[Corrigendum] MicroRNA­1929­3p participates in murine cytomegalovirus­induced hypertensive vascular remodeling through Ednra/NLRP3 inflammasome activation.

Following the publication of this article, the authors have realized that the images selected for the 'MCMV+miR­NC' and 'MCMV+miR­1929­3p' data panels (15 months), as featured in the lower of the two rows of data shown in Fig. 4A on p. 726, were derived from the same experimental group. The authors re­examined their original data, and discovered that an error had inadvertently been made on account of the similar file names of the two images. The corrected version of Fig. 4, featuring the correct data for the 'MCMV+miR­NC' experiment, is shown on the next page. The authors regret that this error was not picked up upon before the paper was sent to press, and thank the Editor of International Journal of Molecular Medicine for allowing them the opportunity to publish a corrigendum. Note that the error did not affect either the results or the conclusions reported in the study, and all the authors agree to this corrigendum. Furthermore, the authors regret any inconvenience caused to the readership. [the original article was published in International Journal of Molecular Medicine 47: 719-731, 2021; DOI: 10.3892/ijmm.2020.4829].

MicroRNA­1929­3p participates in murine cytomegalovirus­induced hypertensive vascular remodeling through Ednra/NLRP3 inflammasome activation.

MicroRNAs (miRNAs) play an important role in the development of vascular remodeling in essential hypertension (EH) by mediating the effects of human cytomegalovirus (HCMV) on the vascular system. Therefore, the aim of the present study was to investigate the effects of murine cytomegalovirus (MCMV) infection on blood pressure and vascular function in mice, in order to elucidate the role of miR­1929­3p in this process. For model development, 7­month­old C57BL/6J mice were infected with the Smith strain of MCMV, and MCMV DNA, IgG and IgM were detected. Subsequently, blood pressure was measured via the carotid artery, and the morphological changes of the aorta were evaluated by hematoxylin and eosin and Masson's trichrome staining. miR­1929­3p transfection was performed using an adeno­associated virus packaged vector and the changes in vascular structure were then observed. The levels of nitric oxide (NO) and endothelial NO synthase were also assessed with colorimetry. Vascular remodeling and expression of NLRP3 inflammasome pathway­related proteins were detected by immunohistochemistry and western blotting. Endothelin­1 (ET­1), interleukin (IL)­1ß and IL­18 were assayed by ELISA. The results revealed that MCMV infection increased the blood pressure, promoted vascular remodeling, caused endothelial cell injury, and downregulated miR­1929­3p. However, these effects were alleviated by miR­1929­3p overexpression, which downregulated endothelin A receptor (Ednra) and NLRP3 inflammasome, as well as endothelial injury­ and vascular remodeling­related genes. Taken together, the findings of the present study indicated that overexpression of miR­1929­3p may improve MCMV­induced vascular remodeling, possibly via the deactivation of the NLRP3 inflammasome by ET­1/Ednra.

Dynamic Behaviour of Bridge Girders with Trapezoidal Profiled Webs Subjected to Moving Loads.

The aim of this study is to find out the degradation of dynamic behaviour of bridge girders with trapezoidal profiled webs when subjected to different vehicle moving loads. Finite element modelling based parametric analysis is demonstrated to be desirable in capturing the dynamic deflection and stress state of critical structural details of girders. The model is validated in the modal analysis through a comparison with theoretical eigenfrequencies. The vibration characteristics are shown to be significantly affected by the corrugation details. The structural service life results of analysed bridge girders are in close agreement with experimental data. It is shown that the dynamic nodal velocity and deflection of analysed bridge girders are greatly affected by the magnitude of the load corresponding to the overload of the vehicle in contrast to the vehicle travel speed. Similar observations can be made for the fatigue life prediction analysis related to the crack initiation when unfavourable effects of the overload vehicle are concerned. Presented analytical results using a fracture mechanics approach could be taken as a good basis for the service life assessment of related bridges with the desired level of performance or functionality.

Screening and validation of differentially expressed microRNAs and target genes in hypertensive mice induced by cytomegalovirus infection.

