bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hypoxia preconditioned human adipose derived mesenchymal stem cells enhance angiogenic potential via secretion of increased VEGF and bFGF
Authors: Liu Linqi , Gao Jianhua , Yuan Yi , Chang Qiang , Liao Yunjun , Lu Feng 
Published: August 2013

AbstractMesenchymal stem cells (MSCs) are adult multipotent cells found in bone marrow, adipose tissue, and other adult tissues. MSCs improve regeneration of injured tissues in vivo, but the mechanisms remain unclear. Typically, MSCs are cultured under ambient or normoxic conditions (21% O2). However, the physiological niches of MSCs have much lower oxygen tension. When used as a therapeutic tool to repair tissue injuries, MSCs cultured in standard conditions must adapt from 21% O2 in culture to <1% O2 in ischemic tissue. We have examined the effects of hypoxia preconditioning (1% O2) in human adipose derived mesenchymal stem cells (AD‐MSCs) to discover the conditions that best enhance their tissue regenerative potential. We demonstrate that AD‐MSCs respond positively to hypoxia compared with normoxia preconditioning, show decreased apoptosis even in severe microenvironmental conditions (such as a low‐serum medium), and an increased expression of the angiogenic factors, vascular endothelial growth factor and basic fibroblast growth factor. Human umbilical vein endothelial cells have higher vitality and lower apoptosis when cultured in medium taken from hypoxia‐preconditioned AD‐MSCs, as well as significantly increased capillary‐like structures with this medium on Matrigel. The data suggest that hypoxia preconditioned AD‐MSCs can improve tissue regeneration.
Stromal vascular fraction (SVF) cells enhance long‐term survival of autologous fat grafting through the facilitation of M2 macrophages
Authors: Dong Ziqing , Fu Rong , Liu Linqi , Lu Feng 
Published: August 2013

AbstractOptimum perfusion may be the key to the endurance, and hence survival, of autologous adipose tissue transportation. Stromal vascular fraction (SVF) cell therapy can greatly improve the survival of fat grafts by enhancing angiogenesis. However, SVF cells are poorly retained in later stages of SVF‐assisted adipose tissue transplant. Therefore, it hardly defines the angiogenic effect through long‐term transportation. Adipose tissue suffers from acute hypoxia in the early stage of transportation, leading to the recruitment of macrophages. M2 macrophages enhance angiogenesis in adipose transplantation by acting as an angiogenic signal source, promoting tip cell migration and assisting tip cell fusion. Furthermore, the angiogenic and anti‐inflammatory micro‐environment in the graft created by M2 macrophages may stimulate the transformation of infiltrating macrophages to M2 macrophages. These M2 macrophages may enhance the long‐term retention of graft through angiogenesis. Based on these observations, we postulate that the long‐term angiogenic effect of SVF cells may be achieved through the facilitation of the M2 macrophages.
Downregulation of miRNA‐128 sensitises breast cancer cell to chemodrugs by targeting Bax
Authors: Ji Shufeng , Shao Guoli , Lv Xiaobin , Liu Yuan , Fan Yingfang , Wu Aiguo , Hu Haiyan 
Published: August 2013

AbstractmiR‐128 is more highly expressed in drug‐resistant breast cancer samples than in drug‐sensitive samples. We have confirmed that Bax is the target of miR‐128 by negative post‐transcriptional regulation. miR‐128 and Bax were detected in the breast cancer cell line, MDA‐MB‐231, which was then transfected with miR‐128 MIMIC (precursor of miR‐128) or AMO (antisense‐miR‐128 oligonucleotides). After transfection, the chemosensitivity of MDA‐MB‐231 cell was up‐regulated with increasing of Bax and inhibition of miR‐128.
Experimental study on the facilitative effects of miR‐125b on the differentiation of rat bone marrow mesenchymal stem cells into neuron‐like cells
Authors: Wu Rui , Wang Na , Li Min , Zang Wenqiao , Xu Yuming 
Published: August 2013

