作者机构：
[Yang, Yong-Zong; Gu, Hong-Feng; Wang, Shuang; Tang, Ya Ling; Peng, Juan] Univ South China, Inst Cardiovasc Dis, Key Lab Arteriosclerol Hunan Prov, Hengyang 421001, Peoples R China.;[Liu, Zhu; Jiang, Jian Hong] Univ South China, Chuanshan Coll, Hengyang 421001, Peoples R China.;[Gu, Hong-Feng; Tang, Xiao Qing] Univ South China, Dept Physiol, Hengyang 421001, Peoples R China.;[Gu, Hong-Feng; Tang, Xiao Qing] Univ South China, Inst Neurosci, Hengyang 421001, Peoples R China.
通讯机构：
[Gu, Hong-Feng] Univ South China, Inst Cardiovasc Dis, Key Lab Arteriosclerol Hunan Prov, Hengyang 421001, Peoples R China.
摘要：
Objective Chronic stress is an important risk factor for atherosclerotic diseases. Our previous studies have shown that chronic unpredictable mild stress (CUMS) accelerates atherosclerosis and up-regulates TLR4/NF-kappa B expression in apoE(-/-) mice. However, TLR4/NF-kappa B signaling whether directly contributes to the development of atherosclerosis in CUMS mice is unclear. We hypothesized that the interference of TLR4/NF-kappa B can ameliorate CUMS-induced inflammation and atherosclerosis in apoE(-/-) mice. Methods ApoE(-/-) mice were exposed to 12 weeks CUMS. Ad-siRNA TLR4 was given by tail vein injection (10 mu l/mouse, every 5 days), and PDTC (an inhibitor of NF-kappa B) was given by intraperitoneal injection (60 mg/kg, once a day). Plasma corticosterone concentrations were determined by solid-phase I-125 radioimmunoassay. Atherosclerosis lesions in aortic sinuses were evaluated and quantified by IMAGEPRO PLUS. Western blotting was used to detect the expression of TLR4, NF-kappa B, and IL-1 beta in aortas of the mice. Plasma lipid profiles, IL-1 beta, TNF-alpha, and MCP-1 were measured by ELISA. Results Our results indicated that CUMS apoE(-/-) mice treatment with siRNA TLR4 significantly decreased atherosclerosis and down-regulated TLR4, NF-kappa B, and inflammatory cytokines. PDTC also remarkably reduced atherosclerosis and the levels of IL-1 beta, TNF-alpha and MCP-1 in plasma. However, Treatment with siRNA TLR4 or PDTC had no effect on plasma corticosterone levels, and lipid profiles. Conclusions TLR4/NF-kappa B pathway may participate in CUMS-induced atherosclerosis through activation of proinflammatory cytokines in apoE(-/-) mice. Our data may provide a new potential therapeutic target for prevention of CUMS-induced atherosclerosis.
摘要：
Cardiovascular disease is a growing major global public health problem. Oxidative stress is regarded as one of the key regulators of pathological physiology, which eventually leads to cardiovascular disease. However, mechanisms by which FGF-2 rescues cells from oxidative stress damage in cardiovascular disease is not fully elucidated. Herein this study was designed to investigate the protective effects of FGF-2 in H2O2-induced apoptosis of H9c2 cardiomyocytes, as well as the possible signaling pathway involved. Apoptosis of H9c2 cardiomyocytes was induced by H2O2 and assessed using methyl thiazolyl tetrazolium assay, Hoechst, and TUNEL staining. Cells were pretreated with PI3K/Akt inhibitor LY294002 to investigate the possible PI3K/Akt pathways involved in the protection of FGF-2. The levels of p-Akt, p-FoxO3a, and Bim were detected by immunoblotting. Stimulation with H2O2 decreased the phosphorylation of Akt and FoxO3a, and induced nuclear localization of FoxO3a and apoptosis of H9c2 cells. These effects of H2O2 were abrogated by pretreatment with FGF-2. Furthermore, the protective effects of FGF-2 were abolished by PI3K/Akt inhibitor LY294002. In conclusion, our data suggest that FGF-2 protects against H2O2-induced apoptosis of H9c2 cardiomyocytes via activation of the PI3K/Akt/FoxO3a pathway.
