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[PMID]: 26116571
[Au] Autor:Ding BS; Gomi K; Rafii S; Crystal RG; Walters MS
[Ad] Address:Department of Genetic Medicine, Weill Cornell Medical College, New York, NY 10065, USA....
[Ti] Title:Endothelial MMP14 is required for endothelial-dependent growth support of human airway basal cells.
[So] Source:J Cell Sci;128(16):2983-8, 2015 Aug 15.
[Is] ISSN:1477-9137
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Human airway basal cells are the stem (or progenitor) population of the airway epithelium, and play a central role in anchoring the epithelium to the basement membrane. The anatomic position of basal cells allows for potential paracrine signaling between them and the underlying non-epithelial stromal cells. In support of this, we have previously demonstrated that endothelial cells support growth of basal cells during co-culture through vascular endothelial growth factor A (VEGFA)-mediated signaling. Building on these findings, we found, by RNA sequencing analysis, that basal cells expressed multiple fibroblast growth factor (FGF) ligands (FGF2, FGF5, FGF11 and FGF13) and that only FGF2 and FGF5 were capable of functioning in a paracrine manner to activate classical FGF receptor (FGFR) signaling. Antibody-mediated blocking of FGFR1 during basal-cell-endothelial-cell co-culture significantly reduced the endothelial-cell-dependent basal cell growth. Stimulation of endothelial cells with basal-cell-derived growth factors induced endothelial cell expression of matrix metallopeptidase 14 (MMP14), and short hairpin RNA (shRNA)-mediated knockdown of endothelial cell MMP14 significantly reduced the endothelial-cell-dependent growth of basal cells. Overall, these data characterize a new growth-factor-mediated reciprocal 'crosstalk' between human airway basal cells and endothelial cells that regulates proliferation of basal cells.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1508
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1242/jcs.168179

  2 / 258443 MEDLINE  
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[PMID]: 26163528
[Au] Autor:Biyajima K; Kakizaki F; Shen X; Mori K; Sugai M; Taketo MM; Yokota Y
[Ad] Address:Division of Molecular Genetics, Department of Biochemistry and Bioinformative Sciences, School of Medicine, Faculty of Medical Sciences, University of Fukui, 23-3 Matsuoka-Shimoaizuki, Eiheiji-cho, Yoshida-gun, Fukui 910-1193, Japan biyajima@u-fukui.ac.jp....
[Ti] Title:Id2 deletion attenuates Apc-deficient ileal tumor formation.
[So] Source:Biol Open;4(8):993-1001, 2015.
[Is] ISSN:2046-6390
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The expression level of inhibitor of DNA binding 2 (Id2) is increased in colorectal carcinomas and is positively correlated with poor prognosis. However, the functional significance of Id2 in intestinal tumorigenesis has not been fully defined using genetic approaches. Here, we show that Id2 promotes ileal tumor initiation in Apc-deficient mice. Expression of Id2 was stimulated by Wnt signaling through the enhancer region of the Id2 promoter at the early stage of tumorigenesis in Apc(+/Δ716) (Apc(Δ716)) mice. Genetic depletion of Id2 in Apc(Δ716) mice caused ∼80% reduction in the number of ileal polyps, but had little effect on tumor size. Notably, the lack of Id2 increased the number of apoptotic cells in the normal crypt epithelium of the mice. Furthermore, DNA microarray analysis revealed that the expression level of Max dimerization protein 1 (Mxd1), known as a c-Myc antagonist, was specifically increased by Id2 deletion in the ileal intestinal epithelium of Apc(Δ716) mice. In contrast, the protein level of c-Myc, but not the mRNA level, was decreased by loss of Id2 in these mice. These results indicate that loss of Id2 inhibits tumor initiation by up-regulation of Mxd1 and down-regulation of c-Myc in Apc(Δ716) mice.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1508
[Da] Date of entry for processing:150816
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.1242/bio.012252

  3 / 258443 MEDLINE  
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[PMID]: 26138464
[Au] Autor:Rosekrans SL; Baan B; Muncan V; van den Brink GR
[Ad] Address:Tytgat Institute for Liver and Intestinal Research and Department of Gastroenterology and Hepatology, Academic Medical Center, Amsterdam, the Netherlands....
[Ti] Title:Esophageal development and epithelial homeostasis.
[So] Source:Am J Physiol Gastrointest Liver Physiol;309(4):G216-28, 2015 Aug 15.
[Is] ISSN:1522-1547
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The esophagus is a relatively simple organ that evolved to transport food and liquids through the thoracic cavity. It is the only part of the gastrointestinal tract that lacks any metabolic, digestive, or absorptive function. The mucosa of the adult esophagus is covered by a multilayered squamous epithelium with a remarkable similarity to the epithelium of the skin despite the fact that these tissues originate from two different germ layers. Here we review the developmental pathways involved in the establishment of the esophagus and the way these pathways regulate gut-airway separation. We summarize current knowledge of the mechanisms that maintain homeostasis in esophageal epithelial renewal in the adult and the molecular mechanism of the development of Barrett's metaplasia, the precursor lesion to esophageal adenocarcinoma. Finally, we examine the ongoing debate on the hierarchy of esophageal epithelial precursor cells and on the presence or absence of a specific esophageal stem cell population. Together the recent insights into esophageal development and homeostasis suggest that the pathways that establish the esophagus during development also play a role in the maintenance of the adult epithelium. We are beginning to understand how reflux of gastric content and the resulting chronic inflammation can transform the squamous esophageal epithelium to columnar intestinal type metaplasia in Barrett's esophagus.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1508
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1152/ajpgi.00088.2015