AbstractTo observe the effects of miR‐125b on the differentiation of rat bone marrow mesenchymal stem cells (BMSCs) into neuron‐like cells, rat BMSCs were isolated and transfected with Syn‐rno‐miR‐125b* miScript miRNA Mimic (Mimic + BME group), with anti‐rno‐miR‐125b* miScript miRNA Inhibitor (Inhibitor + BME group) and BME control was set up without transfection. Blank controls without transfection and induction by BME was also set up. BMSCs of three groups including Mimic + BME group, Inhibitor + BME group and BME group were induced to differentiate into neuron‐like cells by β‐mercaptoethanol (BME). Cells in the Blank group were not treated by BME. mRNA expression of miR‐125b was determined with qRT‐PCR in each group. mRNA and protein expressions of seven nerve cell markers, including β3 tubulin, neural microtubule‐associated protein (MAP‐2), neurofilament protein (NF), neuron‐specific enolase (NSE), glial fibrillary acidic protein (GFAP), Nestin and Vimentin in the four groups were determined by RT‐PCR and Western blots. GFAP and Nestin were detected by immunofluorescent and immunocytochemistry assays. Compared with BME group, mRNA and protein expression of β3 tubulin, MAP‐2, NF, NSE, GFAP, Nestin were significantly increased in the Mimic + BME group (P < 0.01), but significantly decreased in the Inhibitor + BME group (P < 0.01). Cells in the Mimic + BME group were more like nerve cells in morphology than cells in the BME groups. Thus miR‐125b can promote BME to induce rat BMSCs differentiation into neuron‐like cells.
Role of melatonin receptor MT2 and quinone reductase II in the regulation of the redox status of 3T3‐L1 preadipocytes in vitro
Authors: Adamczyk‐Sowa Monika , Sowa Pawel , Zwirska‐Korczala Krystyna , Pierzchala Krystyna , Bartosz Grzegorz , Sadowska‐Bartosz Izabela 
Published: August 2013

AbstractWe have examined the role of melatonin receptor MT2 and quinone reductase II in the regulation of the redox status of preadipocytes (3T3‐L1) in vitro. 3T3‐L1 cells were treated with melatonin at a physiological concentration (10−9 mol/L) and a supraphysiological (pharmacological) concentration (10−3 mol/L) for 24 h. Luzindole (10−4 mol/L), an antagonist of MT2 receptor, and prazosin (10−5 mol/L), an inhibitor of quinone reductase II, were added 30 min before subsequent exposure of the cells to melatonin. The level of oxidative stress was determined by the analysis of activities of enzymes neutralising reactive oxygen species, and determination of the malondialdehyde (MDA) content. Melatonin increased activities of manganese and copper‐zinc superoxide dismutase (MnSOD, Cu/ZnSOD) and catalase (CAT) at both a physiological concentration (10−9 mol/L) and a pharmacological concentration (10−3 mol/L). MDA content was unchanged, whereas activities of glutathione peroxidase (GSH‐Px) and glutathione reductase (GSSG‐Rd) were increased only by the physiological concentration. Both effects were partially inhibited by luzindole, but not prazosin. These observations suggest that melatonin, acting at least partially via MT2 receptors, can increase antioxidant enzymes activities in 3T3‐L1 preadipocytes.
A novel therapeutic drug for colon cancer: EpCAM scFv‐truncated protamine (tp)‐siRNA
Authors: Hao Huiwen , Zhen Yansen , Wang Zaicun , Chen Fulin , Xie Xin 
Published: August 2013

