Laboratory Investigation - Table of Contents alert Volume 95 Issue 3

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TABLE OF CONTENTS Volume 95, Issue 3 (March 2015) 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 2015 95: 248-249; 10.1038/labinvest.2015.31 Full Text Research Articles Top GENITOURINARY AND REPRODUCTIVE SYSTEMS Serum amyloid A and inflammation in diabetic kidney disease and podocytes OPEN This paper shows that serum amyloid A is up-regulated in humans and mice with diabetic kidney disease, and is increased in mouse podocytes exposed to advanced glycation end-products. Serum amyloid A exposure also causes an inflammatory response in podocytes, indicating that it may contribute to the progression of kidney disease in diabetes. Robert J Anderberg, Rick L Meek, Kelly L Hudkins, Sheryl K Cooney, Charles E Alpers, Renee C Leboeuf and Katherine R Tuttle 2015 95: 250-262; advance online publication, December 22, 2014; 10.1038/labinvest.2014.163 Abstract | Full Text Exogenous C-type natriuretic peptide infusion ameliorates unilateral ureteral obstruction-induced tubulointerstitial fibrosis in rats Exogenous C-type natriuretic peptide infusion can ameliorate tubulointerstitial fibrosis in animals with ureteral obstruction, indicating its potential therapeutic value. The pathological lesions and collagen IV accumulation in the obstructed kidneys are reduced through down-regulation of tissue inhibitor of metalloproteinase-1 and -2 expression. Peng Hu, Xiao Cen Zhang, Hai Bo Kong, Xun Xia, Bo Hu and Yuan Han Qin 2015 95: 263-272; advance online publication, December 1, 2014; 10.1038/labinvest.2014.149 Abstract | Full Text Glomerular parietal epithelial cell activation induces collagen secretion and thickening of Bowman’s capsule in diabetes This study investigates thickening of the Bowman's capsule in patients with diabetic nephropathy and unravels its pathomechanism by assessing the production of extracellular matrix proteins by activated parietal epithelial cells under diabetic conditions. The authors conclude that the metabolic changes in diabetes activate parietal epithelial cells and cause thickening of Bowman's capsules. Alexander Holderied, Simone Romoli, Jonathan Eberhard, Lukas A Konrad, Satish K Devarapu, Julian A Marschner, Susanna Müller and Hans-Joachim Anders 2015 95: 273-282; advance online publication, December 22, 2014; 10.1038/labinvest.2014.160 Abstract | Full Text The potential of neurotensin secreted from neuroendocrine tumor cells to promote gelsolin-mediated invasiveness of prostate adenocarcinoma cells This study indicates that neuroendocrine cells and neurotensin induce gelsolin-mediated invasiveness of a prostate cancer cell line through neurotensin receptor-1 activation. These findings support the significance of controlling neuroendocrine cells, which may secrete neurotensin and trigger progression of prostate cancer to castration-resistant prostate cancer. Kohei Hashimoto, Yuki Kyoda, Toshiaki Tanaka, Toshihiro Maeda, Ko Kobayashi, Kohsuke Uchida, Hiroshi Kitamura, Koichi Hirata, Taiji Tsukamoto and Naoya Masumori 2015 95: 283-295; advance online publication, January 12, 2015; 10.1038/labinvest.2014.165 Abstract | Full Text ORAL AND GASTROINTESTINAL SYSTEMS Intracellular colon cancer-associated Escherichia coli promote protumoral activities of human macrophages by inducing sustained COX-2 expression Tumors of patients with colorectal cancer are abnormally colonized by E. coli. In this study, the authors provide evidence showing that tumor-infiltrating bacteria can support tumor progression by persisting within immune cells and inducing production of pro-tumoral factors such as COX-2. Jennifer Raisch, Nathalie Rolhion, Anaëlle Dubois, Arlette Darfeuille-Michaud and Marie-Agnès Bringer 2015 95: 296-307; advance online publication, December 29, 2014; 10.1038/labinvest.2014.161 Abstract | Full Text Upregulation of integrin β4 promotes epithelial–mesenchymal