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The Poster Awards of the 53rd ICBL: "Frontiers in Lipid Biology"

The Western style BBQ and meeting banquet was held just outside Banff at the Brewster´s Mountain View Barbeque on
Saturday night, after completion of the scientific sessions. Before commencing line-dancing and the Western-style entertaining, the traditional ICBL Poster Awards were announced.

Members of the 2012 Poster Award Jury were: J Peter Slotte (chairman), Finland; Beatriz Caputto (Argentina); Andrew Brown (Australia), Barbara Karten (Canada), Thomas Lagace (Canada), Christina Leslie (USA), and Charles Rock (USA). From about 80 posters which were presented by young scientists, 30 were pre-selected as finalists by the Poster Award Jury. The pre-selected posters were more closely inspected by all members of the Poster Award Jury during the Conference poster sessions. Criteria for selecting the top posters were the relevance of the topic, originality of the subject, the quality of the presentation, the visual appearance, and discussions with the presenter. In this year’s Award presentation, one award was sponsored by Progress in Lipid Research, whereas two
awards were sponsored by ASBMB. The abstracts of the three winning posters are shown below. The ICBL community is proud of the high quality of the posters presented at the Banff meeting and congratulates the three winners.

J. Peter Slotte, President of ICBL

Progress in Lipid Research Poster Award

Choline Kinase b is an Important Regulator of Endochondral Bone Formation

Zhuo Li1, Gengshu Wu1, Roger B. Sher2, Kayla Rumack3, Gregory A. Cox2, Michael R. Doschak1, Monzur Murshed4, Frank Beier3, Dennis E. Vance1

1 University of Alberta
2 The Jackson Laboratory
3 University of Western Ontario
4 McGill University

Choline kinase is the first enzyme in the choline pathway to generate phosphatidylcholine and converts choline to phosphocholine. Choline kinase has two isoforms encoded by the genes Chka and Chkb. Inactivation of Chka results in embryonic lethality, whereas Chkb mutant mice display neonatal forelimb bone deformation. To understand the mechanisms of the bone deformation phenotype, we characterized the major long bones in the forelimb. We found that the deformation is specific to the radius and ulna and the deformation occurs during the late embryonic stage. We also found that the radius and ulna in mutant mice display abnormal chondrocyte cell morphology, unorganized proliferative columns and expanded hypertrophic zones in their growth plates as well as delayed formation of primary ossification centers. To further understand these phenotypes, we examined chondrocyte differentiation, proliferation, maturation, cartilage extracellular matrix (ECM) degradation and mineralization events. The gene expression analysis suggested that the mutant chondrocytes still maintain normal differentiation, proliferation and maturation properties. However, we found the cartilage in mutant mice may have diminished ECM degradation by matrix metalloproteinase 9 and 13. In addition, matrix of mutant chondrocytes shows impaired mineralization both in vivo and in vitro. Taken together, our data suggests that choline kinase beta plays an important role in endochondral bone formation through regulation of growth plate chondrocyte physiology.

ASBMB Poster award I

An EPR-based assay to measure ApoA-I displacement from HDL in human plasma reveals lower levels of displacement for individuals with coronary artery disease and diabetes

Mark S. Borja1, Kalistyn H. Lemke1, Bradley Hammerson1, Jacques Genest2, Michael N. Oda1

1 Children's Hospital Oakland Research Institute, CA 94609
2 McGill University, Montreal, QC H3A 1A1, Canada

High density lipoprotein (HDL) prevents coronary artery disease (CAD) by mediating reverse cholesterol transport, a process wherein cholesterol is effluxed from peripheral cells to the liver and steroidogenic organs. Cholesterol efflux requires the presentation of cholesterol by an energydependent process (ATP binding cassette transporter A1
(ABCA1)) and the availability of lipoprotein recipients/carriers of cholesterol. In the arterial wall, desorption of lipidfree/lipid-poor apolipoprotein A-I (ApoA-I) from HDL is the most plausible source of cholesterol acceptor, required to initiate de novo ABCA1-mediated cholesterol efflux and is this a rate-limiting factor. Recently, CAD status has been strongly associated with cholesterol efflux capacity. Importantly, chronic inflammation leads to an increase in oxidative events, particularly oxidation of ApoA-I by the enzyme myeloperoxidase, which impairs cholesterol efflux capacity with a concomitant reduction in the displacement/desorption of lipid-free/lipid-poor ApoA-I from HDL. Current processes for quantifying HDL efflux potential of human plasma are laborious, time consuming, costly, and employ cell culture and radioactive compounds. Here, we present an electron paramagnetic resonance (EPR) based assay to measure the exchange of ApoA-I on and off HDL particles in human plasma. By adding nitroxide spin-labeled ApoA-I directly to plasma, we can observe changes in the EPR spectrum indicative of binding to HDL particles and displacement of resident endogenous ApoA-I. Analysis of plasma samples from individuals with active CAD and/or diabetes reveal reduced levels of ApoA-I displacement when compared to healthy individuals, which is an indicator of reduced cholesterol efflux capacity in these patients. Our findings demonstrate that our EPR-based assay may be a promising new method to detect changes in plasma HDL that reflect a reduced capacity to mobilize cholesterol.

ASBMB Poster award II

The Liver X Receptor agonist GW3965 improves behavioral and neuropathological outcomes after mild repetitive closed head injury in mice

Dhananjay Namjoshi1, Georgina Martin1, James Donkin1, Anna Wilkinson1, Jianjia Fan1, Sophie Stukas1, Mike Carr1, Jeniffer Chan1, Cheryl Wellington1

1 The University of British Columbia, Vancouver, BC, Canada

Traumatic brain injury (TBI) increases Alzheimer’s Disease (AD) risk and leads to deposition of neurofibrillary tangles and amyloid deposits similar to those found in AD, suggesting that therapeutic strategies in development for AD may also be of potential interest for TBI. Agonists of Liver-X-Receptors (LXR), which regulate the expression of many genes involved in lipid homeostasis and inflammation, consistently improve cognitive function and reduce neuropathology in AD mice. One pathway by which LXR agonists exert their beneficial effects is through ABCA1-mediated lipid transport to apolipoprotein E (apoE), which enhances apoE function.

To test the therapeutic utility of the LXR agonist GW3965 for TBI, we subjected male wild-type (WT) and apoE-/- mice to mild repetitive traumatic brain injury (mrTBI) followed by treatment with vehicle or GW3965 at 15 mg/kg/day.

mrTBI impaired novel object recognition memory of WT and apoE-/- mice in both control and treatment groups within 2d with no spontaneous recovery in untreated mice. GW3965 restored memory in WT but not apoE-/- mice by 7d. Accelerating rotarod test revealed significant motor deficits in injured WT and apoE-/- mice within 24h, followed by spontaneous recovery by 14d independent of GW3965 treatment. Total soluble endogenous amyloid beta 40 and 42 levels were significantly elevated in WT and apoE-/- within 2d post-injury, a response that was suppressed by GW3965 in both genotypes. WT mice showed mild but significant axonal damage as determined by silver staining at 2d post-mrTBI, which was suppressed by GW3965 treatment. In contrast, apoE-/- mice showed severe axonal damage from 2 to 14d that was unresponsive to GW3965 treatment. These results suggest that GW3965 can reduce some of the phenotypes induced by mrTBI in an apoE-dependent manner.

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