AbstractColon cancer is a type of malignant tumor that causes considerable mortality worldwide. Epithelial cellular adhesion molecule (EpCAM), a tumor‐associated antigen of colon tumors, is a target for colon cancer therapy. EpCAM‐specific monoclonal antibodies (mAbs) have been applied in human colon cancer since the 1990s; however, the therapeutic effects are limited. EpCAM activates nuclear signaling pathways by releasing its intracellular domain (EpICD). The released EpICD stimulates the Wnt/β‐catenin signaling pathway, which is also strongly associated with tumorigenesis. EpCAM is also a target gene of the Wnt/β‐catenin signaling pathway. EpCAM and the Wnt/β‐catenin signaling pathway form a functional interaction cycle in colon cancer. Thus, we propose a new therapeutic drug for colon cancer: an EpCAM single‐chain fragment variable antibody (scFv)‐truncated protamine‐siRNA. EpCAM scFv can recognize and bind colon cancer cells through its EpCAM antigen activity. Furthermore, the specific siRNA transferred into colon cancer cells specifically inhibits Wnt/β‐catenin signal transmission. Therefore, this new drug may efficiently interrupt the functional cycle between EpCAM and Wnt/β‐catenin signaling and be an effective therapeutic strategy for colon cancer.
Role of CD271 enrichment in the isolation of mesenchymal stromal cells from umbilical cord blood
Authors: Attar Armin , Ghalyanchi Langeroudi Arash , Vassaghi Attyieh , Ahrari Iman , Maharlooei Mohsen Khosravi , Monabati Ahmad 
Published: August 2013

AbstractIsolation of mesenchymal stromal cells (MSCs) from the umbilical cord blood (UCB) has a success rate of 25% and is frequently contaminated by osteoclast‐like cells (OLCs). CD271 is a well‐known marker for the enrichment of bone marrow (BM) MSCs. We have assessed the effect of CD271 isolation on the isolation rate of MSCs from UCB. Twenty‐one samples of UCB were collected. Ten samples of UCB and five of BM underwent CD271 isolation using magnetic activated cell sorting. The other 11 UCB samples were used as the control. The isolated cells were cultured and MSC isolation was confirmed with respect to morphology, flow cytometry, adipogenic and osteogenic differentiation potentials. CD271‐positive UCB cells did not show outgrowth despite 54.5% MSCs isolation in the non‐enriched portion. No OLC was noted in the CD271‐enriched group, but 66% of the non‐enriched samples were contaminated. All the CD271‐positive BM cells formed MSC colonies. Although the per cent of CD271+ cells showed no difference between BM‐mononuclear cells (MNCs) and UCB‐MNCs, the haematopoietic marker, CD45, was found in a higher percentage of CD271‐positive UCB‐MNCs. The results of our study indicate that, although CD271 is a valuable marker for enrichment of MSCs from BM, it does not contribute to isolation of MSCs from UCB. In this source, most of the CD271+ cells are from haematopoietic origin, and possibly the process of isolation may eliminate the very low frequent MSCs and the isolation therefore fails.
AEG‐1 participates in TGF‐beta1‐induced EMT through p38 MAPK activation
Authors: Wei Jiali , Li Zhuori , Chen Wenfang , Ma Chunyang , Zhan Feng , Wu Wei , Peng Youming 
Published: August 2013

AbstractEpithelial–mesenchymal transition (EMT) is an important cellular event in organogenesis, cancer and renal tubulointerstitial fibrosis. Transforming growth factor‐beta1 (TGF‐beta1) is the key inducer of EMT and the p38 mitogen‐activated protein kinases (p38 MAPK), an major intracellular signal transduction pathway is involved in TGF‐beta1‐induced EMT. Astrocyte elevated gene‐1 (AEG‐1) represents an chief genetic determinant regulating multiple events in tumorigenesis. Our present study is to explore the role of AEG‐1 in TGF‐beta1‐induced p38 MAPK activation and EMT process in human renal tubular epithelial (HK‐2) cells. The protein expressions of AEG‐1, the markers of EMT and p38 phosphorylation were measured by Western blot. The protein expression of AEG‐1 was increased in HK‐2 cells treated with TGF‐beta1. Knockdown of AEG‐1 potently inhibited phosphorylation of p38 MAPK and reversed TGF‐beta1‐induced EMT. Over‐expression of AEG‐1 via AEG‐1 transfection elicited p38 MAPK phosphorylation and promoted EMT. The effects of AEG‐1 during EMT were blocked by a p38‐specific inhibitor. Our findings suggest that AEG‐1 plays an important role in TGF‐beta1‐induced EMT through activation of p38 MAPK in proximal tubular epithelial cells.
SDF‐1 promotes ox‐LDL induced vascular smooth muscle cell proliferation
Authors: Li Ling‐Xing , Zhang Xian‐Feng , Bai Xue , Tong Qian 
Published: August 2013

