Laboratory Investigation - Table of Contents alert Volume 96 Issue 6

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TABLE OF CONTENTS Volume 96, Issue 6 (June 2016) In this issue Inside the USCAP Journals Research Articles Technical Reports Also new AOP Sign up for e-alerts Recommend to your library Web feed Subscribe Inside the USCAP Journals Top Inside the USCAP Journals 2016 96: 600-601; 10.1038/labinvest.2016.59 Full Text Research Articles Top GENITOURINARY AND REPRODUCTIVE SYSTEMS Effects of combination PPARγ agonist and angiotensin receptor blocker on glomerulosclerosis A combination of a PPARγ agonist and angiotensin receptor blocker (ARB) is more beneficial for ameliorating glomerulosclerosis than either monotherapy. The combined mechanisms include downregulation of injurious renin-angiotensin-aldosterone system components and decreased inflammation, resulting in increased antifibrotic activity and enhanced podocyte preservation. Keizo Matsushita, Hai-Chun Yang, Manu M Mysore, Jianyong Zhong, Yu Shyr, Li-Jun Ma and Agnes B Fogo 2016 96: 602-609; advance online publication, March 21, 2016; 10.1038/labinvest.2016.42 Abstract | Full Text Ursodeoxycholic acid and 4-phenylbutyrate prevent endoplasmic reticulum stress-induced podocyte apoptosis in diabetic nephropathy This paper describes the effects of the ER stress inhibitors ursodeoxycholic acid (UDCA) and 4-phenylbutyrate (4-PBA) on diabetic nephropathy (DN) in mice. UDCA and 4-PBA prevent hyperglycemia-induced podocyte apoptosis stress and restorine autophagy, decrease urinary albuminuria, attenuate mesangial expansion and prevent apoptosis in podocytes. Ai-Li Cao, Li Wang, Xia Chen, Yun-Man Wang, Heng-Jiang Guo, Shuang Chu, Cheng Liu, Xue-Mei Zhang and Wen Peng 2016 96: 610-622; advance online publication, March 21, 2016; 10.1038/labinvest.2016.44 Abstract | Full Text ANGIOGENESIS, CARDIOVASCULAR AND PULMONARY SYSTEMS Secretory leukocyte protease inhibitor gene deletion alters bleomycin-induced lung injury, but not development of pulmonary fibrosis Protease-mediated transforming growth factor-β activation has been proposed as a pathogenic mechanism of lung fibrosis. Secretory leukocyte protease inhibitor (SLPI) null mice have enhanced metalloproteinase activity and reduced collagen gene synthesis in the lung following bleomycin-induced lung fibrosis. However, these changes do not protect against the development of fibrosis. These data suggest that the absence of SLPI does not modify the development of lung fibrosis. Anthony N Habgood, Amanda L Tatler, Joanne Porte, Sharon M Wahl, Geoffrey J Laurent, Alison E John, Simon R Johnson and Gisli Jenkins 2016 96: 623-631; advance online publication, March 14, 2016; 10.1038/labinvest.2016.40 Abstract | Full Text Inhibition of endotoxin-induced airway epithelial cell injury by a novel family of pyrrol derivates There is no specific therapy for acute respiratory distress syndrome (ARDS). This study evaluated the ability of a pyrrol compound, DTA0118, to attenuate lipopolysaccharide-induced injury in an airway epithelial cell injury model. The potent anti-inflammatory and anti-apoptotic properties of DTA0118 suggest that it is a potential drug therapy for the acute phase of sepsis and septic ARDS. Nuria E Cabrera-Benítez, Eduardo Pérez-Roth, Ángela Ramos-Nuez, Ithaisa Sologuren, José M Padrón, Arthur S Slutsky and Jesús Villar 2016 96: 632-640; advance online publication, March 21, 2016; 10.1038/labinvest.2016.46 Abstract | Full Text Inhibition of development of laser-induced choroidal neovascularization with suppression of infiltration of macrophages in Smad3-null mice Choroidal neovascularization (CNV) and associated fibrotic tissue formation are major features of age-related macular degeneration. The authors used a mouse model of CNV lesions to show that loss of Smad3 activity decreases growth factor levels, suppresses inflammation and attenuates the growth of CNV. Hiroki Iwanishi, Norihito Fujita, Katsuo Tomoyose, Yuka Okada, Osamu Yamanaka, Kathleen C Flanders and Shizuya Saika 2016 96: 641-651; advance online publication, March 7, 2016; 10.1038/labinvest.2016.30 Abstract | Full Text ORAL AND GASTROINTESTINAL SYSTEMS PIK3C2A is a gene-specific target of microRNA-518a-5p in