共查询到20条相似文献,搜索用时 46 毫秒
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I. C. Lopez-Mejia J. Castillo-Armengol S. Lagarrigue L. Fajas 《Cellular and molecular life sciences : CMLS》2018,75(6):975-987
In the course of the last decades, metabolism research has demonstrated that adipose tissue is not an inactive tissue. Rather, adipocytes are key actors of whole body energy homeostasis. Numerous novel regulators of adipose tissue differentiation and function have been identified. With the constant increase of obesity and associated disorders, the interest in adipose tissue function alterations in the XXIst century has become of paramount importance. Recent data suggest that adipocyte differentiation, adipose tissue browning and mitochondrial function, lipogenesis and lipolysis are strongly modulated by the cell division machinery. This review will focus on the function of cell cycle regulators in adipocyte differentiation, adipose tissue function and whole body energy homeostasis; with particular attention in mouse studies. 相似文献
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A. L.-F. Mui 《Cellular and molecular life sciences : CMLS》1999,55(12):1547-1558
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Reconstruction of gene association network reveals a transmembrane protein required for adipogenesis and targeted by PPARγ 总被引:1,自引:0,他引:1
Juliane G. Bogner-Strauss Andreas Prokesch Fatima Sanchez-Cabo Dietmar Rieder Hubert Hackl Kalina Duszka Anne Krogsdam Barbara Di Camillo Evelyn Walenta Ariane Klatzer Achim Lass Montserrat Pinent Wing-Cheong Wong Frank Eisenhaber Zlatko Trajanoski 《Cellular and molecular life sciences : CMLS》2010,67(23):4049-4064
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Agnieszka Siejka Andrew V. Schally Nektarios Barabutis 《Cellular and molecular life sciences : CMLS》2010,67(6):959-964
Growth hormone-releasing hormone (GHRH) can act as a potent growth factor in various cancers. The mitogenic activity of this
neuropeptide is exerted through binding to the pituitary type receptors (GHRH-R) or their splice variants (SV). In the present
work, we studied whether this hormone can activate the JAK2/STAT3 pathway which plays a crucial role in cancer cell proliferation
and is also linked to carcinogenesis. We transfected HeLa human cervical cancer cells, which are not sensitive to GHRH analogs
with the pGHRH-R. Transfected cells responded to the GHRH or its antagonist with an increase or a decrease in proliferation,
respectively. These results were confirmed by the expression of proliferating cell nuclear antigen. We then showed that these
effects are linked to the activation of the JAK2/STAT3 pathway. Our work demonstrates the activation of JAK/STAT3 pathway
by GHRH and sheds further light to the mechanisms of the antitumorogenic action of GHRH antagonists. 相似文献
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JAKs and STATs in invertebrate model organisms 总被引:5,自引:0,他引:5
C. R. Dearolf 《Cellular and molecular life sciences : CMLS》1999,55(12):1578-1584
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Profiling of the secreted proteins during 3T3-L1 adipocyte differentiation leads to the identification of novel adipokines 总被引:3,自引:0,他引:3
Wang P Mariman E Keijer J Bouwman F Noben JP Robben J Renes J 《Cellular and molecular life sciences : CMLS》2004,61(18):2405-2417
Adipose tissue is an endocrine organ capable of secreting a number of adipokines with a role in the regulation of
adipose tissue and whole-body metabolism. We used two-dimensional gel electrophoresis combined with mass spectrometry to
profile the secreted proteins from (pre)adipocytes. The culture medium of 3T3-L1 cells during adipocyte differentiation
was screened, and 41 proteins that responded to blocking of secretion by 20°C treatment and/or brefeldin A treatment
were identified. Prohibitin, stress-70 protein, and adhesion-regulating molecule 1 are reported for the first time as
secreted proteins. In addition, procollagen C-proteinase enhancer protein, galectin-1, cyclophilin A and C, and SF20/IL-25
are newly identified as adipocyte secreted factors. Secretion profiles indicated a dynamic environment including an
actively remodeling extracellular matrix and several factors involved in growth regulation.Received 15 June 2004; received after revision 26 July 2004; accepted 2 August 2004 相似文献
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Mireia Pérez-Verdaguer Jesusa Capera María Ortego-Domínguez Joanna Bielanska Núria Comes Rafael J. Montoro Marta Camps Antonio Felipe 《Cellular and molecular life sciences : CMLS》2018,75(21):4059-4075
