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TABLE OF CONTENTS
|  |  |  | Volume 93, Issue 7 (July 2013) |  | In this issue Inside LI Research Articles
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| |  |  |  | | Advertisement |  | | |  |  | Inside LI | Top |  | Inside Lab Invest2013 93: 746-747; 10.1038/labinvest.2013.78 Full Text |  | Research Articles | Top |  | ANGIOGENESIS, CARDIOVASCULAR AND PULMONARY SYSTEMS | MicroRNA-206 is involved in hypoxia-induced pulmonary hypertension through targeting of the HIF-1α/Fhl-1 pathwayThis paper reveals the role of muscle-specific microRNA-206 in a rat model of hypoxia-induced pulmonary hypertension. Hypoxia induces down-regulation of miR-206 by means of the hypoxia-inducible factor-1α/four-and-a-half LIM domain 1 pathway in pulmonary artery smooth muscle cells, suggesting that miR-206 may be an important factor in chronic obstructive pulmonary disease. Junqiu Yue, Jing Guan, Xiaoyan Wang, Lili Zhang, Zixuan Yang, Qilin Ao, Yunte Deng, Pengcheng Zhu and Guoping Wang 2013 93: 748-759; advance online publication, April 29, 2013; 10.1038/labinvest.2013.63 Abstract | Full Text |  |  |  | An endovascular canine stroke model: middle cerebral artery occlusion with autologous clots followed by ipsilateral internal carotid artery blockadeA new reproducible canine stroke model that mimics human ischemic stroke was generated by middle cerebral artery occlusion with two autologous clots and temporary ipsilateral internal carotid artery blockade. The infarct lesions were confirmed by magnetic resonance imaging and pathological examination. This model may be useful in revealing the pathophysiological mechanisms of stroke. Qing-Quan Zu, Sheng Liu, Xiao-Quan Xu, Shan-Shan Lu, Lei Sun and Hai-Bin Shi 2013 93: 760-767; advance online publication, May 6, 2013; 10.1038/labinvest.2013.65 Abstract | Full Text |  |  |  | Expression of CXCL1 in human endothelial cells induces angiogenesis through the CXCR2 receptor and the ERK1/2 and EGF pathwaysA novel mechanism for pathological angiogenesis is revealed in this study. Chemokine (C-X-C motif) ligand 1 (CXCL1), expressed by vasculature, stimulates angiogenesis by an autocrine response and supports the growth of surrounding epithelial tissue via a paracrine response. CXCL1 and its receptor CXCR2 activate the ERK1/2 signaling pathway, leading to expression and secretion of epidermal growth factor, a potent stimulator of angiogenesis. Makito Miyake, Steve Goodison, Virginia Urquidi, Evan Gomes Giacoia and Charles J Rosser 2013 93: 768-778; advance online publication, June 3, 2013; 10.1038/labinvest.2013.71 Abstract | Full Text |  |  |  | A practical and sensitive method of quantitating lymphangiogenesis in vivoThis paper describes a directed in vivo lymphangiogenesis assay that simultaneously quantitates lymphangiogenesis and angiogenesis in mice using multiple approaches and markers. It is highly suited for identifying pro- and anti-lymphangiogenic agents, as well as shared or distinct mechanisms regulating lymphangiogenesis vs. angiogenesis, and is widely applicable to research in vascular and tumor biology. Mousumi Majumder, Xiping Xin and Peeyush K Lala 2013 93: 779-791; advance online publication, May 27, 2013; 10.1038/labinvest.2013.72 Abstract | Full Text |  |  |  | TLR4 as receptor for HMGB1-mediated acute lung injury after liver ischemia/reperfusion injuryAcute lung injury (ALI) is caused by pro-inflammatory mediators released from damaged liver after liver ischemia/reperfusion (I/R). This paper reveals that high mobility group box protein 1 (HMGB1), a pro-inflammatory cytokine, contributes to the mechanism for liver I/R injury-induced ALI via toll-like receptor 4 (TLR4), p38 mitogen-activated protein kinase (p38MAPK), and activator protein-1 (AP-1) signaling pathways. Zhongwei Yang, Yuxiao Deng, Diansan Su, Jie Tian, Yuan Gao, Zhengyu He and Xiangrui Wang 2013 93: 792-800; advance online publication, April 29, 2013; 10.1038/labinvest.2013.66 Abstract | Full Text |  |  |  | GENITOURINARY AND REPRODUCTIVE SYSTEMS | Interleukin-10 deficiency aggravates kidney inflammation and fibrosis in the unilateral ureteral obstruction mouse modelIn a murine model