Biochemical and Biophysical Research Communications (Biochem Biophys Res Comm )

Publisher: Elsevier

Description

Biochemical and Biophysical Research Communications is the premier international journal devoted to the very rapid dissemination (six weeks) of timely and significant experimental results in the diverse fields of biological research. Frequent publication (36 issues per year) ensures a steady stream of information. The development of the "Breakthroughs and Views" section brings the minireview format to the journal. In addition, the editors have expanded the journalís scope. Research Areas now include: Biochemistry Cell Biology; Developmental Biology; Immunology; Neurobiology; Biophysics; Molecular Biology; Plant Biology.

Impact factor 2.28

  • 5-year impact
    2.50
  • Cited half-life
    8.50
  • Immediacy index
    0.40
  • Eigenfactor
    0.14
  • Article influence
    0.78
  • Website
    Biochemical and Biophysical Research Communications website
  • Other titles
    Biochemical and biophysical research communications (Online), Biochemical and biophysical research communications
  • ISSN
    1090-2104
  • OCLC
    35247010
  • Material type
    Document, Periodical, Internet resource
  • Document type
    Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Elsevier

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Pre-print allowed on any website or open access repository
    • Voluntary deposit by author of authors post-print allowed on authors' personal website, arXiv.org or institutions open scholarly website including Institutional Repository, without embargo, where there is not a policy or mandate
    • Deposit due to Funding Body, Institutional and Governmental policy or mandate only allowed where separate agreement between repository and the publisher exists.
    • Permitted deposit due to Funding Body, Institutional and Governmental policy or mandate, may be required to comply with embargo periods of 12 months to 48 months .
    • Set statement to accompany deposit
    • Published source must be acknowledged
    • Must link to journal home page or articles' DOI
    • Publisher's version/PDF cannot be used
    • Articles in some journals can be made Open Access on payment of additional charge
    • NIH Authors articles will be submitted to PubMed Central after 12 months
    • Publisher last contacted on 18/10/2013
  • Classification
    ​ green

Publications in this journal

  • Source
    Biochemical and Biophysical Research Communications 01/2015;
  • Shimizu H, Koyama T, Yamada S, Lipton SA, Satoh T.
    [Show abstract] [Hide abstract]
    ABSTRACT: Seaweed-origin electrophilic compounds are proposed as a class of neuroprotective compounds that provide neuroprotection through activation of the Nrf2/ARE pathway. Electrophilic hydroquinones are of particular interest due to their ability to become electrophilic quinones upon auto-oxidation. Although many marine plants produce a variety of electrophilic compounds, the detailed mechanism of action of these compounds remain unknown. Here, we focused on the neuroprotective effects of zonarol (ZO), a para-hydroquinone-type pro-electrophilic compound from the brown algae Dictyopteris undulata. We show that ZO activates the Nrf2/ARE pathway, induces phase-2 enzym es, and protects neuronal cells from oxidative stress. ZO is the first example of a neuroprotective pro-electrophilic compound obtained from brown algae.
    Biochemical and Biophysical Research Communications 01/2015;
  • Ancheng Qin, Qiang Yu, Yuan Gao, Jifu Tan, Hai Huang, Zhiming Qiao, Weifeng Qian
    [Show abstract] [Hide abstract]
    ABSTRACT: Chemotherapeutic resistance indicated the poor prognosis of colorectal cancer. Our study aimed to investigate the role of STAT3/cyclinD1 pathway in the chemotherapeutic resistance of colorectal cancer. We firstly measured the expression of cyclinD1 in the colorectal cancer tissues using immunohistochemistry in tissue microarray. Then cell viability and apoptosis were investigated in the HT-29 cell lines dealing with recombinant lentivirus and shRNA to increase or decrease cyclinD1 expression. Furthermore, luciferase and ChIP assays were applied to investigate whether STAT3 regulated cyclinD1 expression by binding to its promoter. Finally, we determined whether inhibition of STAT3 could decrease cyclinD1 and increase the chemotherapy sensitivity. CyclinD1 expression was significantly increased in the cancer cells and high level of cyclinD1 indicated the poor prognosis. Inhibition of cyclinD1 decreased the cell viability assessed by MTT and increased rate of apoptosis when exposed to 5-FU treatment while overexpression of cyclinD1 showed the reverse effect. ChIP assay showed that STAT3 directly bind to cyclinD1 promoter. Subclone of full promoter of cyclinD1 into pGL4 increased the luciferase activity while delete or mutation of any of STAT3 binding sites resulted in reductions of luciferase activity. Inhibition of STAT3 decreased cyclinD1 expression to decrease the cell viability and increase rate of apoptosis when exposed to 5-FU treatment. Inhibition of STAT3/cyclinD1 pathway increased the sensitivity of colorectal cancer cell to chemotherapy. Copyright © 2015. Published by Elsevier Inc.
