作者:
Kai Zhang;Qionglin Zhou;Yu Guo;Linxi Chen;Lanfang Li
期刊:
生物化学与生物物理学报,2018年50(6):618-619 ISSN:1672-9145
通讯作者:
Chen, L.
作者机构:
[Zhang Kai; Zhou Qionglin; Guo Yu; Chen Linxi; Li Lanfang] Institute of Pharmacy and Pharmacology, University of South China, Learning Key Laboratory for Pharmacoproteomics;[Zhang Kai; Zhou Qionglin; Guo Yu; Chen Linxi; Li Lanfang] Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Hengyang, 421001
通讯机构:
[Chen, L.] L
关键词:
线粒体;机能障碍;蜂窝;胃;真核细胞;膜;细胞器;房间
摘要:
Both endoplasmic reticulum (ER) and mitochondria are fundamental organelles that coordinate high-order cell functions. ER is an extensive network of cisternae and microtubules, which stretches from the nuclear envelope to the cell surface in all eukaryotic cells. ER works as the site for protein synthesis and corrects post-translational ‘folding’ of proteins. ER also has the ability to transport proteins to their destination. Moreover, ER acts as a calcium ion (Ca~(2+)) reservoir which can be activated by both electrical and chemical stimulation.
作者机构:
[Shi, J.-F.; Tian, Q.-X.; Li, M.-X.] Institute of Cardiovascular Disease, Institute of Pharmaceutical and Biological Sciences, University of South China, Hengyang Hunan, 421001, China;[He, P.-C.; She, M.-H.] Dept. of Biotechnology, Institute of Pharmaceutical and Biological Sciences, University of South China, Hengyang Hunan, 421001, China;[Zhang, X.-H.] Aier Eye Hospital of Hengyang, Hengyang Hunan, 421001, China;[Zhang, Y.] First People's Hospital of Changde, Changde Hunan, 415000, China;[Moshe, L.] Neurim Pharmaceuticals Ltd., Israel
作者机构:
[Fu, Nian; Chen, Linxi; Zhao, Hong] Institute of Pharmacy and Pharmacology, Hunan Province Cooperative Innovation Center for Molecular Target New Drugs Study, University of South China, Hengyang, 421001, China;[Yao, Pingbo] Intensive Care Units of the Affiliated Nanhua Hospital, University of South China, Hengyang, 421002, China
通讯机构:
[Fu, N.] I;Institute of Pharmacy and Pharmacology, Hunan Province Cooperative Innovation Center for Molecular Target New Drugs Study, University of South China, Hengyang, China
摘要:
Hepatocellular carcinoma (HCC),one of the most common malignant cancers, is the third leading cause of cancer-related mortality worldwide. The etiological factors of HCC include alcohol intake, smoking, viral infections, cirrhosis, non-alcoholic steatohepatitis, hemochromatosis, and diabetes. Nowadays, despite much advance in HCC treatment, the 5-year survival rate for patients keeps dismal due to recurrence and metastases of HCC. Cancer stem cells (CSCs), also termed tumor-initiating cells, have the capability for unrestricted cell division, contributing to heterogeneous cell progenies. CSCs exist in both solid tumors and hematological malignancy. Till now, some cell surface markers are widely used to identify a subpopulation of cells with CSC features in liver such as CD24,CD 133, and epithelial cell adhesion molecule. Therefore, identification of CSC subpopulations in tumor will provide a novel understanding for cancer progress.
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.
作者机构:
[张晓一] Dept of Pharmacy, Changzhi Medical College, Changzhi Shanxi, 046000, China;[秦旭平; 刘玉环; 杨丽; 郭峰; 阳芳; 王珍] Institute of Pharmacy and Pharmacology, University of South China, Hengyang Hunan, 421001, China
作者机构:
[江振涛; 刘盛权; 唐芬; 龙俊蓉; 谭文婷] Department of Cardiology, First A ffi liated Hospital of South China University, Hengyang Hunan 421001, China;[Chu, Chun] Department of Pharmacy, Second A ffi liated Hospital of South China University, Hengyang Hunan 421001, China
通讯机构:
Department of Pharmacy, Second Affiliated Hospital, South China University, Hengyang Hunan, China
摘要:
Apelin is the endogenous peptide APJ receptor, while APJ is a member of the G protein-coupled receptors family. Recent evidence strongly suggests that Apelin/APJ system influences apoptosis in various diseases through different signal pathways. In this review, we discuss the possible mechanisms by which the Apelin/APJ system inhibits apoptosis, including the phosphatidylinositol-3-kinase (PI3K)/Akt, ERK1/2, caspase signaling, and autophagy pathway. We also summarize the role of Apelin/APJ system in apoptosis in myocardial ischemia-reperfusion (l/R) injury, pulmonary artery hypertension, retinal neovascular disease, acute renal injury, skeletal homeostasis, and gastrointestinal diseases. Apelin/APJ system decreases myocardial infarction size and alleviates myocardial l/R injury by inhibiting cardiomyocytes apoptosis. However, Apelin/APJ system improves pulmonary artery hypertension via increasing apoptosis. Apelin/APJ system exerts neuroprotective effect by blocking apoptosis and participates in the recovery of retinal neovascular disease by suppressing apoptosis. Apelin/APJ system also shows anti-apoptotic effect against acute renal injury and plays a role in regulating skeletal homeostasis. In gastrointestinal disease, Apelin/APJ system plays a potential physiological role in gastrointestinal cytoprotection by regulating apoptosis. We hope that a better understanding of the Apelin/APJ system will help to discover new disease pathogenesis and find possible therapeutic targets of the Apelin/APJ system essential for various diseases.
