Laboratory Investigation - Table of Contents alert Volume 92 Issue 2

TABLE OF CONTENTS Volume 92, Issue 2 (February 2012) In this issue Inside LI Research Articles Also new AOP Sign up for e-alerts Recommend to your library Web feed Subscribe Advertisement Announcing Open Laboratory Investigation now offers authors the option to publish their articles with immediate open access upon publication. Open access articles will also be deposited on PubMed Central at the time of publication and will be freely available immediately. Find out more from the FAQs page.   Inside LI Top Inside Lab Invest 2012 92: 164-165; 10.1038/labinvest.2011.202 Full Text Research Articles Top BLOOD, LYMPHATICS, IMMUNE SYSTEM, STEM CELLS The anti-TNF-α antibody infliximab indirectly regulates PECAM-1 gene expression in two models of in vitro blood cell activation Activation of leukocytes induces PECAM-1 downregulation and simultaneous ICAM-1- and VCAM-1-upregulation through the action of TNF-α and/or IFN-γ; this can be reverted by antibodies to TNF-α. The anti-inflammatory effect of anti-TNF-α antibodies administered to patients suffering from chronic inflammatory diseases may be explained by this mechanism. Federico Moriconi, Ihtzaz Ahmed Malik, Ahmad Amanzada, Martina Blaschke, Dirk Raddatz, Sajjad Khan and Giuliano Ramadori 2012 92: 166-177; advance online publication, October 31, 2011; 10.1038/labinvest.2011.160 Abstract | Full Text Bevacizumab attenuates major signaling cascades and eIF4E translation initiation factor in multiple myeloma cells Bevacizumab, an anti-VEGF antibody, influences major pathways critically activated in multiple myeloma independent of its established effect on angiogenesis. The cytostatic effect of VEGF inhibition on multiple myeloma cells underscores its potential in combined therapy. Oshrat Attar-Schneider, Liat Drucker, Victoria Zismanov, Shelly Tartakover-Matalon, Gloria Rashid and Michael Lishner 2012 92: 178-190; advance online publication, November 14, 2011; 10.1038/labinvest.2011.162 Abstract | Full Text Galectin-1-mediated cell death is increased by CD30-induced signaling in anaplastic large cell lymphoma cells but not in Hodgkin lymphoma cells The role of the endogenous β-galactose-binding lectins galectin-1 and -3 are elucidated in lymphoma. CD30 signaling stimulates galectin-1-induced cell death of anaplastic large cell lymphoma cells but Hodgkin lymphoma cells are not susceptible. Unexpectedly, galectin-3 has no effect on CD30/galectin-1-induced cell death. Osamu Suzuki, Burkhard Hirsch, Masafumi Abe, Horst Dürkop and Harald Stein 2012 92: 191-199; advance online publication, October 10, 2011; 10.1038/labinvest.2011.151 Abstract | Full Text BREAST, SKIN, SOFT TISSUE AND BONE ERp29 induces breast cancer cell growth arrest and survival through modulation of activation of p38 and upregulation of ER stress protein p58IPK ERp29 overexpression in breast cancer cells significantly inhibits cell proliferation and improves cell survival. Mechanistic studies reveal that the ERp29-regulated activation of p38 and up-regulation of ER stress protein p58IPK are the key in modulation of cell fate. Targeting ERp29 and its downstream signaling is therefore a potential therapeutic strategy. Danmei Gao, I Fon Bambang, Thomas C Putti, Yuan Kun Lee, Des R Richardson and Daohai Zhang 2012 92: 200-213; advance online publication, November 7, 2011; 10.1038/labinvest.2011.163 Abstract | Full Text Therapeutic potential of fibroblast growth factor-2 for hypertrophic scars: upregulation of MMP-1 and HGF expression Fibroblast growth factor-2 up-regulates the expression of matrix metalloproteinase-1 and hepatocyte growth factor in a model of hypertrophic scars, resulting in reversal of the condition. These findings may suggest a new therapeutic approach. Hitomi Eto, Hirotaka Suga, Noriyuki Aoi, Harunosuke Kato, Kentaro Doi, Shinichiro Kuno, Yasuhiko Tabata and Kotaro Yoshimura 2012 92: 214-223; advance online publication, September 26, 2011; 10.1038/labinvest.2011.127 Abstract | Full Text ANGIOGENESIS, CARDIOVASCULAR AND PULMONARY SYSTEMS Antioxidant N-acetyl cysteine reverses cigarette smoke-induced myocardial infarction by inhibiting inflammation and oxidative stress in a rat model N-acetyl cysteine, an antioxidant and anti-inflammatory agent, is presented as a novel post-infarction therapy for amelioration of the adverse effects of tobacco exposure on infracted myocardium, as it may reverse cardiovascular adverse effects of cigarette smoke. Ashwani K Khanna, Jianping Xu and Mandeep R Mehra 2012 92: 224-235; advance online publication, October 3, 2011; 10.1038/labinvest.2011.146 Abstract | Full Text Pentosan polysulfate inhibits atherosclerosis in Watanabe heritable hyperlipidemic rabbits: differential modulation of metalloproteinase-2 and -9 Pentosan polysulfate prevents progression of established atherosclerosis in an animal model. This effect is mediated by matrix metalloproteinase-2 and tissue inhibitors of metalloproteinase activities in the aortic wall, as reduced TNFα-stimulates inflammation and metaloproteinase activation in macrophages. Enrico Lupia, Feng Zheng, Fabrizio Grosjean, Ivan Tack, Sophie Doublier, Sharon J Elliot, Helen Vlassara and Gary E Striker 2012 92: 236-245; advance online publication, October 31, 2011; 10.1038/labinvest.2011.154 Abstract | Full Text WNT3A induces a contractile and secretory