Genetic variation of pharmacogenomic VIP variants in Zhuang nationality of southern China.

Drug gene polymorphisms are strongly associated with disease. Previous studies have shown that the frequency of drug genes varies in different populations. At present, there are no reports about the polymorphism of the drug genome in the Zhuang population in southern China. This study conducted a pharmacogenomics study on the Zhuang population in southern China. Therefore, we conducted genotyping on 105 Zhuang samples, and compared the genotyping results with those of other 11 ethnic groups after statistical analysis. Our results show that, compared with the 11 populations in the HapMap data set, the differences between the CYP2E1 rs2070676 and CYP2D6 rs1065852 of the Zhuang nationality are the largest. This study fills in the blank of the drug genome information of the Zhuang nationality in southern China. The two sites of Rs2070676 (CYP2E1) and rs1065852 (CYP2D6) provide a reliable basis for the prediction of the efficacy of certain drugs. Its main purpose is to provide theoretical basis for safe drug use in the Zhuang region of southern China.

Cadmium sulfate induces apoptosis in planarians.

With rapid socio-economic development, heavy metal pollution in water has become common and affects both environment and human health. Cadmium (Cd) has been recognized as one of the heavy metals which cause acute or chronic toxic effects if ingested. Although its toxicity is undisputed, the underlying molecular mechanisms in vivo are not fully understood. Planarians, a model organism famous for their regenerative prowess, have long been utilized to study the effects of chemical exposure. In this study, we observed apoptosis with TUNEL assay in planarians induced by cadmium sulfate (CdSO4) in a dose-dependent manner. The apoptosis-related genes were detected with quantitative RT-PCR. Significant changes in c-Myc, P53, and BcL-2 were indicated, which may play a partial role in the regulation of the process of apoptosis in the planarians. H&E staining showed that Cd had obvious biological toxicity in the planarians. Here, new insights on metal toxicity mechanisms are provided, contributing to understand how CdSO4 induces the pathological and physiological processes of apoptosis in the living bodies. Meanwhile, planarians are proved to be a freshwater pollution indicator and toxicological research model.

Tenascin-c renders a proangiogenic phenotype in macrophage via annexin II.

Tenascin-c is an extracellular matrix glycoprotein, the expression of which relates to the progression of atherosclerosis, myocardial infarction and heart failure. Annexin II acts as a cell surface receptor of tenascin-c. This study aimed to delineate the role of tenascin-c and annexin II in macrophages presented in atherosclerotic plaque. Animal models with atherosclerotic lesions were established using ApoE-KO mice fed with high-cholesterol diet. The expression of tenascin-c and annexin II in atherosclerotic lesions was determined by qRT-PCR, Western blot and immunohistochemistry analysis. Raw 264.7 macrophages and human primary macrophages were exposed to 5, 10 and 15 µg/ml tenascin-c for 12 hrs. Cell migration as well as the proangiogenic ability of macrophages was examined. Additionally, annexin II expression was delineated in raw 264.7 macrophages under normal condition (20% O2 ) for 12 hrs or hypoxic condition (1% O2 ) for 6-12 hrs. The expression of tenascin-c and annexin II was markedly augmented in lesion aorta. Tenascin-c positively regulated macrophage migration, which was dependent on the expression of annexin II in macrophages. VEGF release from macrophages and endothelial tube induction by macrophage were boosted by tenascin-c and attenuated by annexin II blocking. Furthermore, tenascin-c activated Akt/NF-κB and ERK signalling through annexin II. Lastly, hypoxia conditioning remarkably facilitates annexin II expression in macrophages through hypoxia-inducible factor (HIF)-1α but not HIF-2α. In conclusion, tenascin-c promoted macrophage migration and VEGF expression through annexin II, the expression of which was modulated by HIF-1α.