BioFactors

Cover image for Vol. 41 Issue 3

Edited By: Angelo Azzi

Impact Factor: 4.592

ISI Journal Citation Reports © Ranking: 2014: 26/128 (Endocrinology & Metabolism); 60/289 (Biochemistry & Molecular Biology)

Online ISSN: 1872-8081

Associated Title(s): Biochemistry and Molecular Biology Education, Biotechnology and Applied Biochemistry, IUBMB Life

Featured

  • HDL particle subpopulations: Focus on biological function

    HDL particle subpopulations: Focus on biological function

    Intravascular HDL particle remodelling and metabolism. Lipid-free apolipoprotein A-I (apoA-I) or lipid-poor prebeta HDL are small precursors of mature HDL primarily generated by the liver or intestine that acquire cholesterol and phospholipids from cells lipids via the ATP binding cassette transporter (ABC) A1-mediated efflux. Acting on discoidal HDL, lecithin:cholesterol acyltransferase (LCAT)-mediated cholesterol esterification subsequently produces small (HDL3) and large spherical (HDL2) HDL. They can further undergo remodeling via particle fusion and surface remnant transfer mediated by phospholipids transfer protein (PLTP). Both HDL2 and HDL3 combine with cholesterol via cellular efflux mediated by ATP binding cassette G1 (ABCG1) transporter and scavenger receptor class B Type I (SR-BI). CETP-mediated transfer heteroexchange of cholesteryl esters (CE) and triglycerides (TG) occurs between HDL and TG-rich lipoproteins, TG-rich HDLs are generated, which can be further hydrolyzed by hepatic lipase (HL) to small, TG-rich particles. The concerted action of CETP and HL promotes reduction in HDL size, formation of lipid-poor HDL particles and shedding from HDL of lipid-free apoA-I which can interact with ABCA1 in the next lipidation cycle. HDL lipids are catabolized primarily in the liver, either by selective uptake via SR-BI, or via CETP-mediated transfer to apoB-containing lipoproteins, or as holoparticles via uptake through receptors for HDL holoparticles (HDLR); LDL particles are removed from the circulation primarily via the LDL receptor (LDLR).

  • Punica granatum and its therapeutic implications on breast carcinogenesis: A review

    Punica granatum and its therapeutic implications on breast carcinogenesis: A review

    Implication of Punica extract in breast cancer: Punica extract or its components individually or in combination is found to reduce proliferation, invasion, migration, angiogenesis, and its metastasis to various tissues.

  • Caffeic acid, a phyto polyphenol mitigates fluoride induced hepatotoxicity in rats: A possible mechanism

    Caffeic acid, a phyto polyphenol mitigates fluoride induced hepatotoxicity in rats: A possible mechanism

    Immunoblot analysis of hepatic SOD2, CAT, and GSTpi class expression (A) in control and test animals. β-actin was used as a loading control. L 1: Control; L2: fluoride-induced; L3: CA alone; L4: CA+F. (B) Data expressing the respective proteins with densitometric analysis and were expressed in relative intensity (arbitrary units). Values are mean ± SD (n = 3). *P < 0.05 as compared to control, +P < 0.05 as compared to F treated group (One way ANOVA followed by Tukey's multiple comparison test).

  • U937 cell apoptosis induced by arsenite is prevented by low concentrations of mitochondrial ascorbic acid with hardly any effect mediated by the cytosolic fraction of the vitamin

    U937 cell apoptosis induced by arsenite is prevented by low concentrations of mitochondrial ascorbic acid with hardly any effect mediated by the cytosolic fraction of the vitamin

    Arsenite promotes mitochondrial permeability transition-dependent U937 cell apoptosis via a mechanism sensitive to low concentrations of AA. (A) Counts of cells exposed for 24, 48, or 72 h to increasing concentrations of arsenite. Results represent the means ± SD calculated from at least three separate experiments. *P < 0.01, **P < 0.001 as compared to untreated cells (two-way ANOVA followed by Bonferroni's test). (B–F) Cells were exposed for 15 min to 10 µM AA, DHA, or the two agents combined, and subsequently treated for 16 (B and C) or 48 h (D-F) with 2.5 µM arsenite. In some experiments, cells were also exposed to CsA (0.5 μM, 15 min) or FK506 (1 μM, 15 min), before incubation with arsenite. Cells were analyzed for oxygen consumption (B), MitoTracker Red CMXRos-fluorescence (C), number and viability (D), and detection of apoptosis (E and F). Representative micrographs of Hoechst 33342-loaded nuclei (inset to panel E) and microgel-electrophoresed U937 DNA (inset to panel F) after treatment for 48 h with 0 or 2.5 µM arsenite. Apoptotic cells display a pear-shaped morphology. Results represent the means ± SD calculated from at least three separate experiments. *P < 0.01, as compared to untreated cells, (*)P < 0.01, or cells treated with arsenite (one-way ANOVA followed by Dunnet's test).