phenotype in cultured vascular smooth muscle cells that is associated with increased gap junction communication Wnt3a, a canonical Wnt ligand, induces the expression of smooth muscle contractile proteins along with extracellular matrix components in cultures of vascular smooth muscle cells. These findings suggest Wnt3a simultaneously induces a contractile and secretory phenotype in these cells and thus may have important implications in vascular wound healing and disease. Jon M Carthy, Zongshu Luo and Bruce M McManus 2012 92: 246-255; advance online publication, November 21, 2011; 10.1038/labinvest.2011.164 Abstract | Full Text GENITOURINARY AND REPRODUCTIVE SYSTEMS Wnt activation downregulates olfactomedin-1 in Fallopian tubal epithelial cells: a microenvironment predisposed to tubal ectopic pregnancy Wnt-activation and down-regulation of olfactomedin-1 occur in the receptive endometrium and coincide with embryo implantation in vivo. It is now shown that Wnt-activation suppresses expression olfactomedin-1 in the Fallopian tube and may create a favorable microenvironment for retention of an embryo, leading to ectopic pregnancy. Suranga P Kodithuwakku, Ronald T K Pang, Ernest H Y Ng, Annie N Y Cheung, Andrew W Horne, Pak-Chung Ho, William S B Yeung and Kai-Fai Lee 2012 92: 256-264; advance online publication, October 3, 2011; 10.1038/labinvest.2011.148 Abstract | Full Text HEPATIC AND PANCREATIC SYSTEMS A novel murine model for non-alcoholic steatohepatitis developed by combination of a high-fat diet and oxidized low-density lipoprotein A murine model of non-alcoholic steatohepatitis (NASH) is established by the combination of a high-fat diet (HFD) and oxidized low-density lipoprotein (oxLDL). An increased oxidative state resulting from HFD-induced intracellular lipid peroxidation and oxLDL is the trigger for hepatic inflammation. CD36 expressed on hepatocytes and hepatic macrophages mediate the pathophysiology of NASH.  Yimin, Hiroaki Furumaki, Shiho Matsuoka, Toshihiro Sakurai, Masashi Kohanawa, Songji Zhao, Yuji Kuge, Nagara Tamaki and Hitoshi Chiba 2012 92: 265-281; advance online publication, November 7, 2011; 10.1038/labinvest.2011.159 Abstract | Full Text Histamine stimulates the proliferation of small and large cholangiocytes by activation of both IP3/Ca2+ and cAMP-dependent signaling mechanisms The proliferative mechanisms of different subpopulations of bile duct cells are differentially targeted by liver injury and toxins. Histamine stimulates the proliferation of small and large cholangiocytes by interaction with H1 and H2 histamine receptors, respectively, activating Ca2+ in small cholangiocytes and cAMP-signaling in large cholangiocytes. Heather L Francis, Sharon DeMorrow, Antonio Franchitto, Julie K Venter, Romina A Mancinelli, Mellanie A White, Fanyin Meng, Yoshiyuki Ueno, Guido Carpino, Anastasia Renzi, Kimberly K Baker, Hannah E Shine, Taylor C Francis, Eugenio Gaudio, Gianfranco D Alpini and Paolo Onori 2012 92: 282-294; advance online publication, November 7, 2011; 10.1038/labinvest.2011.158 Abstract | Full Text HBcAg induces PD-1 upregulation on CD4+T cells through activation of JNK, ERK and PI3K/AKT pathways in chronic hepatitis-B-infected patients Expression of PD-1, a hallmark of exhausted T-cells, is up-regulated in CD4+ T cells in every phase of chronic hepatits-B virus (HBV) infection, and is induced by hepatitis B core antigen through JNK, ERK, and PI3K/AKT signaling pathways. Understanding such changes in PD-1 expression in each phase of chronic HBV infection may be crucial to the management of HBV carriers. Man Li, Xue-Hua Sun, Xiao-Jun Zhu, Shu-Gen Jin, Zhen-Jun Zeng, Zhen-Hua Zhou, Zhuo Yu and Yue-Qiu Gao 2012 92: 295-304; advance online publication, October 31, 2011; 10.1038/labinvest.2011.157 Abstract | Full Text The function of integrin-linked kinase in normal and activated stellate cells: implications for fibrogenesis in wound healing Integrin-linked kinase (ILK) is implicated in signal transduction between integrins and growth factor/extracellular receptors and mediates the fibrogenic phenotype of hepatic stellate cells by engaging the small GTPase Rho in a signal transduction pathway linked to fibrogenesis. A downstream ILK signaling pathway including the G protein coupled receptor system also mediates critical stellate cell attributes. Mahnoush S Shafiei and Don C Rockey 2012 92: 305-316; advance online publication, November 7, 2011; 10.1038/labinvest.2011.155 Abstract | Full Text Advertisement Ensure your access If you are unable to access the articles in this alert, your library may not subscribe to this journal. Our online recommendation form is a simple way to make your librarian aware that this journal is valuable to your research. Recommend now!   Please note that you need to be a subscriber or site-licence holder to enjoy full-text access to Laboratory Investigation. In order to do so, please purchase a subscription. You have been sent this Table of Contents Alert because you have opted in to receive it. You can change or discontinue your e-mail alerts at any time, by modifying your preferences on your nature.com account at: www.nature.com/nams/svc/myaccount (You will need to log in to be recognised as a nature.com registrant). For further technical assistance, please contact our registration department. 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