排序方式: 共有28条查询结果,搜索用时 15 毫秒
1.
《Redox report : communications in free radical research》2013,18(6):317-324
AbstractThe cardiotoxic effect of anthracyclines limits their use in the treatment of a variety of cancers. The reason for the high susceptibility of cardiac muscle to anthracyclines remains unclear, but it appears to be due, at least in part, to the interaction of these drugs with intracellular iron (Fe). The suggestion that Fe plays an important role in anthracycline cardiotoxicity has been strengthened by observation that the chelator, dexrazoxane (ICRF-187), has a potent cardioprotective effect. In the present review, the role of Fe in the cardiotoxicity of anthracyclines is discussed together with the possible role of Fe chelation therapy as a cardioprotective strategy that may also result in enhanced antitumour activity. 相似文献
2.
Sumiyuki Mii Jennifer Duong Yasunori Tome Aisada Uchugonova Fang Liu Yasuyuki Amoh Norimitsu Saito Kensei Katsuoka Robert M. Hoffman PhD 《Journal of cellular biochemistry》2013,114(7):1674-1684
We have previously reported that nestin‐expressing hair follicle stem cells can differentiate into neurons, Schwann cells, and other cell types. In the present study, vibrissa hair follicles, including their sensory nerve stump, were excised from transgenic mice in which the nestin promoter drives green fluorescent protein (ND‐GFP mice), and were placed in 3D histoculture supported by Gelfoam®. β‐III tubulin‐positive fibers, consisting of ND‐GFP‐expressing cells, extended up to 500 µm from the whisker nerve stump in histoculture. The growing fibers had growth cones on their tips expressing F‐actin. These findings indicate that β‐III tubulin‐positive fibers elongating from the whisker follicle sensory nerve stump were growing axons. The growing whisker sensory nerve was highly enriched in ND‐GFP cells which appeared to play a major role in its elongation and interaction with other nerves in 3D culture, including the sciatic nerve, the trigeminal nerve, and the trigeminal nerve ganglion. The results of the present report suggest a major function of the nestin‐expressing stem cells in the hair follicle is for growth of the follicle sensory nerve. J. Cell. Biochem. 114: 1674–1684, 2013. © 2013 Wiley Periodicals, Inc. 相似文献
3.
GDNF From Human Periodontal Ligament Cells Treated With Pro‐Inflammatory Cytokines Promotes Neurocytic Differentiation of PC12 Cells
下载免费PDF全文
![点击此处可从《Journal of cellular biochemistry》网站下载免费的PDF全文](/ch/ext_images/free.gif)
4.
5.
F1FO ATP Synthase Is Expressed at the Surface of Embryonic Rat Heart‐Derived H9c2 Cells and Is Affected by Cardiac‐Like Differentiation
下载免费PDF全文
![点击此处可从《Journal of cellular biochemistry》网站下载免费的PDF全文](/ch/ext_images/free.gif)
Marina Comelli Rossana Domenis Alessia Buso Irene Mavelli 《Journal of cellular biochemistry》2016,117(2):470-482
Taking advantage from the peculiar features of the embryonic rat heart‐derived myoblast cell line H9c2, the present study is the first to provide evidence for the expression of F1FO ATP synthase and of ATPase Inhibitory Factor 1 (IF1) on the surface of cells of cardiac origin, together documenting that they were affected through cardiac‐like differentiation. Subunits of both the catalytic F1 sector of the complex (ATP synthase‐β) and of the peripheral stalk, responsible for the correct F1‐FO assembly/coupling, (OSCP, b, F6) were detected by immunofluorescence, together with IF1. The expression of ATP synthase‐β, ATP synthase‐b and F6 were similar for parental and differentiated H9c2, while the levels of OSCP increased noticeably in differentiated cells, where the results of in situ Proximity Ligation Assay were consistent with OSCP interaction within ecto‐F1FO complexes. An opposite trend was shown by IF1 whose ectopic expression appeared greater in the parental H9c2. Here, evidence for the IF1 interaction with ecto‐F1FO complexes was provided. Functional analyses corroborate both sets of data. i) An F1FO ATP synthase contribution to the exATP production by differentiated cells suggests an augmented expression of holo‐F1FO ATP synthase on plasma membrane, in line with the increase of OSCP expression and interaction considered as a requirement for favoring the F1‐FO coupling. ii) The absence of exATP generation by the enzyme, and the finding that exATP hydrolysis was largely oligomycin‐insensitive, are in line in parental cells with the deficit of OSCP and suggest the occurrence of sub‐assemblies together evoking more regulation by IF1. J. Cell. Biochem. 9999: 1–13, 2015. © 2015 Wiley Periodicals, Inc. J. Cell. Biochem. 117: 470–482, 2016. © 2015 Wiley Periodicals, Inc. 相似文献
6.