INTRODUCTION: Multiple studies have suggested an association between cytomegalovirus (CMV) infection and essential hypertension (EH). MicroRNAs (miRNAs) play a critical role in the development of EH by regulating the expression of specific target genes. However, little is known about the role of miRNAs in CMV-induced EH. In the present study, we compared the miRNA expression profiles of samples from normal and murine cytomegalovirus (MCMV)-infected C57BL/6 mice using high-throughput sequencing analysis. METHODS: We collected the thoracic aorta, heart tissues, and peripheral blood from 20 normal mice and 20 MCMV-infected mice. We identified differentially expressed miRNAs in the peripheral blood samples and predicted their target genes using bioinformatics tools. We then experimentally validated them using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and the target genes with double luciferase reporter gene assay. RESULTS: We found 118 differentially expressed miRNAs, among which 9 miRNAs were identified as potential MCMV infection-induced hypertension regulators. We then validated the expression of two candidate miRNAs, mmu-miR-1929-3p and mcmv-miR-m01-4-5p, using qRT-PCR. Furthermore, the dual-luciferase reporter gene assay revealed that the 3'-untranslated region (UTR) of endothelin A receptor (Ednra) messenger RNA (mRNA) contained a binding site for mmu-miR-1929-3p. Collectively, our data suggest that MCMV infection can raise the blood pressure and reduce mmu-miR-1929-3p expression in C57BL/6 mice. Moreover, we found that mmu-miR-1929-3p targets the 3'-UTR of the Ednra mRNA. CONCLUSION: This novel regulatory axis could aid the development of new approaches for the clinical prevention and control of EH.

miR-1929-3p Overexpression Alleviates Murine Cytomegalovirus-Induced Hypertensive Myocardial Remodeling by Suppressing Ednra/NLRP3 Inflammasome Activation.

MicroRNAs (miRNAs) play crucial roles in the development of essential hypertension (EH). Previously, we found that the expression of miR-1929-3p was decreased in C57BL/6 mice with hypertension induced by murine cytomegalovirus (MCMV). In this study, we explored the role of miR-1929-3p in hypertension myocardial remodeling in MCMV-infected mice. First, we measured MCMV DNA and host IgG and IgM after infection and determined the expression of miR-1929-3p and its target gene endothelin A receptor (Ednra) mRNA in the myocardium of mice. Then, we performed invasive blood pressure (BP) monitoring. Heart-to-body weight ratio (HW/BW%), along with mRNA levels of B-type natriuretic peptide (BNP) and beta myosin heavy chain (ß-MHC), revealed myocardial remodeling. Hematoxylin/eosin and Masson's trichrome staining indicated morphological changes in the myocardium. Cardiac function was assessed via echocardiography. Moreover, MCMV-infected mice were injected with recombinant adeno-associated virus- (rAAV-) miR-1929-3p overexpression vector. Immunohistochemistry and western blotting showed the expression of Ednra and the activation of NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome. And enzyme-linked immunosorbent assay (ELISA) revealed the concentrations of endothelin-1 (ET-1), interleukin-1ß (IL-1ß), and interleukin-18 (IL-18). In this study, we found that decreased expression of miR-1929-3p in MCMV-infected mice induced high BP and further development of myocardial remodeling cardiac function injury through increased expression of Ednra. Strikingly, overexpression of miR-1929-3p ameliorated these pathological changes of the heart. The positive effect was shown to be associated with inhibition of NLRP3 inflammasome activation and decreased expression of key proinflammatory cytokine IL-1ß. Collectively, these results indicate that miR-1929-3p overexpression may effectively alleviate EH myocardial remodeling by suppressing Ednra/NLRP3 inflammasome activation in MCMV-infected mice.

[English translation of culture-specific lexicon commonly seen in Huangdi Neijing].

HuangDi NeiJing, the Yellow Emperor's Classic of Internal Medicine, a foundational classic of Chinese medical theory, is ranked as the first among the four most important classics of traditional Chinese medicine. Translation of culture-specific Lexicon is a pivot, also a nodus in translating Huangdi Neijing, so, chewing over it is of important meaning for English translation of the Chinese classic or even for that of whole Chinese medicine. In expectation of somewhat contribution to the development of the Chinese medical English discipline, the classification and translation strategy for culture-specific lexicon were discussed by the authors in this paper through an empirical study on comparing the different terms translated in two versions of Huangdi Neijing translation.

[On the English translation of TCM pulse picture terms].

At present, the English translation of TCM terms of pulse picture are various, which would bring confusion to the study and research on TCM diagnostics. In this paper, four principles for the translation are suggested by the authors: to distinguish the nomenclature of term with its connotative explanation, to translate with commonly used words in general, to create new word with common affix and to differentiate the terms similar in meaning. The authors tried to make choice the best translation for each kind pulse picture, and explained the reasons for selection.