The voltage-dependent potassium channel Kv1.3 participates in peripheral insulin sensitivity. Genetic ablation of Kv1.3 triggers resistance to diet-induced weight gain, thereby pointing to this protein as a pharmacological target for obesity and associated type II diabetes. However, this role is under intense debate because Kv1.3 expression in adipose tissue raises controversy. We demonstrated that Kv1.3 is expressed in white adipose tissue from humans and rodents. Moreover, other channels, such as Kv1.1, Kv1.2, Kv1.4 and especially Kv1.5, from the same Shaker family are also present. Although elevated insulin levels and adipogenesis remodel the Kv phenotype, which could lead to multiple heteromeric complexes, Kv1.3 markedly participates in the insulin-dependent regulation of glucose uptake in mature adipocytes. Adipocyte differentiation increased the expression of Kv1.3, which is targeted to caveolae by molecular interactions with caveolin 1. Using a caveolin 1-deficient 3T3-L1 adipocyte cell line, we demonstrated that the localization of Kv1.3 in caveolar raft structures is important for proper insulin signaling. Insulin-dependent phosphorylation of the channel occurs at the onset of insulin-mediated signaling. However, when Kv1.3 was spatially outside of these lipid microdomains, impaired phosphorylation was exhibited. Our data shed light on the putative role of Kv1.3 in weight gain and insulin-dependent responses contributing to knowledge about adipocyte physiology. 相似文献
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Tongxing Song Yang Yang Yuanfei Zhou Hongkui Wei Jian Peng 《Cellular and molecular life sciences : CMLS》2017,74(15):2723-2733
It is well known that adipose tissue has a critical role in the development of obesity and metabolic diseases and that adipose tissue acts as an endocrine organ to regulate lipid and glucose metabolism. Accumulating in the adipose tissue, fatty acids serve as a primary source of essential nutrients and act on intracellular and cell surface receptors to regulate biological events. G protein-coupled receptor 120 (GPR120) represents a promising target for the treatment of obesity-related metabolic disorders for its involvement in the regulation of adipogenesis, inflammation, glucose uptake, and insulin resistance. In this review, we summarize recent studies and advances regarding the systemic role of GPR120 in adipose tissue, including both white and brown adipocytes. We offer a new perspective by comparing the different roles in a variety of homeostatic processes from adipogenic development to adipocyte metabolism, and we also discuss the effects of natural and synthetic agonists that may be potential agents for the treatment of metabolic diseases. 相似文献
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Jing Lu Jimin Zhao Kangdong Liu Jun Zhao Hongyan Yang Youtian Huang Zhenzhu Qin Ruihua Bai Pei Li Junfen Ma Wenhai Yan Mingyao Zhao Ziming Dong 《Cellular and molecular life sciences : CMLS》2010,67(12):2091-2106
Endothelial-like differentiation of dendritic cells (DCs) is a new phenomenon, and the mechanism is still elusive. Here, we show that the tumor microenvironment derived from the human esophageal squamous cell carcinoma (ESCC) cell line EC9706 can induce immature DCs (iDCs) differentiate toward endothelial cells, and become endothelial-like cells, but it has no obvious influence on mature DCs. During the course of endothelial-like differentiation of iDCs, a sustained activation of mitogen-activated protein kinase/extracelluar signal-regulated kinase1/2 (MAPK/ERK1/2) and cAMP response element-binding protein (CREB) was detected. Incubation of iDCs with MEK phosphorylation inhibitor PD98059 blocked the MAPK/ERK1/2 and CREB phosphorylation as well as the endothelial-like differentiation of iDCs. Inhibition of vascular endothelial growth factor-A (VEGF-A) in the microenvironment with its antibody blocked the endothelial-like differentiation and the phosphorylation of MAPK/ERK1/2 and CREB. These data suggest that MAPK/ERK1/2 signaling pathway activated by VEGF-A could mediate endothelial-like differentiation of iDCs in the ESCC microenvironment. 相似文献
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Becatti M Taddei N Cecchi C Nassi N Nassi PA Fiorillo C 《Cellular and molecular life sciences : CMLS》2012,69(13):2245-2260
SIRT1, an ubiquitous NAD(+)-dependent deacetylase that plays a role in biological processes such as longevity and stress response, is significantly activated in response to reactive oxygen species (ROS) production. Resveratrol (Resv), an important activator of SIRT1, has been shown to exert major health benefits in diseases associated with oxidative stress. In ischemia-reperfusion (IR) injury, a major role has been attributed to the mitogen-activated protein kinase (MAPK) pathway, which is upregulated in response to a variety of stress stimuli, including oxidative stress. In neonatal rat ventricular cardiomyocytes subjected to simulated IR, the effect of Resv-induced SIRT1 activation and the relationships with the MAPK pathway were investigated. Resv-induced SIRT1 overexpression protected cardiomyocytes from oxidative injury, mitochondrial dysfunction, and cell death induced by IR. For the first time, we demonstrate that SIRT1 overexpression positively affects the MAPK pathway-via Akt/ASK1 signaling-by reducing p38 and JNK phosphorylation and increasing ERK phosphorylation. These results reveal a new protective mechanism elicited by Resv-induced SIRT1 activation in IR tissues and suggest novel potential therapeutic targets to manage IR-induced cardiac dysfunction. 相似文献