    Biochemical and Biophysical Research Communications 01/2015;
  • [Show abstract] [Hide abstract]
    ABSTRACT: We set out to identify the Candida glabrata cell wall attached proteases which may play a role as virulence factors in candidosis, particularly in the immunocompromized host. We studied a clinical Candida glabrata strain T-1639, which was isolated from a patient from the Helsinki University Central Hospital. With non-reducing 2-D electrophoresis using parallel fluorogenic gels and mass spectrometry we identified a novel appr. 25 kDa (192 aa in length) cell wall located protease with an estimated pI of 7.6. The LC-MS/MS peptides matched with the ORF of predicted Candida glabrata CBS138 cell wall protein Cwp1.2p /pI 7.7/ 212 aa (http://cbi.labri.fr/Génolevures/[NCBI access 49525604, UniProt access Q6FTZ7]), which is an orthologue to Saccharomyces cerevisiae cell wall protein Cwp1p (UniProt access P28319). The novel serine protease was released by β-1,3-glucanase treatment from the cell wall. In contrast to previous predictions this protease has an enzymatic function instead of being merely a structural cell wall protein. The protease showed gelatinolytic activity and was inhibited by PMSF, a known serine protease inhibitor. Further characterization of the protease may give insight to its role in infections caused by Candida glabrata and possibly aid in the development of new kinds of antifungal drugs. Copyright © 2015. Published by Elsevier Inc.
    Biochemical and Biophysical Research Communications 01/2015;
  • Harrison Pride, Zhen Yu, Bharath Sunchu, Jillian Mochnick, Alexander Coles, Yiqiang Zhang, Rochelle Buffenstein, Peter J Hornsby, Steven N Austad, Viviana I Pérez
    [Show abstract] [Hide abstract]
    ABSTRACT: Our previous studies have shown that the liver from Naked Mole Rats (NMRs), a long-lived rodent, has increased proteasome activity and lower levels of protein ubiquitination compared to mice. This suggests that protein quality control might play a role in assuring species longevity. To determine whether enhanced proteostasis is a common mechanism in the evolution of other long-lived species, here we evaluated the major players in protein quality control including autophagy, proteasome activity, and heat shock proteins (HSPs), using skin fibroblasts from three phylogenetically-distinct pairs of short- and long-lived mammals: rodents, marsupials, and bats. Our results indicate that in all cases, macroautophagy was significantly enhanced in the longer-lived species, both at basal level and after induction by serum starvation. Similarly, basal levels of most HSPs were elevated in all the longer-lived species. Proteasome activity was found to be increased in the long-lived rodent and marsupial but not in bats. These observations suggest that long-lived species may have superior mechanisms to ensure protein quality, and support the idea that protein homeostasis might play an important role in promoting longevity. Copyright © 2015. Published by Elsevier Inc.
    Biochemical and Biophysical Research Communications 01/2015;
  • [Show abstract] [Hide abstract]
    ABSTRACT: In this study, a necrosis-inducing protein was purified from the culture filtrate of the necrotrophic fungus Botrytis cinerea BC-98 strain. Secreted proteins were collected and fractionated by liquid chromatography. The fraction with the highest necrosis-inducing activity was further purified. A glycoprotein named BcGs1 was identified by 2D electrophoresis and mass spectrometry. The BcGs1 protein consisted of 672 amino acids with a theoretical molecular weight of 70.487 kDa. Functional domain analysis indicated that BcGs1 was a glucan 1,4-alpha-glucosidase, a cell wall-degrading enzyme, with a Glyco_hydro_15 domain and a CBM20_glucoamylase domain. The BcGs1 protein caused necrotic lesions that mimicked a typical hypersensitive response and H2O2 production in tomato and tobacco leaves. BcGs1-treated plants exhibited resistance to B. cinerea, Pseudomonas syringae pv. tomato DC3000 and tobacco mosaic virus in systemic leaves. In addition, BcGs1 triggered elevation of the transcript levels of the defence-related genes PR-1a, TPK1b and Prosystemin. This is the first report of a Botrytis glucan 1,4-alpha-glucosidase triggering host plant immunity as an elicitor. These results lay a foundation for further study of the comprehensive interaction between plants and necrotrophic fungi. Copyright © 2015. Published by Elsevier Inc.