imatinib mesylate-resistant gastrointestinal stromal tumor Microarray analysis reveals that miR-518a-5p is down-regulated in imatinib-resistant gastrointestinal stromal tumors, and that phosphatidylinositol-4-khosphate 3-kinase C2A (PIK3C2A) is its gene-specific target. MiR-518a-5p reduces proliferation and promotes apoptosis, so that low expression of miR-518a-5p up-regulates PIK3C2A and affects the cellular response to the drug, causing imatinib resistance. Yuan Shi, Xiaodong Gao, Qin Hu, Xiaojing Li, Jianfang Xu, Shaohua Lu, Yalan Liu, Chen Xu, Dongxian Jiang, Jiaqian Lin, Anwei Xue, Yunshan Tan, Kuntang Shen and Yingyong Hou 2016 96: 652-660; advance online publication, March 7, 2016; 10.1038/labinvest.2015.157 Abstract | Full Text Gastric adenocarcinoma microRNA profiles in fixed tissue and in plasma reveal cancer-associated and Epstein-Barr virus-related expression patterns The authors examined human and Epstein-Barr virus (EBV)-encoded microRNA expression in gastric adenocarcinoma samples. They found that expression of viral microRNAs in concert with unique human microRNAs provides novel insights into viral oncogenesis and reinforces the potential for microRNA profiles to aid in classification of gastric cancer subtypes. Amanda L Treece, Daniel L Duncan, Weihua Tang, Sandra Elmore, Douglas R Morgan, Ricardo L Dominguez, Olga Speck, Michael O Meyers and Margaret L Gulley 2016 96: 661-671; advance online publication, March 7, 2016; 10.1038/labinvest.2016.33 Abstract | Full Text Technical Reports Top MODELS AND TECHNIQUES Development of an in vitro model to test antifibrotic drugs on primary human liver myofibroblasts This paper describes the development of an in vitro test with normal human liver myofibroblasts that may be useful for predicting the antifibrotic properties of drug candidates for treatment of liver disease. Inter-subject variations in a-smooth muscle actin and collagen 1 expression enabled the classification of subjects as potentially low or high fibrosers, and as proof of concept, the authors show that the cells from high fibrosers respond to a currently used drug. Lynda Aoudjehane, Pierre-Yves Boelle, Grégoire Bisch, Rolland Delelo, François Paye, Olivier Scatton, Chantal Housset, Jérôme Becquart, Yvon Calmus and Filomena Conti 2016 96: 672-679; advance online publication, March 7, 2016; 10.1038/labinvest.2016.36 Abstract | Full Text Severe ocular phenotypes in Rbp4-deficient mice in the C57BL/6 genetic background Retinol binding protein 4 (RBP4) is a specific carrier for retinol in the blood. The authors produced Rbp4-deficient mice on a C57BL/6 genetic background. These mice display more severe and longer lasting retinal structural abnormalities than an older model using mice with a mixed genetic background. Furthermore, with the new model they show that RBP4 is critical for the mobilization of retinol from hepatic storage pools, and that such mobilization is necessary for ocular development and visual function. Jingling Shen, Dan Shi, Tomohiro Suzuki, Zunping Xia, Hanli Zhang, Kimi Araki, Shigeharu Wakana, Naoki Takeda, Ken-ichi Yamamura, Shoude Jin and Zhenghua Li 2016 96: 680-691; advance online publication, March 14, 2016; 10.1038/labinvest.2016.39 Abstract | Full Text Longitudinal, in vivo assessment of invasive pulmonary aspergillosis in mice by computed tomography and magnetic resonance imaging To enable non-invasive, longitudinal monitoring of pulmonary aspergillosis, the authors optimized computed tomography and magnetic resonance imaging techniques with A. fumigatus-infected mice. These techniques may prove to be valuable tools for the evaluation of dynamic disease-related changes and differences in disease severity in individual animals, and might be applied as rapid and cost-efficient drug screening protocols in preclinical models. Jennifer Poelmans, Amy Hillen, Liesbeth Vanherp, Kristof Govaerts, Johan Maertens, Tom Dresselaers, Uwe Himmelreich, Katrien Lagrou and Greetje Vande Velde 2016 96: 692-704; advance online publication, March 28, 2016; 10.1038/labinvest.2016.45 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. For other enquiries, please contact our customer feedback department. 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