摘要：
A variety of cardiovascular diseases is accompanied by the loss of vascular contractility. This study sought to investigate the effects of curcumin, a natural polyphenolic compound present in turmeric, on mouse vascular contractility and the underlying mechanisms. After mice were administered curcumin (100 mg·kg~(-1)·d~(-1), ig) for 6 weeks, the contractile responses of the thoracic aorta to KCI and phenylephrine were significantly enhanced compared with the control group. Furthermore, the contractility of vascular smooth muscle (SM) was significantly enhanced after incubation in curcumin (25 pmol/L) for 4 d, which was accompanied by upregulated expression of SM marker contractile proteins SM22a and SM a-actin. In cultured vascular smooth muscle cells (VSMCs), curcumin (10, 25, 50 µmol/L) significantly increased the expression of myocardin, a “master regulator” of SM gene expression. Curcumin treatment also significantly increased the levels of caveolin-1 in VSMCs. We found that as a result of the upregulation of caveolin-1, curcumin blocked the activation of Notch 1 and thereby abolished Notchl-inhibited myocardin expression. Knockdown of caveolin-1 or activation of Notch 1 signaling with Jagged 1 (2 pg/mL) diminished these effects of curcumin in VSMCs. These findings suggest that curcumin induces the expression of myocardin in mouse smooth muscle cells via a variety of mechanisms, including caveolin-l-mediated inhibition of Notch 1 activation and Notch 1-mediated repression of myocardin expression. This may represent a novel pathway, through which curcumin protects blood vessels via the beneficial regulation of SM contractility.
摘要：
Hepatocellular carcinoma (HCC), a disease that is a major health care issue across the globe, includes the deviant expression of miRNAs in its development, progression, and resistance to treatment. We focused our study on miR-503 expression and its role in HCC. miR-503 was found in HCC tissues and cell lines using quantitative real-time PCR (RT-qPCR). Western blot analyses and the luciferase reporter assay were used to determine the miR-503 potential target in the HCC cells. We used MTT to analyze cell proliferation activity and noted that there was a considerable decrease of miR-503 in HCC tissues and cell lines when measured against the controls. miR-503 upregulation decreased expression of eukaryotic translation initiation factor 4E (EIF4E), and reduced HCC cell proliferation and sensitized HCC cells to anticancer drugs. miR-503 overexpression hindered luciferase activity of EIF4E 3' untranslated region-based reporter construct among HepG2, BEL-7402, and SMMC-7721 cells, revealing that miR-503 may increase sensitivity to therapies at least partially through targeting EIF4E suppression of HCC proliferation.
作者机构：
[杨晓燕] Institute of Biologic Research;[杨晓燕] Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang Hunan 421001, China;[殷杰; 谢红艳] Institute of Biologic Research, University of South China, Hengyang Hunan 421001, China;[向琼; 雷小勇; 虞佳] Institute of Pharmacy and Pharmacology, University of South China, Hengyang Hunan 421001, China;[甘润良; 雷小勇] Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study
通讯机构：
Cancer Research Institute, University of South China, Hengyang Hunan, China
摘要：
Self-assembled peptide nanomaterials display the advantageous properties of injectability, biodegradability and biocompatibility. These peptide nanomaterials, by self-assembling, can be widely applied in such fields as drug delivery (small molecules and large molecules), regenerative medicine and nanobiotechnology. In this review, we mainly discuss the properties of these peptide nanomaterials in their physical, chemical and biological aspects. Also discussed are recent advances in their potential applications as drug delivery systems and for uses in regenerative medicine. These current advances show a bright future for the development and clinical applications of self-assembled peptide-based nanotechnology and nanomedicine. However, there are still some big challenges for us to face before these peptide nanomaterials eventually can be used for the treatment of human diseases.
通讯机构：
[Tang, Shengsong] H;[Tang, Shengsong] U;Hunan Univ Med, Biomed Res Ctr, Huaihua 418000, Peoples R China.;Univ South China, Inst Pharm & Pharmacol, Dept Histol & Embryol, Hengyang 421001, Peoples R China.