    Biochemical and Biophysical Research Communications 01/2015;
  • [Show abstract] [Hide abstract]
    ABSTRACT: The biosensor based on total internal reflection imaging ellipsometry (TIRIE), regarded as an automotive real-time research approach for biomolecular interaction, is introduced to analyze the kinetic process of the weak interaction between tris and lysozyme. The experiment is performed by delivering lysozyme solution diluted to different concentrations to the biosensor substrate interface immobilized with tris. By applying pseudo-first-order interaction kinetics model, we are able to obtain the kinetic parameters from fitting experimental data. The calculated association rate constant and dissociation rate constant of tris and lysozyme interaction are in 10-2 mol-1s-1 and 103 s-1 magnitude, respectively. To further improve TIRIE‵s ability for kinetically characterizing biomolecular interaction, a theoretical method to deduce associate rate constant before experiment is proposed.
    Biochemical and Biophysical Research Communications 01/2015;
  • Shuang Li, Yongwei Huo, Hong Tian, Qiannan Zhang, Yifei Lv, Zhiming Hao
    [Show abstract] [Hide abstract]
    ABSTRACT: Connective tissue growth factor (CTGF) is a secreted matricellular protein possessing complex biological functions. CTGF modulates a number of signaling pathways that are involved in cell adhesion, migration, angiogenesis, myofibroblast activation, extracellular matrix deposition and tissue remodeling. Aptamers are oligonucleic acid chains or polypeptides that bind with specific target molecules hence have the potential to be used in the detection and blockade of the targets. In this study, we selected CTGF-targeting DNA aptamers by using systematic evolution of ligands by exponential enrichment (SELEX). After 8 iterative rounds of selection, cloning, DNA sequencing and affinity determination, six aptamers with high affinities to CTGF were obtained. Among them, one (C-ap17P) binds with the N-terminal region (aa 1-190) and the other five (C-ap11, 12, 14, 15 and 18) bind with the C-terminal region (aa 191-350) of hCTGF specifically. The biological stability assay indicated that a representative aptamer, C-ap17P, could keep its integrity at a rather high level for at least 24 hours in complete DMEM cell culture medium. These CTGF aptamers might be used as a easy and fast detection tool for CTGF and be developed as CTGF-specific inhibitors for both research works and clinical applications. Copyright © 2015. Published by Elsevier Inc.
    Biochemical and Biophysical Research Communications 01/2015;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Multidrug resistance (MDR) is the major cause of cancer treatment failure. The ATP-binding cassette-B1 (ABCB1) transporter, also known as MDR1 or P-glycoprotein, is thought to promote the efflux of drugs from cells. MDR is also associated with the multidrug resistance-associated protein 1 (ABCC1) and the lung resistance-related protein (LRP), a human major vault protein. Moreover, MDR has a complex relationship with lipids. The ABCB1 has been reported to modulate cellular cholesterol homeostasis. Conversely, cholesterol has been reported to modulate multidrug transporters. However, results reported to date are contradictory and confusing. The aim of this study was to investigate whether LDL, HDL, and serum deprivation could influence ABCB1, ABCC1, and LRP expression in a human doxorubicin-resistant uterine sarcoma cell line. ABCB1 and ABCC1 expression increased after 24 h of serum deprivation, and expression returned to basal levels after 72 h. LDL, depending on concentration, increased ABCB1, ABCC1, and LRP expression. ABCB1 expression increased at low HDL, and decreased at high HDL concentrations. We demonstrated that serum deprivation and lipoproteins, particularly LDL, modulated ABCB1 expression and, to a lesser extent, ABCC1 expression. This finding may link the phenomena of drug transport, cholesterol metabolism and cancer. Copyright © 2015. Published by Elsevier Inc.
    Biochemical and Biophysical Research Communications 01/2015;
  • [Show abstract] [Hide abstract]
    ABSTRACT: microRNAs (miRNAs) are frequently dysregulated in human malignancies. It was recently shown that miR-204-5p is downregulated in papillary thyroid carcinoma (PTC); however, the functional significance of this observation is not known. This study investigated the role of miR-204-5p in PTC. Overexpressing miR-204-5p suppressed PTC cell proliferation and induced cell cycle arrest and apoptosis. The results of a luciferase reporter assay showed that miR-204-5p can directly bind to the 3' untranslated region (UTR) of insulin-like growth factor-binding protein 5 (IGFBP5) mRNA, and IGFBP5 overexpression partially reversed the growth-inhibitory effects of miR-204-5p. These results indicate that miR-204-5p acts as a tumor suppressor in PTC by regulating IGFBP5 expression and that miR-204-5p can potentially serve as an antitumorigenic agent in the treatment of PTC.