摘要:
Atherosclerotic lesions are characterized by the accumulation of abundant lipids and chronic inflammation. Previous researches have indicated that macrophage-derived lipoprotein lipase (LPL) promotes atherosclerosis progression by accelerating lipid accumulation and proinflammatory cytokine secretion. Although apelin-13 has been regarded as an atheroprotective factor, it remains unclear whether it can regulate the expression of LPL. The aim of this study was to explore the effects of apelin-13 on the expression of LPL and the underlying mechanism in THP-1 macrophage-derived foam cells. Apelin-13 significantly decreased cellular levels of total cholesterol, free cholesterol, and cholesterol ester at the concentrations of 10 and 100 nM. ELISA analysis confirmed that treatment with apelin-13 reduced pro-inflammatory cytokine secretion, such as interleukin-6 (IL-6), interleukin-1β (IL-1β) and tumor necrosis factor-alpha (TNF-α). It was also found that apelin-13 inhibited the expression of LPL as revealed by western blot and real-time PCR analyses. Bioinformatics analyses and dual-luciferase reporter assay indicated that miR-361-5p directly downregulated the expression of LPL by targeting the 3'UTR of LPL. In addition, apelin-13 + miR-361-5p mimic significantly downregulated the expression of LPL in cells. Finally, we demonstrated that apelin-13 downregulated the expression of LPL through activating the activity of PKCa. Taken together, our results showed that apelin-13 downregulated the expression of LPL via activating the APJ/PKCa/miR-361 -5p signaling pathway in THP-1 macrophage-derived foam cells, leading to inhibition of lipid accumulation and proinflammatory cytokine secretion. Therefore, our studies provide important new insight into the inhibition of lipid accumulation and pro-inflammatory cytokine secretion by apelin-13, and high-light appelin-13 as a promising therapeutic target in atherosclerosis.
作者机构:
Dept of Genetics, Changde Maternal and Child Health-Care Hospital, Changde, Hunan, 415000, China;[张敏; Yu X.-X.; 田英; Duan U.-R.; 龙石银; 麻燕妮; 张彩平] Dept of Biotechnology, University of South China, Hengyang, Hunan, 421001, China;[刘英] Dept of Medicine, Changde Vocational Technical College, Changde, Hunan, 415000, China;[欧露] Dept of Genetics, Changde Maternal and Child Health-Care Hospital, Changde, Hunan, 415000, China, Dept of Biotechnology, University of South China, Hengyang, Hunan, 421001, China
作者机构:
[Lanfang Li; Liqun Lu; Jiangang Cao; Linxi Chen] Institute of Pharmacy and Pharmacology, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Learning Key Laboratory for Pharmacoproteomics, University of South China, Hengyang 421001, China
通讯机构:
[Li, L.] I;Institute of Pharmacy and Pharmacology, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Learning Key Laboratory for Pharmacoproteomics, University of South China, Hengyang, China
摘要:
Apelin is an endogenous ligand of the APJ receptor (also known as Aplnr) which is a G protein-coupled receptor. Elabela (also known as Toddler, Apela), which shares little sequence similarity with Apelin (Fig.1),has been identified as a new endogenous ligand for APJ receptor. Elabela is encoded by AK092578 gene from a region of the human genome which was previously classified as 'non-coding'. Elabela is initially translated into a peptide of 54 amino acids including a secretory signal peptide. However, its mature form only contains 32 amino acids. The Elabela/Aplnr axis mainly acts in embryonic development compared with Apelin/APJ system which has abundant biological functions in different physiological and pathological processes. During zebrafish embryogenesis, Elabela is proved to be indispensable for the proper differentiation of endodermal precursors which guide the overlying cardiac progenitors to the heart-forming region to initiate cardiogenesis. Therefore, loss of Elabela causes severe cardiac dysplasia ranging from a rudimentary heart to no heart, and has little to no blood circulation. Elabela expresses concomitantly with Aplnr before the onset of gastrulation, and loss of Elabela phenocopies the loss of Aplnr during early heart development. However, Apelin is not expressed until midgastrulation and Apelin zebrafish morphants are not presented with overt congenital cardiac anomalies. Thus, the Elabela/Aplnr axis appears to be exclusive for endoderm differentiation and subsequent cardiogenesis (Fig.2).
作者机构:
[Hongtao Qu; Lu He; Hong Liu] Department of Neurosurgery, The First Affiliated Hospital, University of South China, Hengyang 421001, China;[Hong Zhou] Department of Radiology, The First Affiliated Hospital, University of South China, Hengyang 421001, China;[Hong Zhou] Institute of Pharmacy and Pharmacology, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Learning Key Laboratory for Pharmacoproteomics, University of South China, Hengyang 421001, China
通讯机构:
[Hong Liu; Hongtao Qu] 1;1 Department of Neurosurgery , The First Affiliated Hospital , University of South China , Hengyang 421001 , China
关键词:
signal transduction;neoplasms
摘要:
Cell competition possesses a cell fitness-sensing process ranging from Drosophila to mammals that selectively eliminates aberrant cells via apoptosis. The presence of cell competitive interaction will determine whether the cell contributes to the survival of organisms. Yamamoto et al. recently reveal a hitherto unexplored mechanism by which the surrounding normal epithelial cells can recognize oncogenic polarity-deficient neighbors to trigger tumor-suppressive cell competition in Drosophila.