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Experimental Cell Research

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https://www.readbyqxmd.com/read/28826677/extracellular-matrix-remodeling-and-matrix-metalloproteinase-inhibition-in-visceral-adipose-during-weight-cycling-in-mice
#1
Cíntia Rabelo E Paiva Caria, Érica Martins Ferreira Gotardo, Paola Souza Santos, Simone Coghetto Acedo, Thainá Rodrigues de Morais, Marcelo Lima Ribeiro, Alessandra Gambero
Extracellular matrix (ECM) remodeling is necessary for a health adipose tissue (AT) expansion and also has a role during weight loss. We investigate the ECM alteration during weight cycling (WC) in mice and the role of matrix metalloproteinases (MMPs) was assessed using GM6001, an MMP inhibitor, during weight loss (WL). Obesity was induced in mice by a high-fat diet. Obese mice were subject to caloric restriction for WL followed by reintroduction to high-fat diet for weight regain (WR), resulting in a WC protocol...
August 18, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28823833/microrna-21-suppresses-ox-ldl-induced-human-aortic-endothelial-cells-injuries-in-atherosclerosis-through-enhancement-of-autophagic-flux-involvement-in-promotion-of-lysosomal-function
#2
Feng Tang, Tian-Lun Yang, Zhen Zhang, Xiao-Gang Li, Qiao-Qing Zhong, Ting-Ting Zhao, Li Gong
Atherosclerosis is a common pathological basis of cardiovascular disease and remains the leading cause of mortality. Endothelial cell (EC) injury and autophagy dysfunction have been proved to contribute to the development of atherosclerosis. Recently, accumulating evidence confirms that microRNAs (miRNAs) have emerged as vital regulators and fine-tuners of various pathophysiological cellular impacts and molecular signaling pathways involvedin atherosclerosis. Herein, the objective of the present study was to explore the biological function of miR-21 in oxidized low-density lipoprotein (ox-LDL)-induced human aortic endothelial cells (HAECs) injury and the underlying molecular mechanism...
August 17, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28823832/the-adapter-sash1-acts-through-notch1-and-its-inhibitor-dlk1-in-a-3d-model-of-lumenogenesis-involving-ceacam1
#3
Kandis Stubblefield, Jennifer Chean, Tung Nguyen, Charng-Jui Chen, John E Shively
CEACAM1 transfection into breast cancer cells restores lumen formation in a 3D culture model. Among the top up-regulated genes that were associated with restoration of lumen formation, the adaptor protein SASH1 was identified. Furthermore, SASH1 was shown to be critical for lumen formation by RNAi inhibition. Upon analyzing the gene array from CEACAM1/MCF7 cells treated with SASH1 RNAi, DLK1, an inhibitor of NOTCH1 signaling, was found to be down-regulated to the same extent as SASH1. Subsequent treatment of CEACAM1/MCF7 cells with RNAi to DLK1 also inhibited lumen formation, supporting its association with SASH1...
August 17, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28823831/gskj4-an-h3k27me3-demethylase-inhibitor-effectively-suppresses-the-breast-cancer-stem-cells
#4
Ningning Yan, Liang Xu, Xiaobo Wu, Le Zhang, Xiaochun Fei, Yali Cao, Fengchun Zhang
Recently, studies have been suggested that H3K27me3 is implicated with maintenance of cancer stem cells (CSCs), however, the roles of H3K27me3 in Breast cancer stem cells (BCSCs) remain poorly investigated. Here we explore the functionality of H3K27me3 on BCSCs, we identify H3K27me3 as a negative modulator of BCSCs and suggest GSKJ4 is a promising drug targeting BCSCs. We show that the H3K27me3 level is decreased in mammosphere-derived BCSCs. In breast cancer cells, we demonstrate that GSKJ4 could markedly inhibit the proliferation...
August 17, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28822708/mrtf-a-mir-206-wdr1-form-feedback-loop-to-regulate-breast-cancer-cell-migration
#5
Yuan Xiang, Xing-Hua Liao, Ao Yao, Huan Qin, Li-Juan Fan, Jia-Peng Li, Peng Hu, Hui Li, Wei Guo, Jun-Yan Li, Chao-Jiang Gu, Le-Yuan Bao, Tong-Cun Zhang
Breast cancer is the leading cause of cancer death in women worldwide which is closely related to metastasis. Our previous study has shown that MRTF-A promote the migration of MDA-MB-231 cells and WDR1 promotes breast cancer cell migration. But the exact molecular mechanism on metastasis is still not fully understood, we now report that WDR1 enhanced the effect of MRTF-A induced-MDA-MB-231 cell migration by promoting the expression of the EMT markers and migration markers via RhoA-MRTF-A signaling pathway. Importantly, WDR1 promoted the nuclear importion of MRTF-A by affecting the expression of nuclear transport protein importin...