    Biochemical and Biophysical Research Communications 01/2015;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Independently, a high fat diet and hypoxia are associated with vascular endothelial dysfunction (VED) and often occur concurrently in patients. Nevertheless, the effects of a high fat diet on vascular endothelial function combined with hypoxia, a situation occurring with increasing frequency in many parts of the world, remain largely unknown. We investigated the effects of a high fat diet on vascular endothelial function in rats exposed to continuous hypoxia for 4 weeks. Seventy two male Sprague-Dawley rats were randomly divided into 3 groups: a hypoxia group fed regular chow, a combined hypoxia and high fat diet (HFD) group, and for comparison, rats maintained in normoxic, regular chow conditions were set as baseline (BL) group. The experimental data of BL group were got at beginning of hypoxia given in the other groups. Continuous hypoxia was induced in a hypobaric chamber maintained at an altitude of 5000m. Compared to hypoxic conditions alone, hypoxia plus a HFD prevented adaptive changes in plasma nitric oxide (NOx) levels and caused earlier and more severe changes in aortic endothelial structures. Functionally, hypoxia plus a HFD resulted in impaired endothelium-dependent vasodilator responses to acetylcholine and altered the bioavailability of the NOS substrate L-Arginine. At the molecular level, hypoxia plus a HFD blunted increases in eNOS mRNA and protein in aortic endothelial tissue. Taken together, our findings demonstrate that in the setting of hypoxia, a high fat diet leads to earlier and more severe VED than hypoxia alone. These data have important implications for populations residing at high-altitude, as dietary patterns shift towards increased fat intake.
    Biochemical and Biophysical Research Communications 01/2015;
  • [Show abstract] [Hide abstract]
    ABSTRACT: In the past decade, monoclonal antibodies (mAbs) have revolutionized the treatment of non-Hodgkin lymphomas (NHLs). Although Fc-dependent mechanisms of mAb-mediated tumor clearance have been extensively studied, the ability of mAbs to directly evoke programmed cell death (PCD) and the underlying mechanisms involved remain unclear. It is well established that type II anti-CD20 mAb (Tositumomab) potently evoked PCD through a caspases-independent, lysosome-mediated process, which is related to homotypic adhesion (HA) in NHL cell lines. Herein, we reveal that the induction of ceramide generation by anti-CD20 mAbs directly correlates with their ability to induce PCD. The inhibition of ceramide abrogated Tositumomab-induced PCD indicating that ceramide is required for the execution of cell death. Further experimental results revealed that ceramide was generated downstream of mAb-induced HA and upstream of lysosome leakage. These findings provide further insights into a previously unrecognized role for ceramide generation in mediating PCD evoked by type II anti-CD20 mAbs in Burkitt’s lymphoma cells. This newly characterized cell death pathway may potentially be exploited to eliminate malignant cells.
    Biochemical and Biophysical Research Communications 01/2015;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Mesenchymal stem cells found in bone marrow stromal cells (BMSCs) are the common progenitors for both adipocyte and osteoblast. An increase in marrow adipogenesis is associated with age-related osteopenia and anemia. Both extracellular and intracellular Ca2+ ([Ca2+]o and [Ca2+]i) are versatile signaling molecules that are involved in the regulation of cell functions, including proliferation and differentiation. We have recently reported that upon treatment of BMSCs with insulin and dexamethasone, both high [Ca2+]o and high [Ca2+]i enhanced adipocyte accumulation, which suggested that increases in [Ca2+]o caused by bone resorption may accelerate adipocyte accumulation in aging and diabetic patients. In this study, we used primary mouse BMSCs to investigate the mechanisms by which high [Ca2+]o and high [Ca2+]i may enhance adipocyte accumulation. In the process of adipocyte accumulation, two important keys are adipocyte differentiation and the proliferation of BMSCs, which have the potential to differentiate into adipocytes. Use of MTT assay and real-time RT-PCR revealed that high [Ca2+]i (ionomycin)-dependent adipocyte accumulation is caused by enhanced proliferation of BMSCs but not enhanced differentiation into adipocytes. Using fura-2 fluorescence-based approaches, we showed that high [Ca2+]o (addition of CaCl2) leads to increases in [Ca2+]i. Flow cytometric methods revealed that high [Ca2+]o suppressed the phosphorylation of ERK independently of intracellular Ca2+. The inhibition of ERK by U0126 and PD0325901 enhanced the differentiation of BMSCs into adipocytes. These data suggest that increased extracellular Ca2+ provides the differentiation of BMSCs into adipocytes by the suppression of ERK activity independently of increased intracellular Ca2+, which results in BMSC proliferation.