  • Transforming growth factor type-β inhibits Mas receptor expression in fibroblasts but not in myoblasts or differentiated myotubes; Relevance to fibrosis associated to muscular dystrophies

    Transforming growth factor type‐β inhibits Mas receptor expression in fibroblasts but not in myoblasts or differentiated myotubes; Relevance to fibrosis associated to muscular dystrophies

    Profibrotic factor TGF-β reduced Mas expression in fibroblasts. (A) Relative expression of mas receptor from fibroblasts (10T-1/2) that were treated with the profibrotic factor TGF-β1 at 5 ng/mL for 24 H. Student's t-test; *P < 0.05 vs nontreated. Data are presented as mean ± SEM (n = 4). (B) Relative expression of mas receptor from fibroblasts treated with profibrotic factor CTGF at 500 ng/mL for 48 H. (C) Relative expression of mas receptor from fibroblasts treated with profibrotic factor Ang II at 100 nM for 48 H. (D) Relative expression of mas receptor from primary cultured fibroblasts obtained from diaphragms of C57BL6 mice that were treated with the profibrotic factor TGF-β1 at 10 ng/mL for 24 H. Data are presented as mean ± SEM n = 3, Student's t-test; *P < 0.05 vs nontreated. (E) Relative expression of ctgf receptor on primary cultured fibroblasts obtained from diaphragm of C57BL6 mice, that were treated with the profibrotic factor TGF-β1 10 ng/mL for 24 H, data are presented as mean ± SEM, n = 3, Student's t-test; *P < 0.05 vs nontreated. (F) Western blot of Mas receptor from extracts of 10T-1/2 fibroblasts treated, or untreated, with TGF-β1 for 5 ng/mL for 48 H (lanes 3 and 4, respectively). Lanes 1 and 2 correspond to skeletal muscle extracts of gastrocnemius muscle from knockout (KO) Mas mice and wild type (wt) mice, respectively; arrow indicates the Mas receptor band. (G) Graph shows quantitation of three different experiments, data are presented as mean ± SEM, Student's t-test; *P < 0.05 vs nontreated.

  • Evaluating the role of hnRNP-C and FMRP in the cAMP-induced APP metabolism

    Evaluating the role of hnRNP‐C and FMRP in the cAMP‐induced APP metabolism

    Effect of silencing hnRNP-C on APP and Aβ levels in FSK-treated cells. Forty-eight hours after transfection with hnRNP-C siRNA and control siRNA, N2a cells were treated with 1 µM forskolin (FSK) or an equal volume of solvent (DMSO) for 5 H. At the end of the incubation period, conditioned media were subjected to specific Aβ42 ELISA and the cells were processed for total protein extraction followed by immunoblot analysis, performed with anti-hnRNP-C, anti-APP or anti-GAPDH antibodies. Graphed data show mean ± standard error of the mean for three independent experiments. The GAPDH signal represents the internal loading control. *P < 0.05 and **P < 0.01 versus the corresponding control group.

  • Branched-chain amino acids supplementation protects streptozotocin-induced insulin secretion and the correlated mechanism

    Branched‐chain amino acids supplementation protects streptozotocin‐induced insulin secretion and the correlated mechanism

    Fasting blood glucose levels of STZ-induced diabetic rats and control group, and also the glucose levels of different groups after different dose of BCAA treatment. *P < 0.05, **P < 0.01 compared with STZ-induced diabetic group. Data were expressed as means ± SD (n = 6 per group).

