Laboratory Investigation - Table of Contents alert Volume 93 Issue 4

TABLE OF CONTENTS Volume 93, Issue 4 (April 2013) In this issue Inside LI Pathobiology in Focus Research Articles Also new AOP Sign up for e-alerts Recommend to your library Web feed Subscribe Advertisement This month's recommended article by the Editors of LI: Hydroxylases as therapeutic targets in inflammatory bowel disease   Inside LI Top Inside Lab Invest 2013 93: 376-377; 10.1038/labinvest.2013.49 Full Text Pathobiology in Focus Top Hydroxylases as therapeutic targets in inflammatory bowel disease Inflammatory bowel disease occurs when inappropriate immunological activity in the intestinal mucosa results in epithelial barrier dysfunction. Intracellular hydroxylases activate adaptive transcriptional responses to hypoxia. This review discusses the mechanisms of action and therapeutic potential of hydroxylase inhibitors that ameliorate symptoms of colitis through the promotion of intestinal epithelial barrier function. Eoin P Cummins, Glen A Doherty and Cormac T Taylor 2013 93: 378-383; advance online publication, February 18, 2013; 10.1038/labinvest.2013.9 Abstract | Full Text Research Articles Top ORAL AND GASTROINTESTINAL SYSTEMS Bacteroides fragilis enterotoxin upregulates lipocalin-2 expression in intestinal epithelial cells This study reveals that a signaling pathway involving mitogen-activated protein kinases and transcription factor AP-1 is required for induction of lipocalin-2, an antimicrobial protein, in intestinal epithelial cells exposed to enterotoxin from enterotoxigenic Bacteroides fragilis. The secreted lipocalin -2 may facilitate antimicrobial activity within B. fragilis-infected mucosa. Do Young Yoo, Su Hyuk Ko, Jireh Jung, Young-Jeon Kim, Joo Sung Kim and Jung Mogg Kim 2013 93: 384-396; advance online publication, February 4, 2013; 10.1038/labinvest.2013.1 Abstract | Full Text Primary esophageal and gastro-esophageal junction cancer xenograft models: clinicopathological features and engraftment In this paper, primary human esophageal cancer xenograft models were created using freshly resected and endoscopic biopsy-derived tumor specimens from patients. This system has potential as a pre-clinical tool to study tumor biology, to determine resistance to therapy, and to test sensitivity of novel therapeutics. Lorin Dodbiba, Jennifer Teichman, Andrew Fleet, Henry Thai, Bin Sun, Devang Panchal, Devalben Patel, Alvina Tse, Zhuo Chen, Olusola O Faluyi, Daniel J Renouf, Hala Girgis, Bizhan Bandarchi, Joerg Schwock, Wei Xu, Robert G Bristow, Ming-Sound Tsao, Gail E Darling, Laurie E Ailles, Hala El-Zimaity and Geoffrey Liu 2013 93: 397-407; advance online publication, February 11, 2013; 10.1038/labinvest.2013.8 Abstract | Full Text ANGIOGENESIS, CARDIOVASCULAR AND PULMONARY SYSTEMS Neural lineage-specific homeoprotein BRN2 is directly involved in TTF1 expression in small-cell lung cancer A neural cell lineage-specific transcription factor, BRN2, is specifically expressed in small cell lung cancer (SCLC) and up-regulates expression of thyroid transcription factor 1 (TTF1) a protein crucial in thyroid, lung, and developing brain morphogenesis. Expression of TTF1, is lineage-specific in SCLC , as it is in thyroid carcinomas and lung adenocarcinomas with terminal respiratory unit differentiation. Masashi Sakaeda, Hanako Sato, Jun Ishii, Chie Miyata, Hiroshi Kamma, Yukiko Shishido-Hara, Hiroaki Shimoyamada, Masachika Fujiwara, Tetsuya Endo, Ryota Tanaka, Haruhiko Kondo, Tomoyuki Goya, Ichiro Aoki and Takuya Yazawa 2013 93: 408-421; advance online publication, January 28, 2013; 10.1038/labinvest.2013.2 Abstract | Full Text ROS-mediated downregulation of MYPT1 in smooth muscle cells: a potential mechanism for the aberrant contractility in atherosclerosis In cultured smooth muscle cells, superoxide anions and peroxynitrite downregulate the myosin phosphatase regulatory subunit, MYPT1. Aortas of apoE-knockout mice exhibit decreased MYPT1 that correlates with increased sensitivity to vasoconstrictor; this is reversed by estrogen treatment. Oxidative stress therefore mediates the down-regulation of MYPT1 that contributes to the aberrant contractility seen in atherosclerosis. Jung-Chien Cheng, Hui-Pin Cheng, I-Ching Tsai and Meei Jyh Jiang 2013 93: 422-433; advance online publication, February 18, 