    Biochemical and Biophysical Research Communications 01/2015;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Hypoxia inducible factor-1 alpha (HIF-1α) plays an important role in angiogenesis and metastasis and is a promising therapeutic target for the development of anti-cancer drugs. We recently developed a new synthetic small molecule inhibitor of HIF-1α, LW6, which results in inhibition of angiogenesis. To investigate its underlying mechanism, target protein identification was conducted by reverse chemical proteomics using phage display. We identified calcineurin b homologous protein 1 (CHP1) as a target protein of LW6, which specifically binds to CHP1 in a Ca2+ dependent manner. Covalent labeling of LW6 using photoaffinity and click chemistry demonstrated its co-localization with CHP1 in live cells. HIF-1α was decreased by CHP1 knockdown in HepG2 cells, and angiogenesis was not induced in HUVEC cells by treatment with conditioned media from CHP1 knockdown cells compared to the control. These data demonstrated that LW6 inhibited HIF-1α stability via direct binding with CHP1 resulting in suppression of angiogenesis, providing a new insight into the role of CHP1 in HIF-1α regulation. LW6 could serve as a new chemical probe to explore CHP1 function.
    Biochemical and Biophysical Research Communications 01/2015;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Resveratrol is identified as polyphenolic compound with anti-inflammatory, antioxidant, anti-insulin resistance characteristics. Moreover, resveratrol exerts pro-apoptotic effects in varieties of cancer cell lines. However, effects and mechanisms of resveratrol on the regulation of adipocytes apoptosis remain largely unknown. In this study, we found that resveratrol treatment could induce cell apoptosis in murine 3T3-L1 adipocytes. Furthermore, resveratrol activated the mitochondrial apoptotic signaling pathway with the decrease in the mitochondrial membrane potential (MMP), and the activation of caspase 3. Mechanistically, we found that phosphorylation level of AMP-activated protein kinase α (AMPKα) was elevated, accompany with reduced level of phosphorylation of protein kinase B (AKT) when cells were exposed to resveratrol. By using small interfering RNAs of AMPKα and specific inhibitor for p-AKT, it was shown that activation of AMPKα could inhibit downstream of p-AKT, consequently activating mitochondrion-mediated apoptotic pathway. Additionally, we observed similar pro-apoptotic effects of Res on mouse primary adipocytes. Our findings clarified the apoptotic effects and underlying mechanisms of resveratrol in adipocytes, suggesting its potential therapeutic application in the treatment or prevention of obesity and related metabolic symptoms. Copyright © 2015. Published by Elsevier Inc.
    Biochemical and Biophysical Research Communications 01/2015;
  • [Show abstract] [Hide abstract]
    ABSTRACT: A large percentage of energy produced during high-intensity exercise depends on the aerobic glycolytic pathway. Maintenance of a cytoplasmic redox balance ([NADH]/[NAD(+)] ratio) by the glycerophosphate shuttle involves sustained aerobic glycolysis. Glycerol 3-phosphate dehydrogenase 1 (GPD1) catalyzes an oxidation reaction in the glycerophosphate shuttle. In this study, we examined whether GPD1 deficiency decreases exercise capacity due to impairment of aerobic glycolysis by using the GPD1 null mouse model BALB/cHeA (HeA). Unexpectedly, we found that exercise endurance was significantly higher in HeA mice than in BALBc/By (By) mice used as controls. Furthermore, aerobic glycolysis in HeA mice was not impaired. During exercise, lipid oxidation was significantly higher in HeA mice than in By mice, concomitant with an increase in phosphorylation of AMP-activated protein kinase (AMPK). HeA mice also showed a delay in the onset of muscle glycogen usage and lactate production during exercise. These data suggest that contribution of lipid oxidation as a fuel source for exercise is increased in HeA mice, and GPD1 deficiency enhances exercise capacity by increasing lipid oxidation, probably due to activation of AMPK. We propose that GPD1 deficiency induces an adaptation that enhances lipid availability in the skeletal muscle during exercise. Copyright © 2015. Published by Elsevier Inc.
