- Temporal Smad7 Transgene Induction in Mouse Epidermis Accelerates Skin Wound Healing
[作者：Han, GW; Li, FL; ten Dijke, P; Wang, XJ,期刊：American Journal of Pathology, 页码：1768-1779 , 文章类型： Article，,卷期：2011年179-4]
- The expression of Smad7, a tumor growth factor-beta (TGF beta) antagonist, is increased during cutaneous wound healing. To assess this significance, we temporally induced Smad7 transgene expression in wounded skin in gen...
- Autacoid 14S,21R-Dihydroxy-Docosahexaenoic Acid Counteracts Diabetic Impairment of Macrophage Prohealing Functions
[作者：Tian, HB; Lu, Y; Shah, SP; Hong, S,期刊：American Journal of Pathology, 页码：1780-1791 , 文章类型： Article，,卷期：2011年179-4]
- Impaired macrophage functions imposed by diabetic complications and the suppressed formation of 14S, 2 1R-dihydroxydocosa-4Z,7Z,10Z,12E,16Z, 19Z-hexaenoic acid (14S,21R-diHDHA) in wounds contribute significantly to defic...
- Desiccating Stress Induces CD4(+) T-Cell Mediated Sjogren's Syndrome-Like Corneal Epithelial Apoptosis via Activation of the Extrinsic Apoptotic Pathway by Interferon-gamma
[作者：Zhang, XB; Chen, W; De Paiva, CS; Volpe, EA; Gandhi, NB; Farley, WJ; Li, DQ; Niederkorn, JY; Stern, ME; Pflugfelder, SC,期刊：American Journal of Pathology, 页码：1807-1814 , 文章类型： Article，,卷期：2011年179-4]
- We investigated the role of CD4(+) T-cell-produced interferon (IFN)-gamma on corneal epithelial apoptosis in a murine desiccating stress (DS) model that resembles Sjogren's syndrome. The DS model was generated in C57BL/6...
- Membrane-Bound Serine Protease Inhibitor HAI-1 Is Required for Maintenance of Intestinal Epithelial Integrity
[作者：Kawaguchi, M; Takeda, N; Hoshiko, S; Yorita, K; Baba, T; Sawaguchi, A; Nezu, Y; Yoshikawa, T; Fukushima, T; Kataoka, H,期刊：American Journal of Pathology, 页码：1815-1826 , 文章类型： Article，,卷期：2011年179-4]
- Hepatocyte growth factor activator inhibitor type 1 (HAI-1), encoded by the serine protease inhibitor Kunitz type 1 (SPINT1) gene, is a membrane-bound serine protease inhibitor expressed in epithelial tissues. Mutant mou...
- Twist1 Is Up-Regulated in Gastric Cancer-Associated Fibroblasts with Poor Clinical Outcomes
[作者：Sung, CO; Lee, KW; Han, S; Kim, SH,期刊：American Journal of Pathology, 页码：1827-1838 , 文章类型： Article，,卷期：2011年179-4]
- Stromal fibroblasts perform important roles in cancer development and progression. Overexpression of Twist1, a basic helix-loop-helix transcription factor, is often associated with aggressive behavior in many tumors. In ...
- Kupffer Cells Influence Parenchymal Invasion and Phenotypic Orientation, but Not the Proliferation, of Liver Progenitor Cells in a Murine Model of Liver Injury
[作者：Van Hul, N; Lanthier, N; Suner, RE; Quinones, JA; van Rooijen, N; Leclercq, I,期刊：American Journal of Pathology, 页码：1839-1850 , 文章类型： Article，,卷期：2011年179-4]
- Activation of myofibroblasts (MF) and extracellular matrix (ECM) deposition predispose the expansion and differentiation of liver progenitor cells (LPC) during chronic liver injury. Because Kupffer cells (KC) are active ...
- Aquaporin-1 Promotes Angiogenesis, Fibrosis, and Portal Hypertension Through Mechanisms Dependent on Osmotically Sensitive MicroRNAs
[作者：Huebert, RC; Jagavelu, K; Hendrickson, HI; Vasdev, MM; Arab, JP; Splinter, PL; Trussoni, CE; LaRusso, NF; Shah, VH,期刊：American Journal of Pathology, 页码：1851-1860 , 文章类型： Article，,卷期：2011年179-4]
- Changes in hepatic vasculature accompany fibrogenesis, and targeting angiogenic molecules often attenuates fibrosis in animals. Aquaporin-1 (AQP1) is a water channel, overexpressed in cirrhosis, that promotes angiogenesi...
- A Detrimental Role for Invariant Natural Killer T Cells in the Pathogenesis of Experimental Dengue Virus Infection
[作者：Renneson, J; Guabiraba, R; Maillet, I; Marques, RE; Ivanov, S; Fontaine, J; Paget, C; Quesniaux, V; Fayeeuw, C; Ryffel, B; Teixeira, MM; Trottein, F,期刊：American Journal of Pathology, 页码：1872-1883 , 文章类型： Article，,卷期：2011年179-4]
- Dengue virus (DENY), a member of the mosquito-borne flaviviruses, is a serious public health problem in many tropical countries. We assessed the in vivo physiologic contribution of invariant natural killer T (iNKT) cells...
- JNK1, but Not JNK2, Is Required in Two Mechanistically Distinct Models of Inflammatory Arthritis
[作者：Denninger, K; Rasmussen, S; Larsen, JM; Orskov, C; Poulsen, SS; Sorensen, P; Christensen, JP; Illges, H; Odum, N; Labuda, T,期刊：American Journal of Pathology, 页码：1884-1893 , 文章类型： Article，,卷期：2011年179-4]
- The roles of the c-Jun N-terminal kinases (JNKs) in inflammatory arthritis have been investigated; however, the roles of each isotype (ie, JNK1 and JNK2) in rheumatoid arthritis and conclusions about whether inhibition o...
- Mast Cell Function and Death in Trypanosoma cruzi Infection
[作者：Meuser-Batista, M; Correa, JR; Carvalho, VF; Britto, CFDD; Moreira, OD; Batista, MM; Soares, MJ; Farias, FA; Silva, PMRE; Lannes-Vieira, J; Silva, RC; Henriques-Pons, A,期刊：American Journal of Pathology, 页码：1894-1904 , 文章类型： Article，,卷期：2011年179-4]
- Although the roles of mast cells (MCs) are essential in many inflammatory and fibrotic diseases, their role in hypanosoma cruzi-induced cardiomyopathy is unexplored. In this study, we treated infected CBA mice with cromo...
- miR-125b Regulates Calcification of Vascular Smooth Muscle Cells
[作者：Goettsch, C; Rauner, M; Pacyna, N; Hempel, U; Bornstein, SR; Hofbauer, LC,期刊：American Journal of Pathology, 页码：1594-1600 , 文章类型： Article，,卷期：2011年179-4]
- Vascular calcification is a prominent feature of atherosclerosis and is closely linked to osteoporosis. Cellular differentiation is regulated by various microRNAs (miRs), including miR-125b, which is known to be involved...
- CD55 Deficiency Protects against Atherosclerosis in ApoE-Deficient Mice via C3a Modulation of Lipid Metabolism
[作者：Lewis, RD; Perry, MJ; Guschina, IA; Jackson, CL; Morgan, BP; Hughes, TR,期刊：American Journal of Pathology, 页码：1601-1607 , 文章类型： Article，,卷期：2011年179-4]
- Atherosclerosis, the leading cause of death in the Western world, is driven by chronic inflammation within the artery wall. Elements of the complement cascade are implicated in the pathogenesis, because complement protei...
|