摘要：
Attachments of Acidithiobacillus ferrooxidans ATCC 23270 onto elemental sulfur, quartz and complex chalcopyrite were investigated by analysis of its extracellular polymeric substances as well as applying Langmuir and Freundlich equations. The two equations fitted the adsorption equilibrium data with significant correlation coefficient over 0.9. This indicated that bacterial attachment is complicated and involves Langmuir and Freundlich characterizations. Sulfur-grown cells showed the highest affinity for the three solid substrates. The investigated complex chalcopyrite possessed a higher maximum adsorption capacity for A. ferrooxidans than elemental sulfur or quartz. The Freundlich fitting parameters suggested that quartz had a weaker adsorption capacity and smaller adsorption areas than elemental sulfur or the complex chalcopyrite. It is not the content of total carbohydrates or proteins in EPS but their ratios that determine the affinity differences between cells and substrates.
摘要：
P63 null mice have no or truncated limbs and mutations in human p63 cause several skeletal syndromes that also show limb and digit abnormalities, suggesting its essential role in bone development. In the current study, we investigated the effect of ATRA on chondrogenesis using mesenchymal cells from rat hind limb bud and further examined the mRNA and protein expression of Sox9 and Col2a1 and p63 in rat hind limb bud cells. Limb buds were isolated from embryos from euthanized female rats. Growth of hind limb bud mesenchymal cells was determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium (MTT) assays. Formation of cartilage nodules was examined by Alcian blue-nuclear fast red staining. The expression of Sox9, Col2al and p63 was determined by Real-time RT-PCR and immunoblotting assays, respectively. Our MTT assays revealed that ATRA at 1 and 10 mu M significantly suppressed the growth of mesenchymal cells from rat hind limb bud at 24 and 48 h (P <0.01 vs. controls). Alcian blue staining further showed that ATRA caused a significant dose-dependent reduction in the area of cartilage nodules (P <0.05 in all vs. controls). At 1 mu M ATRA, the area of cartilage nodules from hind limb bud cells was reduced to 0.05 +/- 0.03 mm from 0.15 +/- 0.01 mm in controls. Real-time RT-PCR assays further indicated that 1 and 10 mu M ATRA markedly reduced the mRNA expression of Sox9, Col2al and p63 in hind limb bud cells (P < 0.05 in all vs. controls). In addition, ATRA time-dependently inhibits the mRNA expression of p63, Sox9 and Col2al. Western blotting assays additionally showed that ATRA dose-dependently reduced the expression of Sox9, Col2al and p63 (P < 0.05 in all vs. controls). Together, our results suggest that ATRA suppresses chondrogenesis by modulating the expression of Sox9, Col2al and p63 in primary hind limb bud mesenchymal cells. (C) 2014 Elsevier B.V. All rights reserved.
期刊：
Biochemical and Biophysical Research Communications,2019年516(1):278-284 ISSN：0006-291X
通讯作者：
Zhou, Rongrong
作者机构：
[Cheng, Tingting] Cent S Univ, Xiangya Hosp, Dept Prevent Hlth Care, Changsha, Hunan, Peoples R China.;[Zhang, Jing; Zhou, Rongrong; Liang, Zhan; Liu, Zhiyuan; Zhang, Zijian; Chen, Taili; Li, Jiahui; Tan, Zhaohua; Cheng, Tingting; Tang, Jianbing] Cent S Univ, Xiangya Hosp, Dept Oncol, Changsha, Hunan, Peoples R China.;[Zhang, Jing; Zhou, Rongrong; Liang, Zhan; Liu, Zhiyuan; Zhang, Zijian; Chen, Taili; Li, Jiahui; Tan, Zhaohua; Tang, Jianbing] Cent S Univ, Xiangya Hosp, Natl Clin Res Ctr Geriatr Disorders, Changsha, Hunan, Peoples R China.;[Cheng, Yuyu] Univ South China, Chuanshan Coll, Hengyang, Peoples R China.;[Zhao, Jin] Cent S Univ, Key Lab Carcinogenesis, Chinese Minist Hlth, Hunan Canc Hosp, Changsha, Hunan, Peoples R China.