    Biochemical and Biophysical Research Communications 01/2015;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Internal backbone dynamic motions are essential for different protein functions and occur on a wide range of time scales, from femtoseconds to seconds. Molecular dynamic (MD) simulations and nuclear magnetic resonance (NMR) spin relaxation measurements are valuable tools to gain access to fast (nanosecond) internal motions. However, there exist few reports on correlation analysis between MD and NMR relaxation data. Here, backbone relaxation measurements of (15)N-labeled SH3 (Src homology 3) domain proteins in aqueous buffer were used to generate general order parameters (S(2)) using a model-free approach. Simultaneously, 80 ns MD simulations of SH3 domain proteins in a defined hydrated box at neutral pH were conducted and the general order parameters (S(2)) were derived from the MD trajectory. Correlation analysis using the Gromos force field indicated that S(2) values from NMR relaxation measurements and MD simulations were significantly different. MD simulations were performed on models with different charge states for three histidine residues, and with different water models, which were SPC (simple point charge) water model and SPC/E (extended simple point charge) water model. S(2) parameters from MD simulations with charges for all three histidines and with the SPC/E water model correlated well with S(2) calculated from the experimental NMR relaxation measurements, in a site-specific manner. Copyright © 2015 Elsevier Inc. All rights reserved.
    Biochemical and Biophysical Research Communications 01/2015;
  • Yufeng Wu, Ruirui Si, Hong Tang, Zhen He, Hui Zhu, Lili Wang, Yingchao Fan, Suhua Xia, Zelai He, Qiming Wang
    [Show abstract] [Hide abstract]
    ABSTRACT: Inoperable lung adenocarcinoma is currently treated with platinum-based chemotherapy. However, the effectiveness of these chemotherapeutic agents is not the same for all patients. Patients either show quick chemoresistance (QCR) or delayed chemoresistance (DCR), which are defined by 87 and 242 days of progression-free survival (PFS) after initial platinum-based treatment, respectively. We found that QCR patients displayed an elevated level of serum cholesterol and that their tumors showed upregulated ABCG2 expression. We propose that chemoresistance may be attributed to cholesterol-induced ABCG2 expression and hypothesize that blocking ABCG2 may increase the efficacy of platinum-based chemotherapeutic agents. Using the MTT cell viability assay, we observd that cotreatment with ABCG2 blocker Nicardipine and platinum-based drugs Cisplatin, Oxaliplatin or Carboplatin significantly decreased cell viability of tumor cells. Importantly, our results also showed that incubating cells with cholesterol prior to chemotherapy treatment or cotreatment increased cell viability of tumor cells relative to the controls.
    Biochemical and Biophysical Research Communications 01/2015;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Derived from mature adipocytes, dedifferentiated fat (DFAT) cells represent a special group of multipotent cells. However, their phenotype and cellular nature remain unclear. Our study found that human DFAT cells adopted perivascular characteristics and behaviors. Flow cytometry and immunofluorescent staining revealed that human DFAT cells positively expressed markers highly related to perivascular cell lineages, such as CD140b, NG2 and desmin, but were negative for common endothelial markers, including CD31, CD34, and CD309. Furthermore, DFAT cells displayed vascular network formation ability in Matrigel, and they noticeably promoted and stabilized the vessel structures formed by human umbilical vascular endothelial cells (HUVECs) in vitro. These results provide novel evidence on the pericyte nature of human DFAT cells, further supporting the recent model for the perivascular origin of adult stem cells, in which tissue-specific progenitor cells in mesenchymal tissues associate with blood vessels, exhibiting perivascular characteristics and functions.
    Biochemical and Biophysical Research Communications 01/2015;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Heparan sulfate normally binds to heparin cofactor II and modulates the coagulation pathway by inhibiting thrombin. However, when human heparin cofactor II was incubated with heparan sulfate, heparin cofactor II became degraded. Other glycosaminoglycans were tested, including hyaluronic acid, chondroitin sulfates, dermatan sulfate, and heparin, but only dextran sulfate also degraded heparin cofactor II. Pretreatment of heparan sulfate with heparinase reduced its heparin cofactor II-degrading activity. Heparan sulfate and dextran sulfate diminished the thrombin inhibitory activity of heparin cofactor II. Other serpins, including antithrombin III and pigment epithelium-derived factor, were also degraded by heparan sulfate. This is the first evidence of acidic polysaccharides exhibiting protein-degrading activity without the aid of other proteins. Copyright © 2015. Published by Elsevier Inc.
    Biochemical and Biophysical Research Communications 01/2015;