  • HDL particle subpopulations: Focus on biological function
  • Punica granatum and its therapeutic implications on breast carcinogenesis: A review
  • Caffeic acid, a phyto polyphenol mitigates fluoride induced hepatotoxicity in rats: A possible mechanism
  • U937 cell apoptosis induced by arsenite is prevented by low concentrations of mitochondrial ascorbic acid with hardly any effect mediated by the cytosolic fraction of the vitamin
  • Transforming growth factor type‐β inhibits Mas receptor expression in fibroblasts but not in myoblasts or differentiated myotubes; Relevance to fibrosis associated to muscular dystrophies
  • Evaluating the role of hnRNP‐C and FMRP in the cAMP‐induced APP metabolism
  • Branched‐chain amino acids supplementation protects streptozotocin‐induced insulin secretion and the correlated mechanism

Recently Published Issues

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IUBMB Joint Virtual Issue on Cancer Therapies

BTPR online only


We’re pleased to present a new Joint Virtual Issue on Cancer Therapies in celebration of the IUBMB 2015 Miami Winter Symposium, featuring articles from Biofactors, Biotechnology and Applied Biochemistry, and IUBMB Life.

2015 BioFactors Young Investigator Award

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On behalf of the IUBMB, BioFactors and Wiley, it is with great pleasure and honor that we announce Shilpa Thakur as the recipient of the 2015 BioFactors - Wiley Young Investigator Award for her article, Regulation at multiple levels controls the expression of folate transporters in liver cells in conditions of ethanol exposure and folate deficiency.

Shilpa Thakur is a Ph.D student in the Department of Biochemistry, Post Graduate Institute of Medical Education and Research, in Chandigarh, India. She completed her Bachelor’s and Masters' degree in Biotechnology and thereafter joined the Ph.D program under the guidance of Dr. Jyotdeep Kaur, Additional Professor in the Department of Biochemistry. As a part of her thesis work, Dr. Thakur has examined various regulatory mechanisms underlying the effects of folate deficiency and ethanol exposure on folate transport, and has gained expertise in the field of molecular biology and epigenetics during her Ph.D tenure. Presently, Dr. Thakur’s laboratory is focusing on folate deficiency and epigenetic regulation of some imprinting genes.

Shilpa Thakur will be honored with the 2015 BioFactors - Wiley Young Investigator Award at the 23rd International Union for Biochemistry and Molecular Biology (IUBMB) Congress and 44th Annual Meeting of the Brazilian Society for Biochemistry and Molecular Biology in Foz do Iguaçu, Brazil from August 24th to 28th, 2015, and her award-winning article will be FREELY available online through the conference.

Please join us in congratulating Shipla Thakur as the recipient of the annual BioFactors– Wiley Young Investigator Award!

News

2014 Impact Factor:
BioFactors is pleased to announce its 2014 Impact Factor has increased to 4.592!

2015 Release of Journal Citation Reports®
Source: Thomson Reuters 2014 Citation Data

Open Access Highlight

Click below to read this OnlineOpen Review Article in BioFactors for FREE:

Novel insights on interactions between folate and lipid metabolism
Robin P. da Silva, Karen B. Kelly, Ala Al Rajabi, René L. Jacobs
Volume 40, Issue 3, May/June 2014

Folate is an essential B vitamin required for the maintenance of AdoMet-dependent methylation. The liver is responsible for many methylation reactions that are used for post-translational modifications of proteins, methylation of DNA, and the synthesis of hormones, creatine, carnitine, and phosphatidylcholine. Conditions where methylation capacity is compromised, including folate deficiency, are associated with impaired phospatidylcholine synthesis resulting in non-alcoholic fatty liver disease and steatohepatitis. Read the full article FREE!

Now in EarlyView

Fructooligosaccharides suppress high-fat diet-induced fat accumulation in C57BL/6J mice
Yuko Nakamura, Midori Natsume, Akiko Yasuda, Mihoko Ishizaka, Keiko Kawahata, Jinichiro Koga

Alterations in human muscle protein metabolism with aging: Protein and exercise as countermeasures to offset sarcopenia
Tyler A. Churchward-Venne, Leigh Breen, Stuart M. Phillips

Mitochondrial ascorbic acid is responsible for enhanced susceptibility of U937 cells to the toxic effects of peroxynitrite
Andrea Guidarelli, Liana Cerioni, Mara Fiorani, Catia Azzolini, Orazio Cantoni

ATP-binding cassette transporters in live
Katrin Wlcek, Bruno Stieger

A DAF-16/FoxO3a-dependent longevity signal is initiated by antioxidants
Juewon Kim, Naoko Ishihara, Tae Ryong Lee

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