyte structure and function,promotion of cardiac myocyte proliferation and survival,inhibition of cardiac myocyte apoptosis,reduction of myocardial interstitial fibrosis,regulation of energy utilization,and enhancement of angiogenesis and so on.Therefore,NRG-1/ErbBs signaling is involved in the development and treatment of chronic heart failure(CHF).In this review,we bring the growing literature on NRG-1/ErbBs signaling and its significance in cardiovascular development and heart failure.

2.
Acta Biochim Biophys Sin (Shanghai) ; 45(9): 734-41, 2013 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-23824072

RESUMEN

MicroRNAs (miRNAs) are one class of non-coding RNAs that play an important role in post-transcriptional regulation via the degradation or translational inhibition of their target genes. MicroRNA-150 (miR-150) plays a vital role in regulating the development of B and T lymphocytes. Although the dysregulation of miR-150 was confirmed in human myocardial infarction, little is known regarding the biological functions of miR-150 in response to reactive oxygen species (ROS)-mediated gene regulation in cardiac myocytes. Using quantitative real-time reverse transcription-polymerase chain reaction, we demonstrated that the level of miR-150 was up-regulated in cardiac myocytes after treatment with hydrogen peroxide (H2O2). To identify the potential roles of miR-150 in H2O2-mediated gene regulation, we modulated expression of miR-150 using miR-150 inhibitor and miR-150 mimics. Results showed that silencing expression of miR-150 decreased H2O2-induced cardiac cell death and apoptosis. In lymphocytes, c-myb was a direct target of miR-150. In cardiac myocytes, we found that c-myb was also involved in miR-150-mediated H2O2-induced cardiac cell death. These results suggested that miR-150 participates in H2O2-mediated gene regulation and functional modulation in cardiac myocytes. MiR-150 may play an essential role in heart diseases related to ROS, such as cardiac hypertrophy, heart failure, myocardial infarction, and myocardial ischemia/reperfusion injury.


Asunto(s)
Regulación hacia Abajo/efectos de los fármacos , Peróxido de Hidrógeno/farmacología , MicroARNs/genética , Miocitos Cardíacos/efectos de los fármacos , Proteínas Proto-Oncogénicas c-myb/genética , Regiones no Traducidas 3'/genética , Animales , Animales Recién Nacidos , Apoptosis/efectos de los fármacos , Apoptosis/genética , Sitios de Unión/genética , Western Blotting , Células Cultivadas , Relación Dosis-Respuesta a Droga , Expresión Génica/efectos de los fármacos , Células HEK293 , Humanos , MicroARNs/metabolismo , Miocitos Cardíacos/citología , Miocitos Cardíacos/metabolismo , Oxidantes/farmacología , Proteínas Proto-Oncogénicas c-myb/metabolismo , Ratas , Ratas Sprague-Dawley , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa
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