AbstractThe mechanism of the regulatory roles of stromal cell derived factor‐1 (SDF‐1)/C‐X‐C motif receptor 4 (CXCR4) on cell proliferation and apoptosis in vascular smooth muscle cells (VSMCs) via the protein kinase C (PKC) and nuclear factor‐kappa B (NF‐κB) signalling pathways have been investigated. Rat aortic VSMCs were treated with control or an oxidised low‐density lipoprotein (ox‐LDL) atherosclerosis (AS) model. Cells exposed to the AS model were treated with SDF‐1 plus inhibitors specific for PKC (Ro31‐8220), CXCR4 (12G5) or NF‐κB (pyrrolidine dithiocarbamate, PDTC). Cell proliferation was measured with 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) assay, and apoptosis by flow cytometry. NF‐κB protein expression was analysed using Western blotting. The proliferation rate in the AS model group was significantly higher than the control group, but lower than the SDF‐1 group (P < 0.05). Apoptosis in the AS model group (ox‐LDL) was significantly higher than the normal control group (P < 0.05). In addition, the apoptosis rate in the SDF‐1 group was significantly lower than the normal control group (P < 0.05); however, there was no difference from the Ro31‐8220 group. NF‐κB protein expression in the SDF‐1 group was significantly higher than the AS model (ox‐LDL) group (P < 0.05). In conclusion, SDF‐1 can promote the proliferation of VSMCs induced by ox‐LDL and inhibit cell apoptosis, via the SDF‐1/CXCR4 axis.
Ephrin‐As, Eph receptors and integrin α3 interact and colocalise at membrane protrusions of U251MG glioblastoma cells
Authors: Makarov Andrey , Ylivinkka Irene , Nyman Tuula A. , Hyytiäinen Marko , Keski‐Oja Jorma 
Published: August 2013

AbstractGlioblastoma is the most common brain cancer. Ephrins and their Eph receptors play important roles in the development of central nervous system and the regulation of cancer cell migration and invasion. In a search for the Eph receptor complexes, we used tandem affinity purification based interaction screening with tagged ephrins A1, A3 and A4 combined with protein identification by mass‐spectrometry in U251MG glioblastoma cells. Ephrins bound to Eph receptors, mainly to EphA2 in these cells. Integrin α3 was identified in protein complexes with ephrin‐As. Soluble ephrin‐A1 colocalised with integrin α3 at the cell surface, and was rapidly endocytosed by the cells. However, integrin α3 did not colocalise with internalised ephrin‐A1, whereas EphA2 receptor did. In U251MG cells, integrin α3 colocalised with EphA2 receptor at the cell edges and protrusions. Sites of EphA2‐integrin α3 colocalisation were positive for vinculin, focal adhesion kinase and phosphotyrosine, that is, markers for cell adhesion and active signalling. The interaction between ephrin‐As, Eph receptors and integrin α3 is plausibly important for the crosstalk between Eph and integrin signalling pathways at the membrane protrusions and in the migration of brain cancer cells.
Uptake and storage of vitamin A as lipid droplets in the cytoplasm of cells in the lamina propria mucosae of the rat intestine
Authors: Senoo Haruki , Mezaki Yoshihiro , Morii Mayako , Hebiguchi Taku , Miura Mitsutaka , Imai Katsuyuki 
Published: August 2013

