ABSTRACT. Arabidopsis (Arabidopsis thaliana) group A1 heat shock factors (Hsfs), including HsfA1a, are important regulators in the heat shock response. Previous studies have revealed that genetically engineered HsfA1 members result in constitutive Hsf activation and heat shock protein gene (Hsp) expression under normal conditions, eventually enhancing basic thermotolerance in transgenic plants. In this study, we generated transgenic Arabidopsis plants overexpressing HsfA1a. One transgenic line showed a 94-fold increase in the level of HsfA1a mRNA (OE line 1). Overexpressing HsfA1a in OE line 1 plants resulted in higher levels of the inducible expression of Hsp18.2 and Hsp70 genes in response to heat stress, low/high pH changes, and hydrogen peroxide. Analysis of in vivo HsfA1a-promoter binding suggested that the higher level of inducible Hsp expression was mediated by stress-induced activation of elevated levels of HsfA1a in the OE plants. The OE plants showed an increase in tolerance to low/ high pH changes and hydrogen peroxide, in addition to heat shock. These results revealed that overexpressing HsfA1a had positive effects on tolerance to diverse stressors by promoting inducible Hsp expression following stress-induced HsfA1a activation. This study suggests a different mechanism for the activation of genetically engineered Hsfs from that suggested in previous reports, thus providing new insight into complex mechanisms used for achieving stress tolerance by genetic engineering.
ABSTRACT. The aim of this study was to investigate the role of the rat neuregulin-1 (NRG-1) protein in reducing doxorubicin (DOX)-induced myocardial toxicity and its underlying mechanism. The prokaryotic expression of the NRG-1 protein and the CCK8-determined activity of rat primary myocardial cells were evaluated under different DOX concentrations. Myocardial cells were divided into three groups: the control group, the 5 μM DOX (DOX5) group, and the DOX5 + NRG-1 group. Western blotting was used to determine the Na + -Ca 2+ exchanger (NCX-1) and cardiac myosin light-chain kinase (cMLCK) protein expression levels and real-time quantitative polymerase chain reaction methods were used to determine the mRNA expression levels. The prokaryotic expression of NRG-1 in the DOX5 group produced toxicity in the rat myocardial cells, and cell activity was significantly restored with the addition of NRG-1. The protective effect of NRG-1 was limited at higher DOX concentrations (DOX10), and the degree of cellular activity restoration was positively correlated with NRG-1 concentration. The addition of NRG-1 to DOX5 intervention inhibited NCX-1 protein and mRNA expression, and increased cMLCK protein and mRNA expression. In conclusion, DOX-induced toxicity in rat myocardial cells could be protected by NRG-1, and the mechanism may be related to the role of NRG-1 in up-regulating the cMLCK expression level and down-regulating the NCX-1 expression level.
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