关键词：
Macrophage colony-stimulating factor;chemoresistance;apoptosis;autophagy;breast cancer
摘要：
Macrophage colony-stimulating factor is a vital factor in maintaining the biological function of monocyte–macrophage lineage. It is expressed in many tumor tissues and cancer cells. Recent findings indicate that macrophage colony-stimulating factor might contribute to chemoresistance, but the precise mechanisms are unclear. This study was to explore the effect of macrophage colony-stimulating factor on doxorubicin resistance in MCF-7 breast cancer cells and the possible mechanism. In the study, the human breast cancer cells, MCF-7, were transfected with macrophage colony-stimulating factor. We document that cytoplasmic macrophage colony-stimulating factor induces doxorubicin resistance and inhibits apoptosis in MCF-7 cells. Further studies demonstrated that cytoplasmic macrophage colony-stimulating factor-mediated apoptosis inhibition was dependent on the activation of PI3K/Akt/Survivin pathway. More importantly, we found that macrophage colony-stimulating factor-induced autophagic cell death in doxorubicin-treated MCF-7 cells. Taken together, we show for the first time that macrophage colony-stimulating factor-induced doxorubicin resistance is associated with the changes in cell death response with defective apoptosis and promotion of autophagic cell death.
作者机构：
[He, Shuya; Xiao, Xiao; Fu, Liang; Ma, Yun; Tian, Shuai] Univ South China, Dept Biochem & Biol, 28 Western Changsheng Rd, Hengyang City 421001, Hunan, Peoples R China.;[Wang, Zongbao; He, Shuya; Lei, Xiaoyong; Ma, Yun; Lei, XY] Hunan Prov Cooperat Innovat Ctr Mol Target New Dr, 28 Western Changsheng Rd, Hengyang City 421001, Hunan, Peoples R China.;[Chen, Qiong] Cent S Univ, Xiangya Hosp, Dept Resp, Dept Geriatr Med, Changsha 410008, Hunan, Peoples R China.
通讯机构：
[He, Shuya] U;[Ma, Y; Lei, XY] H;Univ South China, Dept Biochem & Biol, 28 Western Changsheng Rd, Hengyang City 421001, Hunan, Peoples R China.;Hunan Prov Cooperat Innovat Ctr Mol Target New Dr, 28 Western Changsheng Rd, Hengyang City 421001, Hunan, Peoples R China.
关键词：
miR-19b;FXR1;RAB18;USP32;Dusp6
摘要：
The biological effects of microRNAs (miRNAs) in the Fragile X Syndrome (FXS) have been widely studied. Dysregulation of miRNAs plays a critical role in the progression of nervous system diseases and in cell proliferation and differentiation. Our previous study validated that miR-19b-3p was associated with FXR1 (Fragile X related gene I), one of homologous genes of FMR1 (Fragile X mental retardation 1). The purpose of this study was to investigate the relationship of FXR1 and miR-19b-3p, and the crucial role of miR-19b-3p in FXS and to validate whether miR-19b-3p could regulate the growth of SH-SY5Y cells. We determined that miR-19b-3p could regulate the expression of not only USP32, RAB18 and Dttsp6 but also FXR1, and FXR1 could in turn regulate the expression of miR-19b-3p. What's more, the overexpression of miR-19b-3p significantly inhibited the proliferation, contributed the apoptosis and slowed down the cycle of SH-SY5Y cells. Taken together, our results indicate that miR-19b-3p plays a significant role in the molecular pathology of FXS by interacting with FXR1 and influencing the growth of SH-SY5Y cells. (C) 2016 Elsevier B.V. All rights reserved.
作者机构：
[潘霞; 管馨馨; 黄楠; 张建华; 刘柳成; 张思; 臧婧蕾] Institute of Pharmacy and Pharmacology, University of South China, Hengyang 421000, China;[雷小勇] Institute of Pharmacy and Pharmacology, University of South China, Hengyang 421000, China. 1622214323@qq.com