August 16, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28821395/extracellular-matrix-type-modulates-cell-migration-on-mechanical-gradients
#6
Christopher D Hartman, Brett C Isenberg, Samantha G Chua, Joyce Y Wong
Extracellular matrix composition and stiffness are known to be critical determinants of cell behavior, modulating processes including differentiation, traction generation, and migration. Recent studies have demonstrated that the ECM composition can modulate how cells migrate in response to gradients in environmental stiffness, altering a cell's ability to undergo durotaxis. These observations were limited to single varieties of extracellular matrix, and typically cells are exposed to environments containing complex mixtures of extracellular matrix proteins...
August 15, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28821394/activation-of-ampk-to-the-neuroprotection-in-the-oxidative-stress-by-advanced-glycosylation-end-products-in-human-neural-stem-cells
#7
Chien-Hung Lin, Yi-Chuan Cheng, Christopher J Nicol, Kuan-Hung Lin, Chia-Hui Yen, Ming-Chang Chiang
Advanced glycosylation end products (AGEs) formation is correlated with the pathogenesis of diabetic neuronal damage, but its links with oxidative stress are still not well understood. Metformin, one of the most widely used anti-diabetic drugs, exerts its effects in part by activation of AMP-activated protein kinase (AMPK). Once activated, AMPK regulates many pathways central to metabolism and energy balance including, glucose uptake, glycolysis and fatty acid oxidation. AMPK is also present in neurons, but its role remains unclear...
August 15, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28811129/microrna-29a-regulates-lipopolysaccharide-lps-induced-inflammatory-responses-in-murine-macrophages-through-the-akt1-nf-%C3%AE%C2%BAb-pathway
#8
Bufu Tang, Xingchen Li, Yanling Ren, Jing Wang, Di Xu, Yiru Hang, Tingting Zhou, Feng Li, Ling Wang
Akt activation in macrophages enhances lipopolysaccharide (LPS)-induced inflammatory responses through upregulation of the NF-κB signal pathway. Akt phosphorylation via microRNA (miR) caused the downregulation of Akt1. Here, we evaluated the role of miR-29a in LPS-triggered inflammatory responses. LPS stimulation of primary macrophages and RAW264.7 cells gradually increased the levels of miR-29a and was dependent on the LPS concentration. Overexpression of miR-29a in macrophages enhanced the expression of proinflammatory cytokines including IL-1β and IL-6, but not TNF-α...
August 12, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28807789/the-expression-of-erk-and-jnk-in-patients-with-an-endemic-osteochondropathy-kashin-beck-disease
#9
XiaoXia Dai, RuiXia Song, YongMin Xiong
Kashin-Beck disease (KBD) is a chronic, endemic osteochondropathy. Its etiopathogenesis is still obscure until now. Epidemiological observation has shown that low selenium play a crucial role in the pathogenesis of KBD. Extracellular signal-regulated kinases (ERKs) and C-Jun N-terminal kinase (JNK), members of the mitogen-activated protein kinase (MAPK) superfamily, play an important role in cell proliferation and differentiation. Nuclear factor-ĸB (NF-ĸB), an important signaling mediator for inflammatory and immune responses, is involved in the regulation of osteoclastogenesis...
August 12, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28807790/the-functional-domains-for-bax%C3%A2-2-aggregate-mediated-caspase-8-dependent-cell-death
#10
Adriana Mañas, Sheng Wang, Adam Nelson, Jiajun Li, Yu Zhao, Huaiyuan Zhang, Aislinn Davis, Bingqing Xie, Natalia Maltsev, Jialing Xiang
Bax∆2 is a functional pro-apoptotic Bax isoform having alterations in its N-terminus, but sharing the rest of its sequence with Baxα. Bax∆2 is unable to target mitochondria due to the loss of helix α1. Instead, it forms cytosolic aggregates and activates caspase 8. However, the functional domain(s) responsible for BaxΔ2 behavior have remained elusive. Here we show that disruption of helix α1 makes Baxα mimic the behavior of Bax∆2. However, the other alterations in the Bax∆2 N-terminus have no significant impact on aggregation or cell death...