AbstractVitamin A (retinyl palmitate) was injected subcutaneously or administered to rats by tube feeding. After subcutaneous injection, vitamin A was taken up and stored in cells of the lamina propria mucosae of the rat intestine. After oral administration, vitamin A was absorbed by the intestinal absorptive epithelial cells and transferred to cells of the lamina propria mucosae, where cells took up and stored the transferred vitamin A. The morphology of these cells was similar to that of hepatic stellate cells (also called vitamin A‐storing cells, lipocytes, interstitial cells, fat‐storing cells or Ito cells). Thus, these cells in the intestine could take up vitamin A from the systemic circulation and as well as by intestinal absorption, and store the vitamin in the lipid droplets in their cytoplasm. The data suggest that these cells are extrahepatic stellate cells of the digestive tract that may play roles in both the absorption and homeostasis of vitamin A.
Titration of lysine residues on adenine nucleotide translocase by fluorescamine induces permeability transition
Authors: Buelna‐Chontal Mabel , Pavón Natalia , Correa Francisco , Hernández‐Esquivel Luz , Chávez Edmundo 
Published: August 2013

AbstractChemical modification of primary amino groups of mitochondrial membrane proteins by the fluorescent probe fluorescamine induces non‐specific membrane permeabilisation. Titration of the lysine ϵ‐amino group promoted efflux of accumulated Ca2+, collapse of transmembrane potential and mitochondrial swelling. Ca2+ release was inhibited by cyclosporin A. Considering the latter, we assumed that fluorescamine induces permeability transition. Carboxyatractyloside also inhibited the reaction. Using a polyclonal antibody for adenine nucleotide translocase, Western blot analysis showed that the carrier appeared labelled with the fluorescent probe. The results point out the importance of the ϵ‐amino group of lysine residues, located in the adenine nucleotide carrier, on the modulation of membrane permeability, since its blockage suffices to promote opening of the non‐specific nanopore.
The HOX genes network in metabolic diseases
Authors: Procino Alfredo , Cillo Clemente 
Published: August 2013

AbstractFat distribution is associated with metabolic risk. Differences in cellular characteristics and metabolic functions of these depots have been described, but the molecular mechanisms involved are not understood. The pathogenesis and pathophysiology of metabolic disease can be better understood by studying the molecular mechanisms that control the development and function of adipose tissue (adipogenesis). Homeobox genes are transcription factors that act during normal development and contain the homeobox, a 183bp DNA sequence coding for a 61 amino acid domain defined as homeodomain (HD). Class 1 homeobox genes (Hox genes) have a critical role in controlling positional information and tissue patterning during development. The expression of the whole HOX gene network in different deposits of normal adult human white adipose tissue (intraperitoneal, extra‐peritoneal and dermis) indicate a marked expression in adipose tissue. Furthermore, this expression seems to vary in different bodily deposits of white adipose tissue and between white and brown adipose tissue. The purpose of this mini‐review is to discuss the role of HOX genes in metabolic diseases.
Kaempferol inhibits cancer cell growth by antagonizing estrogen‐related receptor α and γ activities
Authors: Wang Haibin , Gao Minghui , Wang Junjian 
Published: August 2013

AbstractKaempferol is a dietary flavonoid that can function as a selective estrogen receptor modulator (SERM). Estrogen‐related receptors alpha and gamma (ERRα and ERRγ) are orphan nuclear receptors that play important roles in mitochondrial biogenesis and cancer development. We have shown that kaempferol can functionally antagonize the activities of ERRs based on both response element reporter systems and target gene analysis. Kaempferol modulation of mitochondrial function and suppression cancer cell growth has been confirmed. These findings suggest that kaempferol may exert their anti‐cancer activities through antagonizing ERRs activities.
Study of DNA synthesis and mitotic activity of hepatocytes and its relation to angiogenesis in hepatectomised tumour bearing mice
Authors: Andrini Laura B. , García Marcela N. , Inda Ana María , Errecalde Ana Lía 
Published: August 2013

