Atherosclerosis has been recognized as a chronic inflammatory disease, which can harden the vessel wall and narrow the arteries. MicroRNAs exhibit crucial roles in various diseases including atherosclerosis. However, so far, the role of miR‐328 in atherosclerosis remains barely explored. Therefore, our study concentrated on the potential role of miR‐328 in vascular endothelial cell injury during atherosclerosis. In our current study, we observed that oxidized low‐density lipoprotein (ox‐LDL)‐induced human umbilical vein endothelial cells (HUVECs) apoptosis and inhibited cell viability dose‐dependently and time‐dependently. In addition, indicated dosage of ox‐LDL obviously triggered HUVECs inflammation and oxidative stress process. Then, it was found that miR‐328 in HUVECs was reduced by ox‐LDL. HUVECs apoptosis was greatly repressed and cell survival was significantly upregulated by overexpression of miR‐328. Furthermore, mimics of miR‐328 rescued cell inflammation and oxidative stress process induced by ox‐LDL. Oppositely, inhibitors of miR‐328 strongly promoted ox‐LDL‐induced endothelial cells injury in HUVECs. By using bioinformatics analysis, high‐mobility group box‐1 (HMGB1) was predicted as a downstream target of miR‐328. HMGB1 has been reported to be involved in atherosclerosis development. The correlation between miR‐328 and HMGB1 was validated in our current study. Taken these together, it was implied that miR‐328 ameliorated ox‐LDL‐induced endothelial cells injury through targeting HMGB1 in atherosclerosis.

Acute myocardial infarction (AMI) is a common disease with serious consequences in mortality and cost. Here we aim to screen the differentially expressed genes (DEGs) as biomarkers for early diagnosis of AMI. The microarray data of AMI was downloaded from Gene Expression Omnibus (GEO), including two independent types of research GSE66360 and GSE62646. The DEGs between control and processed samples were screened out by using limma package. Meanwhile, we performed functional analysis of GO terms and/or KEGG pathways to observe the enriched pathways of the DEGs. Finally, regression analysis of raw data was performed by using packet affyPLM in R language. Dataset GSE62646 contained 53 DEGs (FC log2>1 and P value <0.05) between first-day samples from 28 STEMI patients and control samples from 14 patients without myocardial infarction history. There were 12 up-regulated and 41 down-regulated genes, 35 DEGs annotated. In GSE66360, a total of 3034 DEGs between 32 AMI patients and 38 healthy persons were obtained, including 1861 up-regulated and 1173 downregulated DEGs. The comparison of the DEGs in two datasets revealed four common up-regulated genes (EGR1, STAB1, SOCS3, TMEM176A). In enrichment analysis, STAB1, SOCS3, EGR1 involved in metabolic regulation and signaling pathways related to coronary artery disease with a characteristic change (P < 0.05). The DEGs, especially the four up-regulated common genes, could serve as biomarkers for early diagnosis of AMI. Additionally, the relative biological pathways these DEGs enriched in might provide a good reference to explore the molecular expression mechanism of AMI. J. Cell. Biochem. 119: 650-658, 2018. © 2017 Wiley Periodicals, Inc. KEY WORDS: ACUTE MYOCARDIAL INFARCTION; DIFFERENTIALLY EXPRESSED GENES; FUNCTIONAL ANNOTATION; BIOMARKERSA cute myocardial infarction (AMI) can cause heart failure, an irregular heartbeat, cardiogenic shock, or cardiac arrest [Risk et al., 2017]. It is the major cause of morbidity and mortality in the general population. This well-known heart attack is generally classified into ST-elevation MI (STEMI) and non-ST elevation MI (NSTEMI) [Moe and Wong, 2010]. According to the World Health Organization (WHO), annually, more than 3 million people are estimated with acute STEMI and that and more than 4 million suffers from NSTEMI [Organization, 2005;Reed et al., 2017]. In the modern society, the aging of population and comorbidities (e.g., obesity and metabolic syndrome) become more prevalent. All theses public health burden are the high risks of AMI. Besides, other health problems caused by ischemic heart disease are likely to increase even further [Yasuda and Shimokawa, 2009].The main treatments for STEMI include thrombolysis and percutaneous coronary intervention [Bates and Menees, 2012]. Hereinto, the percutaneous coronary intervention (PCI) should be performed within 90-120 min, if not, thrombolysis, preferably within 30 min of arrival to the hospital, is recommended [Bassand et al., 2005]. All these treatments need is extremely a time ...

Background: The members of the Chromobox (CBX) family are important epigenetic regulatory molecules with critical biological roles in many tumors. However, no study has analyzed or verified their role in lung adenocarcinoma (LUAD).Methods: UALCAN and Oncomine databases were used to analyze CBX expression in LUAD, and the cBioPortal database was used to analyze CBX genetic variations. The Kaplan-Meier plotter and UALCAN databases were used to identify molecules with prognostic value. Gene Ontology pathway, receiver operating characteristic curves, and tumor-infiltrating immune cell analyses were used to clarify the biological function of the CBX hub molecules. Paired tumor samples and lung adenocarcinoma cell lines were collected for molecular functional assays to validate the results of the bioinformatics analysis.Results: CBX3/5 may have a cancer-promoting effect and its expression is associated with a poor patient prognosis, while CBX7 shows an opposite trend. CBX3/5/7 can regulate signaling pathways, regulate tumor immune cell infiltration, and has diagnostic value. Molecular biology experiments show that CBX3/5 is highly expressed in LUAD patients; in vitro it promotes the proliferation and migration of the LUAD cell line and can regulate the expression of the corresponding cytokines. CBX7 has opposite effects.Conclusion: Our bioinformatics analysis and subsequent experimental verification confirmed the CBX family members acted as hub signaling molecules in LUAD. The results provide new potential targets for the diagnosis and treatment of this cancer.

Rheumatic heart disease (RHD) is a serious cardiovascular disorder worldwide. Several articles have reported the effect of angiotensin I-converting enzyme gene insertion/deletion (ACE I/D) polymorphism in RHD risk. However, the results still remain inconsistent. The objective of the present study was to assess more precise estimations of the relationship between ACE I/D variant and RHD susceptibility. Relevant case–control studies published between January 2000 and 2016 were searched in the electronic databases. The odds ratio (OR) with its 95% confidence interval (CI) was employed to calculate the strength of the effect. A total of nine articles were retrieved, including 1333 RHD patients and 1212 healthy controls. Overall, our result did not detect a significant association between ACE I/D polymorphism and RHD risk under each genetic model (P > 0.05). Subgroup analysis by ethnicity showed no positive relationship in Asians as well (P > 0.05). With respect to the severity of RHD, our result found that the frequency differences between mitral valve lesion (MVL), combined valve lesion (CVL) and healthy controls were not significantly different. Furthermore, no significant association was found between female, male RHD patients and the controls regarding to the ACE I/D polymorphism. In conclusion, our result indicated that ACE I/D polymorphism might not be a risk factor for RHD progression based on the existing research results. Additional well-designed studies with larger samples are still needed to confirm these findings.