August 11, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28803065/flow-induced-adherens-junction-remodeling-driven-by-cytoskeletal-forces
#11
Deepika Verma, Vivek K Bajpai, Nannan Ye, Mohammad M Maneshi, Deekshitha Jetta, Stelios T Andreadis, Frederick Sachs, Susan Z Hua
Adherens junctions (AJs) are a key structural component for tissue organization and function. Under fluid shear stress, AJs exhibit dynamic assembly/disassembly, but how shear stress couples to AJs is unclear. In MDCK cells we measured simultaneously the forces in cytoskeletal α-actinin and the density and length of AJs using a genetically coded optical force sensor, actinin-sstFRET, and fluorescently labeled E-cadherin (E-cad). We found that shear stress of 0.74dyn/cm(2) for 3h significantly enhanced E-cad expression at cell-cell contacts and this phenomenon has two phases...
August 10, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28803068/improved-therapeutic-efficacy-of-mammalian-expressed-recombinant-interferon-gamma-against-ovarian-cancer-cells
#12
Ali Razaghi, Carina Villacrés, Vincent Jung, Narges Mashkour, Michael Butler, Leigh Owens, Kirsten Heimann
Human interferon gamma (hIFNγ) affects tumour cells and modulates immune responses, showing promise as an anti-cancer biotherapeutic. This study investigated the effect of glycosylation and expression system of recombinant hIFNγ in ovarian carcinoma cell lines, PEO1 and SKOV3. The efficacy of E. coli- and mammalian-expressed hIFNγ (hIFNγ-CHO and HEK293, glycosylated/de-glycosylated) on cytostasis, cell death (MTT, and Guava-ViaCount(®) flow-cytometry) and apoptotic signalling (Western blot of Cdk2, histone H3, procaspase-3, FADD, cleaved PARP, and caspase-3) was examined...
August 9, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28803067/ppargc1a-is-upregulated-and-facilitates-lung-cancer-metastasis
#13
Jin-Dong Li, Qing-Chuan Feng, Yu Qi, Guanghui Cui, Song Zhao
Lung cancer remains a leading cause of cancer-related mortality, with metastatic progression remaining the single largest cause of lung cancer mortality. Hence it is imperative to determine reliable biomarkers for lung cancer prognosis. We performed quantitative real-time PCR (qRT-PCR) analysis to explore epithelial-mesenchymal transition (EMT) inducers that regulate EMT process in three patients with advanced lung cancer disease. Peroxisome proliferator-activated receptor gamma (PPARGC1A) was uniformly the topmost overexpressed gene in all three human non-small cell lung cancer (NSCLC) patient samples...
August 9, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28803066/a-novel-ripk1-inhibitor-that-prevents-retinal-degeneration-in-a-rat-glaucoma-model
#14
Yun-Ju Do, Jee-Won Sul, Ki-Hong Jang, Nam Sook Kang, Young-Hoon Kim, Young-Gwan Kim, Eunhee Kim
In glaucoma, retinal ganglion cells (RGCs) are exposed to ischemic stress with elevation of the intraocular pressure and are subsequently lost. Necroptosis, a type of regulated necrosis, is known to play a pivotal role in this loss. We observed that receptor-interacting protein kinase 1 (RIPK1), the key player of necroptosis, was activated by diverse ischemic stresses, including TCZ, chemical hypoxia (CH), and oxygen glucose deprivation (OGD). In this study, we introduce a RIPK1-inhibitory compound (RIC) with a novel scaffold...
August 9, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28803064/high-glucose-induces-tau-hyperphosphorylation-through-activation-of-tlr9-p38mapk-pathway
#15
Yue Sun, Qian Xiao, Cheng Luo, Yuxing Zhao, Die Pu, Kexiang Zhao, Jinliang Chen, Meili Wang, Zhiyin Liao
Diabetic encephalopathy (DE) is one of the most common complications of diabetes. The major pathological variations include neurofibrillary tangles (NFTs), which are caused by tau hyperphosphorylation, and senile plaques (SPs) consisting of amyloid β- protein(Aβ) deposits. In recent years, DE research studies have focused on exploring the activation of the inflammatory signaling pathway in immune cells. Toll-like receptor 9 (TLR9) is well known to regulate the inflammatory reactions in immune processes. During the tau hyperphosphorylation process, TLR9 in microglia plays bidirectional roles...