通讯机构：
[Zhou, Rongrong] Cent S Univ, Xiangya Hosp, Dept Oncol, Natl Clin Res Ctr Geriatr Disorders, Changsha 410078, Hunan, Peoples R China.
关键词：
Lung adenocarcinoma<&wdkj&>ETV4<&wdkj&>MSI2<&wdkj&>Transcription regulation<&wdkj&>Proliferation and invasion
摘要：
The oncogenic roles of ETV4 have been revealed in multiple cancers. However, its expression and functions in lung cancer are rarely explored. Here, we firstly detected the expression of ETV4 in lung adenocarcinoma (LUAD) via online data and local experiment validation. Furthermore, we explored the functions and corresponding mechanisms of ETV4 in LUAD. Upregulation of ETV4 in LUAD is indicated by online data and our results of qPCR, Western blot and immunohistochemistry in collective tissue samples. ETV4 knockdown significantly inhibits proliferation and invasion in LUAD indicated by the outcomes of CCK8, plate clone formation, and Transwell invasion assays. Mechanistically, chromatin immunoprecipitation and luciferase reporter system assays indicated that ETV4 could directly bind at the promoter of MSI2 and promote its transcription. Furthermore, ectopic expression MSI2 can rescue the inhibitory effects caused by ETV4 knockdown in LUAD. Therefore, we proved that upregulation of ETV4 could promote proliferation and invasion of LUAD by transcriptionally upregulating MSI2 offering a potential therapy treatment target of LUAD. (C) 2019 Elsevier Inc. All rights reserved.
期刊：
Progress in Biochemistry and Biophysics,2013年40(9):834-844 ISSN：1000-3282
通讯作者：
Gu Hong-Feng
作者机构：
[Gu Hong-Feng] Univ South China, Dept Physiol, Hengyang 421001, Peoples R China.;[Gu Hong-Feng; Yang Yong-Zong] Key Lab Arteriosclerol Hunan Prov, Hengyang 421001, Peoples R China.;[Jiang Jian-Hong] Nanhua Univ, Chuanshan Coll, Hengyang 421001, Peoples R China.;[Tong Qiao-Zhen; Liao Duan-Fang] Hunan Univ Chinese Med, Div Stem Cell Regulat & Applicat, State Key Lab Chinese Med Powder & Med Innovat Hu, Changsha 410208, Hunan, Peoples R China.
通讯机构：
[Gu Hong-Feng] Univ South China, Dept Physiol, Hengyang 421001, Peoples R China.
关键词：
GP Ⅱb/Ⅲa;atherosclerosis;HMGB-1;TLR4;NF-κB
摘要：
The effects of glycoprotein (GP) Ⅱb/Ⅲa inhibitors on the development of the atherosclerotic process has received scant attention. To investigate whether GP Ⅱb/Ⅲa blockade influences atherosclerosis lesion and HMGB-1/TLR4 signaling, we compared plaque formation in ApoE~(-/-) mice: control group (n=10); IgG group (n=10, 50 μg) and GP Ⅱb/Ⅲa mAb group (n=10, 50 μg). All mice were fed on a Western diet (10% fat and 1.25% cholesterol) for 10 weeks. GP Ⅱb/Ⅲa blockade significantly decreased the atherosclerotic lesion and platelet adhesion to the vessel wall. Immunohistochemistry analysis showed that blocking GP Ⅱb/Ⅲa diminished MOMA-2 and VCAM-1 expression in aortic plaque in ApoE~(-/-) mice. Western blot results indicated that HMGB-1, TLR4, and NF-κB levels were markedly reduced in arteries of ApoE-/- mice treated with GP Ⅱb/Ⅲa mAb (P < 0.05). Moreover, GP Ⅱb/Ⅲa mAb decreased plasma HMGB-1, IL-1β, TNF-α and MCP-1 concentrations. Our findings demonstrated that GP Ⅱb/Ⅲa mAb significantly decreased atherosclerotic lesions and HMGB-1, TLR4 and NF-κB expression in ApoE~(-/-) mice (P < 0.05). The present study has suggested a possibility that GP Ⅱb/Ⅲa blockade attenuates atherosclerosis by inhibiting the HMGB-1/TLR4 pathway..
