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In the article entitled, “Distinct Expression Profiles of p63 Variants during Urothelial Development and Bladder Cancer Progression” (Volume 178, pages 1350–1360, of the March 2011 issue of The American Journal of Pathology), the third author's name was listed incorrectly. The correct name is Tian Huai Shen.
In the article entitled, “Abnormal Cell Properties and Down-Regulated FAK-Src Complex Signaling in B Lymphoblasts of Autistic Subjects” (Volume 179, pages 66–74 of the July 2011 issue), the current address of Hongen Wei was listed incorrectly. The current address of Dr. Wei is the Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
In the article entitled, “Spatiotemporal and Functional Behavior of Airway Dendritic Cells Visualized by Two-Photon Microscopy” (Volume 179, pages 603–609 of the August 2011 issue), the first author's name was listed incorrectly. The correct name is Tibor Z. Veres.
In the article entitled, “Annexin 1 Released by Necrotic Human Glioblastoma Cells Stimulates Tumor Cell Growth through the Formyl Peptide Receptor 1” (Volume 179, pages 1504–1512 of the September 2011 issue), the last author's surname was listed incorrectly. The correct surname is Wang.
In the article entitled, “EMMPRIN Modulates Epithelial Barrier Function through a MMP–Mediated Occludin Cleavage Implications in Dry Eye Disease” (Volume 179, pages 1278–1286 of the September 2011 issue), the last author's affiliation was listed incorrectly. The correct author affiliation is Fondation A de Rothschild,∥ Paris, France; and INSERM UMR S 968,** and the Institut de la Vision, Paris, France; Université Paris 7,†† Diderot, Paris, France.
In the article entitled “Selective Stimulation of VEGFR2 Accelerates Progressive Renal Disease” (Volume 179, pages 155–166 of the July 2011 issue), part of panel J was inadvertently omitted in Figure 2; the figure appears correctly online (HTML and PDF versions). The corrected Figure 2 with legend appears on the following page.
Recent studies suggest that one of the major pathways to the pathogenesis of autism is reduced cell migration. Focal adhesion kinase (FAK) has an important role in neural migration, dendritic morphological characteristics, axonal branching, and synapse formation. The FAK-Src complex, activated by upstream reelin and integrin β1, can initiate a cascade of phosphorylation events to trigger multiple intracellular pathways, including mitogen-activated protein kinase–extracellular signal–regulated kinase and phosphatidylinositol 3-kinase–Akt signaling.
Highly malignant human gliomas overexpress the G-protein–coupled chemoattractant receptor formyl peptide receptor (FPR1), which promotes tumor progression when activated. Our previous studies demonstrated that necrotic glioblastoma cells release chemotactic agonist(s) that activate FPR1 on viable tumor cells. In the present study, we identified an FPR1 agonist released by necrotic human glioblastoma cells. Necrotic tumor cell supernatant (NecSup) contained Annexin 1 (Anx A1), a chemotatic polypeptide agonist for FPR1.
The TP63 gene, a member of the TP53 tumor suppressor gene family, can be expressed as at least six isoforms due to alternative promoter use and alternative splicing. The lack of p63 isoform–specific antibodies has limited the analysis of the biological significance of p63. We report a novel set of well-defined antibodies to examine p63 isoforms in mouse and human urothelium during embryogenesis and tumor progression, respectively. We provide evidence that basal and intermediate urothelial cells express p63 isoforms, with the TAp63 variant the first to be detected during development, whereas umbrella cells are characterized by a p63-negative phenotype.
Airway mucosal dendritic cells (DCs), located beneath the epithelium of the conducting airways, are believed to be specialized for immunosurveillance via sampling of antigens from the airway luminal surface. However, the dynamics of airway DC activity has not yet been visualized. We used two-photon microscopy to illuminate the endogenous mucosal DC network in the airways of mice. To characterize DC behavior, we used lung section preparations and an intravital microscopic approach. DCs displayed a heterogeneous movement pattern according to their localization within the airway mucosa: sessile intraepithelial DCs with a dendritiform shape exhibited active probing movements and occasionally formed transepithelial extensions into the airway lumen.
Vascular endothelial growth factor A (VEGF-A) can play both beneficial and deleterious roles in renal diseases, where its specific function might be determined by nitric oxide bioavailability. The complexity of VEGF-A in renal disease could in part be accounted for by the distinct roles of its two receptors; VEGFR1 is involved in the inflammatory responses, whereas VEGFR2 predominantly mediates angiogenesis. Because nondiabetic chronic renal disease is associated with capillary loss, we hypothesized that selective stimulation of VEGFR2 could be beneficial in this setting.
Dry eye is a common disease that develops as a result of alteration of tear fluid, leading to osmotic stress and a perturbed epithelial barrier. Matrix metalloproteinase-9 (MMP-9) may be important in dry eye disease, as its genetic knockout conferred resistance to the epithelial disruption. We show that extracellular matrix metalloproteinase inducer (EMMPRIN; also termed CD147), an inducer of MMP expression, participates in the pathogenesis of dry eye through MMP-mediated cleavage of occludin, an important component of tight junctions.