2013; 10.1038/labinvest.2013.40 Abstract | Full Text GENITOURINARY AND REPRODUCTIVE SYSTEMS Matrix metalloproteinase-9 of tubular and macrophage origin contributes to the pathogenesis of renal fibrosis via macrophage recruitment through osteopontin cleavage MMP-9 promotes epithelial to mesenchymal transition (EMT) of renal tubular epithelial cells (TECs), leading to renal fibrosis. Two waves of MMP-9 expression occur; the first from TECs and the second from TECs, macrophages, and myofibroblasts. Initially, MMP-9 cleaves osteopontin, stimulating the influx of macrophages, again amplifying MMP-9 production. Inhibition of MMP-9 at early and late stages in renal fibrosis could therefore result in improved renal function. Thian Kui Tan, Guoping Zheng, Tzu-Ting Hsu, So Ra Lee, Jianlin Zhang, Ye Zhao, Xinrui Tian, Yiping Wang, Yuan Min Wang, Qi Cao, Ya Wang, Vincent WS Lee, Changqi Wang, Dong Zheng, Stephen I Alexander, Erik Thompson and David C H Harris 2013 93: 434-449; advance online publication, January 28, 2013; 10.1038/labinvest.2013.3 Abstract | Full Text Blockade of Smad signaling by 3′-deoxyadenosine: a mechanism for its anti-fibrotic potential Cordycepin, or 3′-deoxyadenosine, is a major nucleoside derivative isolated from the mushroom Cordyceps militaris. This compound interferes with fibrogenic processes in the kidney, suppressing TGF-β and bone morphogenetic protein signaling via down-regulation of Smads. Cordycepin may therefore be useful for therapeutic intervention in TGF-β-related fibrotic disorders. Liubao Gu, Hisashi Johno, Shotaro Nakajima, Hironori Kato, Shuhei Takahashi, Ryohei Katoh and Masanori Kitamura 2013 93: 450-461; advance online publication, February 25, 2013; 10.1038/labinvest.2013.4 Abstract | Full Text BLOOD, LYMPHATICS, IMMUNE SYSTEM AND STEM CELLS Sphingosine-1-phosphate receptor 1 in classical Hodgkin lymphoma: assessment of expression and role in cell migration Sphingosine-1-phosphate receptor 1 (S1PR1) is expressed in a subset of classical Hodgkin lymphoma (CHL) cases, and acts a functional receptor on Hodgkin-Reed Sternberg (HRS) cells. S1PR1 governs migration via Gi-protein/phosphatidylinositol-3-kinase, and S1PR1 antagonists inhibit sphingosine-1-phosphate-induced migration in HRS cells. S1PR1 may therefore be an attractive target in the therapy of refractory or recurrent S1PR1-positive CHL. Michael J Kluk, Kieran P Ryan, Bonnie Wang, Guoqi Zhang, Scott J Rodig and Teresa Sanchez 2013 93: 462-471; advance online publication, February 18, 2013; 10.1038/labinvest.2013.7 Abstract | Full Text BREAST, SKIN, SOFT TISSUE AND BONE CXCL5 stimulation of RANK ligand expression in Paget’s disease of bone Paget's disease of bone (PDB) is marked by localized areas of bone turnover. Enhanced levels of RANKL, a protein critical for osteoclast differentiation/bone resorption, are associated with PDB. This study describes a mechanism for PDB: Measles virus nucleocapsid protein upregulates the cytokine CXCL5, which stimulates RANKL expression and results in increased p-CREBP binding to the hRANKL promoter region in stromal/preosteoblast cells. Kumaran Sundaram, D Sudhaker Rao, William L Ries and Sakamuri V Reddy 2013 93: 472-479; advance online publication, February 25, 2013; 10.1038/labinvest.2013.5 Abstract | Full Text Quantitation of fixative-induced morphologic and antigenic variation in mouse and human breast cancers In an empirically heterogeneous tissue such as neoplasia, a basis must be established for comparing sets of observations. This paper shows how quantitative image analysis of whole slide images for morphometric parameters and immunohistochemistry of breast cancer antigens was used to evaluate the reproducibility, biological variability and intratumoral heterogeneity in transplantable mouse models of human breast cancer. Robert D Cardiff, Neil E Hubbard, Jesse A Engelberg, Robert J Munn, Claramae H Miller, Judith E Walls, Jane Q Chen, Héctor A Velásquez-García, Jose J Galvez, Katie J Bell, Laurel A Beckett, Yue-Ju Li and Alexander D Borowsky 2013 93: 480-497; advance online publication, February 11, 2013; 10.1038/labinvest.2013.10 Abstract | Full Text 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. For print subscription enquiries, please contact our subscription department. 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