of renal tubulointerstitial fibrosis, interleukin-10 (IL-10 )-deficiency enhances renal fibrosis. The IL-10-deficient mice develop more severe renal inflammation, increased inflammatory cell infiltration, and upregulation of inflammatory chemokines and cytokines through activation of TGF-β/Smad3 and NF-κB signaling pathways. Enhancement of IL-10 expression may therefore be a potential anti-fibrosis therapy for chronic kidney diseases. Yuanmeng Jin, Ruijie Liu, Jingyuan Xie, Huabao Xiong, John Cijiang He and Nan Chen 2013 93: 801-811; advance online publication, April 29, 2013; 10.1038/labinvest.2013.64 Abstract | Full Text |  |  |  | The C-terminal module IV of connective tissue growth factor is a novel immune modulator of the Th17 responseEmerging evidence suggests that pro-inflammatory T helper (Th) 17 cells, and their effector cytokine IL-17A, participate in chronic inflammatory diseases. This study defines a role for connective tissue growth factor (CTGF/CCN2) (IV) as a regulator of the Th17 response. The C-terminal module of CCN2 induces Th17 differentiation and causes a renal Th17 inflammatory response. Thus, IL-17A targeting may be a promising tool for chronic inflammatory diseases, including renal pathologies. Raquel Rodrigues-Díez, Raúl R Rodrigues-Díez, Sandra Rayego-Mateos, Beatriz Suarez-Alvarez, Carolina Lavoz, Luiz Stark Aroeira, Elsa Sánchez-López, Macarena Orejudo, Matilde Alique, Carlos Lopez-Larrea, Alberto Ortiz, Jesús Egido and Marta Ruiz-Ortega 2013 93: 812-824; advance online publication, May 6, 2013; 10.1038/labinvest.2013.67 Abstract | Full Text |  |  |  | PERIPHERAL AND CENTRAL NERVOUS SYSTEM | The modest impact of transcription factor Nrf2 on the course of disease in an ALS animal modelNuclear factor erythroid 2-related factor 2 (Nrf2) target genes are induced in spinal cords of amyotrophic lateral sclerosis (ALS) mice. However, Nrf2 knockout only modestly accelerates disease progression in these mice. Among all known Nrf2 regulated-phase II enzymes, only NAD(P)H:quinone oxidoreductase induction is Nrf2-dependent, suggesting that Nrf2 is not the key protective mechanism against neurodegeneration in ALS mice. Yansu Guo, Yuesheng Zhang, Di Wen, Weisong Duan, Ting An, Pengxiao Shi, Jingjing Wang, Zhongyao Li, Xiaoyu Chen and Chunyan Li 2013 93: 825-833; advance online publication, May 27, 2013; 10.1038/labinvest.2013.73 Abstract | Full Text |  |  |  | PANCREATIC AND GASTROINTESTINAL SYSTEMS | Butyric acid attenuates intestinal inflammation in murine DSS-induced colitis model via milk fat globule-EGF factor 8Butyric acid exerts potent anti-inflammatory effects by inhibiting histone deacetylases. In a murine model of colitis, acetyl-histone 3K9 levels at the promoter region of milk fat globule-epidermal growth factor 8 (MFG-E8) are significantly increased by butyric acid exposure. These findings suggest that butyric acid exerts anti-inflammatory effects through MFG-E8. Tsuyoshi Mishiro, Ryusaku Kusunoki, Aya Otani, Md Mesbah Uddin Ansary, Miki Tongu, Nanae Harashima, Takaya Yamada, Shuichi Sato, Yuji Amano, Kazuhito Itoh, Shunji Ishihara and Yoshikazu Kinoshita 2013 93: 834-843; advance online publication, June 10, 2013; 10.1038/labinvest.2013.70 Abstract | Full Text |  |  |  | M2-polarized tumor-associated macrophages promoted epithelial–mesenchymal transition in pancreatic cancer cells, partially through TLR4/IL-10 signaling pathwayIn pancreatic cancer, infiltration intensity of M2-polarized tumor-associated macrophages (TAMs) correlates negatively with prognosis. When pancreatic cancer cells are co-cultured with M2-polarized TAMs, increased proliferation, migration, and proteolytic activity of the pancreatic cells is observed. Mechanistically, M2-polarized TAMs promote epithelial-mesenchymal transition of pancreatic cancer cells through TLR4/interleukin-10 signaling, which may suggest novel therapeutic strategies for pancreatic cancer. Chao-Ying Liu, Juan-Ying Xu, Xiao-Yan Shi, Wei Huang, Ting-Yan Ruan, Ping Xie and Jun-Li Ding 2013 93: 844-854; advance online publication, June 10, 2013; 10.1038/labinvest.2013.69 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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