Durand JL Nawrocki AR Scherer PE Jelicks LA 《Journal of cellular biochemistry》2012,113(10):3276-3287
Left ventricular hypertrophy (LVH) is a risk factor for cardiovascular disease, a leading cause of death. Alterations in endothelial nitric oxide synthase (eNOS), an enzyme involved in regulating vascular tone, and in adiponectin, an adipocyte‐derived secretory factor, are associated with cardiac remodeling. Deficiency of eNOS is associated with hypertension and LVH. Adiponectin exhibits vaso‐protective, anti‐inflammatory, and anti‐atherogenic properties. We hypothesized that increased levels of adiponectin would alleviate cardiac pathology resulting from eNOS deficiency, while decreased levels of adiponectin would exacerbate the pathology. Male and female mice, deficient in eNOS, and either lacking or over‐expressing adiponectin, were fed high fat diet (HFD) or normal chow. Cardiac magnetic resonance imaging was performed to serially assess heart morphology and function up to 40 weeks of age. Thirty‐two weeks of HFD feeding led to significantly greater LV mass in male mice deficient in eNOS and either lacking or over‐expressing adiponectin. Heart function was significantly reduced when the mice were deficient in either eNOS, adiponectin or both eNOS and adiponectin; for female mice, heart function was only reduced when both eNOS and adiponectin were lacking. Thus, while over‐expression of adiponectin in the eNOS deficient HFD fed male mice preserved function at the expense of significantly increased LV mass, female mice were protected from decreased function and increased LVH by over‐expression of adiponectin. Our results demonstrate a sexual dimorphism in response of the heart to alterations in eNOS and adiponectin during high fat feeding and suggest that adiponectin might require eNOS for some of its metabolic effects. J. Cell. Biochem. 113: 3276–3287, 2012. © 2012 Wiley Periodicals, Inc. 相似文献
7.
8.
9.
Sodium Butyrate Protects Against High Fat Diet‐Induced Cardiac Dysfunction and Metabolic Disorders in Type II Diabetic Mice
下载免费PDF全文
![点击此处可从《Journal of cellular biochemistry》网站下载免费的PDF全文](/ch/ext_images/free.gif)
10.
Wang C Wang S Zhao P Wang X Wang J Wang Y Song L Zou Y Hui R 《Journal of cellular biochemistry》2012,113(6):2040-2046
Cardiac hypertrophy has been known as an independent predictor for cardiovascular morbidity and mortality. Molecular mechanisms underlying the development of heart failure remain elusive. Recently, microRNAs (miRs) have been established as important regulators in cardiac hypertrophy. Here, we reported miR-221 was up-regulated in both transverse aortic constricted mice and patients with hypertrophic cardiomyopathy (HCM). Forced expression of miR-221 by transfection of miR-221 mimics increased myocyte cell size and induced the re-expression of fetal genes, which were inhibited by the knockdown of endogenous miR-221 in cardiomyocytes. The TargetScan algorithm-based prediction identified that p27, a cardiac hypertrophic suppressor, is the putative target of miR-221, which was confirmed by luciferase assay and Western blotting. In conclusion, our results demonstrated that miR-221 regulated cardiomyocyte hypertrophy probably through down-regulation of p27, suggesting that miR-221 may be a new intervention target for cardiac hypertrophy. 相似文献