August 9, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28800962/contacting-co-culture-of-human-retinal-microvascular-endothelial-cells-alters-barrier-function-of-human-embryonic-stem-cell-derived-retinal-pigment-epithelial-cells
#16
H Skottman, J Muranen, H Lähdekorpi, E Pajula, K Mäkelä, L Koivusalo, A Koistinen, H Uusitalo, K Kaarniranta, K Juuti-Uusitalo
Here we evaluated the effects of human retinal microvascular endothelial cells (hREC) on mature human embryonic stem cell (hESC) derived retinal pigment epithelial (RPE) cells. The hESC-RPE cells (Regea08/017, Regea08/023 or Regea11/013) and hREC (ACBRI 181) were co-cultured on opposite sides of transparent membranes for up to six weeks. Thereafter barrier function, small molecule permeability, localization of RPE and endothelial cell marker proteins, cellular fine structure, and growth factor secretion of were evaluated...
August 8, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28800961/functional-consequences-of-inducible-genetic-elements-from-the-p53-sos-response-in-a-mammalian-organ-system
#17
O'neil W Guthrie
In response to DNA damage from ultraviolet (UV) radiation, bacteria deploy the SOS response in order to limit cell death. This bacterial SOS response is characterized by an increase in the recA gene that transactivates expression of multiple DNA repair genes. The current series of experiments demonstrate that a mammalian organ system (the cochlea) that is not evolutionarily conditioned to UV radiation can elicit SOS responses that are reminiscent of that of bacteria. This mammalian SOS response is characterized by an increase in the p53 gene with activation of multiple DNA repair genes that harbor p53 response elements in their promoters...
August 8, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28800960/ets-transcription-factor-elf5-induces-lumen-formation-in-a-3d-model-of-mammary-morphogenesis-and-its-expression-is-inhibited-by-jak2-inhibitor-tg101348
#18
Jennifer Chean, Charng-Jui Chen, John E Shively
The loss of expression of a single gene can revert normal tissue to a malignant phenotype. For example, while normal breast has high lumenal expression of CEACAM1, the majority of breast cancers exhibit the early loss of this gene with the concurrent loss of their lumenal phenotype. MCF7 cells that lack CEACAM1 expression and fail to form lumena in 3D culture, regain the normal phenotype when transfected with CEACAM1. In order to probe the mechanism of this gain of function, we treated these cells with the clinically relevant Jak2 inhibitor TG101348 (TG), expecting that disruption of the prolactin receptor signaling pathway would interfere with the positive effects of transfection of MCF7 cells with CEACAM1...
August 8, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28800959/mybph-inhibits-vascular-smooth-muscle-cell-migration-and-attenuates-neointimal-hyperplasia-in-a-rat-carotid-balloon-injury-model
#19
Ting Zhu, Yi He, Jue Yang, Weiguo Fu, Xin Xu, Yi Si
Vascular smooth muscle cell (VSMC) migration is implicated in restenosis. Myosin binding protein H (MYBPH) is capable of reducing cell motility and metastasis. In this study, we sought to determine whether MYBPH is involved in VSMC migration and neointima formation in response to vascular injury. To determine the expression of MYBPH in injured artery, we used a standard rat carotid artery balloon-injury model. In vivo studies have demonstrated that MYBPH is upregulated after vascular injury. VSMCs treated with platelet-derived growth factor (PDGF)-BB displayed increased MYBPH mRNA and protein levels...
August 8, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28793234/microrna-132-upregulation-promotes-matrix-degradation-in-intervertebral-disc-degeneration
#20
Wei Liu, Ping Xia, Jing Feng, Liang Kang, Mi Huang, Kun Wang, Yu Song, Shuai Li, Xinghuo Wu, Shuhua Yang, Cao Yang
MicroRNAs (miRNAs) have been shown to be involved in the pathogenesis of intervertebral disc degeneration (IDD). This experiment was designed to study the expression and role of the miRNA, miR-132, in IDD. MiR-132 expression in human nucleus pulposus (NP) tissue was assessed by quantitative real-time PCR. The methylation status of the miR-132 was assessed with methylation-specific PCR and bisulfite sequencing PCR. The regulation of growth differentiation factor5 (GDF5) expression by miR-132 was evaluated by luciferase reporter assay...
August 6, 2017: Experimental Cell Research
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