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Jiong-Yu Hu Zhi-Gang Chu Jian Han Yong-ming Dang Hong Yan Qiong Zhang Guang-ping Liang Yue-Sheng Huang 《Cellular and molecular life sciences : CMLS》2010,67(2):321-333
In both cardiomyocytes and HeLa cells, hypoxia (1% O2) quickly leads to microtubule disruption, but little is known about how microtubule dynamics change during the early stages
of hypoxia. We demonstrate that microtubule associated protein 4 (MAP4) phosphorylation increases while oncoprotein 18/stathmin
(Op18) phosphorylation decreases after hypoxia, but their protein levels do not change. p38/MAPK activity increases quickly
after hypoxia concomitant with MAP4 phosphorylation, and the activated p38/MAPK signaling leads to MAP4 phosphorylation and
to Op18 dephosphorylation, both of which induce microtubule disruption. We confirmed the interaction between phospho-p38 and
MAP4 using immunoprecipitation and found that SB203580, a p38/MAPK inhibitor, increases and MKK6(Glu) overexpression decreases
hypoxic cell viability. Our results demonstrate that hypoxia induces microtubule depolymerization and decreased cell viability
via the activation of the p38/MAPK signaling pathway and changes the phosphorylation levels of its downstream effectors, MAP4
and Op18. 相似文献
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The mitogen-activated protein kinase (MAPK) pathways are known to be involved in various processes of growth, differentiation
and cell death. In spite of their ubiquitous presence and seemingly enormous cross-talk with each other, their action is very
specific. This review deals with various aspects of the three different MAPK pathways (ERK, p38 and JNK) and how their specificity
is brought about.
Received 1 April 2008; received after revision 18 June 2008; accepted 18 June 2008 相似文献
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Bing Liu Hengchi Yu Guangyong Sun Xiaojing Sun Hua Jin Chunpan Zhang Wen Shi Dan Tian Kai Liu Hufeng Xu Xinmin Li Jie Yin Xu Hong Dong Zhang 《Cellular and molecular life sciences : CMLS》2017,74(20):3827-3840
Adaptive immunity plays a critical role in IR and T2DM development; however, the biological mechanisms linking T cell costimulation and glucose metabolism have not been fully elucidated. In this study, we demonstrated that the costimulatory molecule OX40 controls T cell activation and IR development. Inflammatory cell accumulation and enhanced proinflammatory gene expression, as well as high OX40 expression levels on CD4+ T cells, were observed in the adipose tissues of mice with diet-induced obesity. OX40-KO mice exhibited significantly less weight gain and lower fasting glucose levels than those of WT mice, without obvious adipose tissue inflammation. The effects of OX40 on IR are mechanistically linked to the promotion of T cell activation, Th1 cell differentiation and proliferation—as well as the attenuation of Treg suppressive activity and the enhancement of proinflammatory cytokine production—in adipose tissues. Furthermore, OX40 expression on T cells was positively associated with obesity in humans, suggesting that our findings are clinically relevant. In summary, our study revealed that OX40 in CD4+ T cells is crucial for adipose tissue inflammation and IR development. Therefore, the OX40 signaling pathway may be a new target for preventing or treating obesity-related IR and T2DM. 相似文献
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Lethal toxin (LT) is a major virulence factor secreted by anthrax bacteria. It is composed of two proteins, PA (protective antigen) and LF (lethal factor). PA transports the LF inside the cell, where LF, a zinc-dependent metalloprotease cleaves the mitogen activated protein kinase kinase (MAPKK) enzymes of the mitogen activated protein kinase (MAPK) signaling pathway, thereby impairing their function. This disruption of the MAPK pathway, which serves essential functions such as proliferation, survival and inflammation in all cell types, results in multisystem dysfunction in the host. The inactivation of the MAPK pathway in both macrophages and dendritic cells leads to inhibition of proinflammatory cytokine secretion, downregulation of costimulatory molecules such as CD80 and CD86, and ineffective T cell priming. The net result is an impaired innate and adaptive immune response. Endothelial cells of the vascular system undergo apoptosis upon LT exposure, also likely due to inactivation of the MAPK pathway. The activity of various hormone receptors such as glucocorticoids, progesterone and estrogen is also blocked, due to inhibition of p38 MAPK phosphorylation, thus affecting the bodys response to stress. The present review summarizes the various disarming effects of Bacillus anthracis through the use of a single weapon, the lethal toxin.Received 12 June 2004; received after revision 13 July 2004; accepted 28 July 2004 相似文献