AbstractPartial hepatectomy (PH) alters serum concentrations of substances involved in cellular proliferation, leading to the compensatory liver hyperplasia. Furthermore, angiogenesis is mainly stimulated by vascular endothelial growth factor (VEGF) and is a fundamental requirement either in liver regeneration or in tumours growth. This study looks at the expression of VEGF, DNA synthesis (DNAs) and mitotic activity (MA) in hepatectomised (H) and hepatectomised‐tumour bearing (HTB) mice throughout a 24 h period. Adult male mice were sacrificed every 4 h from 26 to 50 h post‐hepatectomy. H mice show a circadian rhythm in VEGF expression with a maximum value of 2.6 ± 0.1 at 08/46 h of day/hours posthepatectomy (HD/HPH); in DNAs, the maximum value was 3.4 ± 0.3 at 16/30 (HD/HPH) and in MA it was 2.3 ± 0.01 at 12/50 (HD/HPH). In HTB animals the peak of VEGF expression appears at 16/30 (HD/HPH) with a maximum value of 3.7 ± 0.1, the peak of DNAs was at 00/38 (HD/HPH) with a value of 4.6 ± 0.3 and the maximum value of MA of 08/46 (HD/HPH) with a value of 3.01 ± 0.3. We can conclude that the presence of the tumour induces modifications in the intensity and the temporal distribution of the circadian curves of VEGF expression, DNAs and MA of hepatectomised animals.
Effect of 3‐bromopyruvic acid on human erythrocyte antioxidant defense system
Authors: Sadowska‐Bartosz Izabela , Bartosz Grzegorz 
Published: August 2013

Abstract3‐Bromopyruvate (3‐BP) is a promising compound for anticancer therapy, its main mode of action being the inhibition of glycolytic enzymes, but this compound also induces oxidative stress. This study aimed at characterisation of the effect of 3‐BP on the antioxidant defense system of erythrocytes. Suspensions of erythrocytes in PBS containing 5 mM glucose were treated with different concentration of 3‐BP at 37°C for 1 h. Activities of antioxidant enzymes were estimated by standard colorimetric methods. The antioxidant capacity of erythrocytes was estimated using the 2,2′‐azinobis(3‐ethylbenzthiazoline‐6‐sulphonic acid) (ABTS•+) decolorisation assay and ferricyanide reduction. The content of reduced and oxidized glutathione was estimated fluorimetrically with o‐phtalaldehyde. 3‐BP did not affect the integrity of the erythrocyte membrane (lack of changes in the osmotic fragility). However, it induced oxidative stress in erythrocytes, as evidenced by the decrease in the content of acid‐soluble thiols and reduced glutathione (GSH). Superoxide dismutase (SOD) and glutathione S‐transferase (GST) activities were significantly decreased. 3‐BP also decreased the transmembrane reduction of ferricyanide. Thus induction of oxidative stress in erythrocytes by 3‐BP is due to depletion of glutathione and inhibition of antioxidant enzymes.
Continuous CO2 Capture in a 1‐MWth Carbonate Looping Pilot Plant
Authors: Kremer J. , Galloy A. , Ströhle J. , Epple B. 
Published: August 2013

AbstractThe carbonate looping process is an efficient technology for post‐combustion CO2 capture from fossil‐fired power plants. Testing campaigns with continuous CO2 capture were performed in a 1‐MWth carbonate looping pilot plant at the Technische Universität Darmstadt. During two distinguished experimental campaigns the heat for the regeneration of the calcium‐based sorbent in the calciner was provided by propane combustion and combustion of pulverized hard coal, respectively. For several hours of operation, the CO2 concentration in the flue gas was reduced to chemical equilibrium conditions. High overall CO2 capture efficiencies above 90 % were achieved.
Effects of Wall Confinement and Power‐Law Fluid Viscosity on Nusselt Number of Confined Spheres
Authors: Rajasekhar Reddy C. , Kishore N. 
Published: August 2013

AbstractEffects of wall confinement on the heat transfer phenomena of confined spherical particles in power‐law fluids are numerically investigated. The spherical particle is held at constant temperature and a power‐law fluid is flowing past the particle in a confining tube. Heat transfer takes place from the heated sphere to the surrounding fluid. The governing conservation equations of mass, momentum, and energy are solved using computational fluid dynamics‐based software. The numerical solver is thoroughly validated by comparing the present average Nusselt numbers with existing literature values. On the basis of numerical results, an empirical correlation for the average Nusselt number of a confined sphere in Newtonian and power‐law fluids is proposed which can be used in new applications.