transition and is a novel prognostic marker in pancreatic ductal adenocarcinoma This paper reveals the clinicopathological significance of integrin beta 4 (ITGb4) up-regulation in pancreatic cancer and also suggest a potential role for ITGb4 in the regulation of epithelial-mesenchymal transition. ITGb4 enhances the migratory and invasive ability of pancreatic ductal adenocarcinoma cells via modulation of E-cadherin and vimentin expresssion. Y Masugi, K Yamazaki, K Emoto, K Effendi, H Tsujikawa, M Kitago, O Itano, Y Kitagawa and M Sakamoto 2015 95: 308-319; advance online publication, January 19, 2015; 10.1038/labinvest.2014.166 Abstract | Full Text DEVELOPMENT, MATRIX BIOLOGY AND AGING Extracellular deposition of mouse senile AApoAII amyloid fibrils induced different unfolded protein responses in the liver, kidney, and heart Extracellular deposition of mouse apolipoprotein A-II amyloid fibrils increases expression of heat shock protein A5 (GRP78) and several endoplasmic reticulum stress-related proteins, and apoptosis-positive cells in the liver and kidney, but not in the heart. This study indicates that unfolded protein responses differ among tissues with amyloid deposition. Hongmin Luo, Jinko Sawashita, Geng Tian, Yingye Liu, Lin Li, Xin Ding, Zhe Xu, Mu Yang, Hiroki Miyahara, Masayuki Mori, Jinze Qian, Yaoyong Wang and Keiichi Higuchi 2015 95: 320-333; advance online publication, December 29, 2014; 10.1038/labinvest.2014.158 Abstract | Full Text MODELS AND TECHNIQUES Preanalytical variables and phosphoepitope expression in FFPE tissue: quantitative epitope assessment after variable cold ischemic time A tissue microarray of breast cancer specimens was used to evaluate changes in antigenicity of 12 phospho-epitopes frequently used in research settings as a function of cold ischemic time. The majority of the epitopes revealed changes in expression levels with increasing time to formalin fixation. Therefore, specimen collection should be closely subjected to quality control measures to ensure accurate measurement of these epitopes. Maria Vassilakopoulou, Fabio Parisi, Summar Siddiqui, Allison M England, Elizabeth R Zarella, Valsamo Anagnostou, Yuval Kluger, David G Hicks, David L Rimm and Veronique M Neumeister 2015 95: 334-341; advance online publication, November 24, 2014; 10.1038/labinvest.2014.139 Abstract | Full Text Technical Reports Top A modified murine model of systemic sclerosis: bleomycin given by pump infusion induced skin and pulmonary inflammation and fibrosis The authors established a murine model of systemic sclerosis by implanting an osmotic mini-pump containing bleomycin. This procedure led to tissue inflammation and fibrosis in the local skin and the distant lung, closely resembling human systemic sclerosis with interstitial lung disease-like manifestations. This improved model can be used to investigate immunological mechanisms and test therapeutic interventions for the human disease. Minrui Liang, Jiaoyan Lv, Linlin Zou, Wei Yang, Yingluo Xiong, Xiangjun Chen, Ming Guan, Rui He and Hejian Zou 2015 95: 342-350; advance online publication, December 15, 2014; 10.1038/labinvest.2014.145 Abstract | Full Text Generation of a murine hepatic angiosarcoma cell line and reproducible mouse tumor model Notch1 behaves as a tumor suppressor gene in endothelial cells. Knockout of Notch1 leads to formation of spontaneous hepatic angiosarcoma in mice. Isolated angiosarcoma cells show Myc pathway activation, sensitivity to the tyrosine kinase inhibitor sorafenib, and can be transplanted into NOD/SCID mice for pre-clinical drug testing. Sonja Rothweiler, Michael T Dill, Luigi Terracciano, Zuzanna Makowska, Luca Quagliata, Ruslan Hlushchuk, Valentin Djonov, Markus H Heim and David Semela 2015 95: 351-362; advance online publication, November 24, 2014; 10.1038/labinvest.2014.141 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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