  4 / 258443 MEDLINE  
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[PMID]: 26124168
[Au] Autor:Wagers PO; Tiemann KM; Shelton KL; Kofron WG; Panzner MJ; Wooley KL; Youngs WJ; Hunstad DA
[Ad] Address:Department of Chemistry and Center for Silver Therapeutics Research, University of Akron, Akron, Ohio, USA....
[Ti] Title:Imidazolium Salts as Small-Molecule Urinary Bladder Exfoliants in a Murine Model.
[So] Source:Antimicrob Agents Chemother;59(9):5494-502, 2015 Sep.
[Is] ISSN:1098-6596
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:We present a novel family of small-molecule urinary bladder exfoliants that are expected to be of great value in preclinical studies of urologic conditions and have improved potential for translation compared with prior agents. There is broad urologic interest in the therapeutic potential of such exfoliating agents. The primary agent used in preclinical models, the cationic peptide protamine sulfate (PS), has limited translational potential due to concerns including systemic adverse reactions and bladder tissue injury. Intravesical application of a safe, systemically nontoxic exfoliant would have potential utility in the eradication of Escherichia coli and other uropathogens that reside in the bladder epithelium following cystitis, as well as in chronic bladder pain and bladder cancer. Here, we introduce a family of imidazolium salts with potent and focused exfoliating activity on the bladder epithelium. Synthesis and purification were straightforward and scalable, and the compounds exhibited prolonged stability in lyophilized form. Most members of the compound family were cytotoxic to cultured uroepithelial cells, with >10-fold differences in potency across the series. Upon topical (intravesical) administration of selected compounds to the murine bladder, complete epithelial exfoliation was achieved with physiologically relevant imidazolium concentrations and brief contact times. The exfoliative activity of these compounds was markedly improved in comparison to PS, as assessed by microscopy, immunofluorescence, and immunoblotting for uroplakins. Bladder uroepithelium regenerated within days to yield a histologically normal appearance, and no toxicity was observed. Finally, the chemical scaffold offers an opportunity for inclusion of antimicrobials or conjugation with chemotherapeutic or other moieties.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1508
[Cu] Class update date: 150815
[Lr] Last revision date:150815
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1128/AAC.00881-15

  5 / 258443 MEDLINE  
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[PMID]: 26269737
[Au] Autor:Larraaga JJ; Sahovaler A; Picco PI; Mazzaro EL; Figari MF
[Ad] Address:Division of Head and Neck, Department of General Surgery, Hospital Italiano de Buenos Aires, Buenos Aires, Argentina....
[Ti] Title:Management Issues in the Treatment of an Ameloblastoma with an Atypical Presentation.
[So] Source:Craniomaxillofac Trauma Reconstr;8(3):257-61, 2015 Sep.
[Is] ISSN:1943-3875
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Benign ameloblastoma (BA) is the most common tumor arising from the odontogenic epithelium. Surgical resection with adequate margins is the mainstay of treatment due to the high index of tumor recurrence when not completely excised. Although locoregional spread has been described in the literature, it is very uncommon. We describe the treatment and follow-up of a 22-year-old woman with multiple recurrences and locoregional spread of a mandibular ameloblastoma who was referred to our center after several tumor resections with subsequent reconstructions. After a complete macroscopical removal of a new recurrence, the mandible was primarily reconstructed. A local homolateral recurrence and a second lesion in the contralateral maxilla were detected after 1-year follow-up and accordingly treated. After 4 years the patient showed a new tumor in the temporal fossa and was reoperated. The histopathology was consistent with a BA in all cases. Even though it is rare, locoregional spread of BA has been reported previously. Recurrences discovered during follow-up may require further resections. A close follow-up is mandatory, and treatment of these cases may result demanding requiring a multiple team approach, including oncologists and radiotherapists.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1508
[Cu] Class update date: 150815
[Lr] Last revision date:150815
[Da] Date of entry for processing:150813
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.1055/s-0035-1549012

  6 / 258443 MEDLINE  
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[PMID]: 26109068
[Au] Autor:Mongan M; Meng Q; Wang J; Kao WW; Puga A; Xia Y
[Ad] Address:From the Departments of Environmental Health and....
[Ti] Title:Gene-Environment Interactions Target Mitogen-activated Protein 3 Kinase 1 (MAP3K1) Signaling in Eyelid Morphogenesis.
[So] Source:J Biol Chem;290(32):19770-9, 2015 Aug 7.
[Is] ISSN:1083-351X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Gene-environment interactions determine the biological outcomes through mechanisms that are poorly understood. Mouse embryonic eyelid closure is a well defined model to study the genetic control of developmental programs. Using this model, we investigated how exposure to dioxin-like environmental pollutants modifies the genetic risk of developmental abnormalities. Our studies reveal that mitogen-activated protein 3 kinase 1 (MAP3K1) signaling is a focal point of gene-environment cross-talk. Dioxin exposure, acting through the aryl hydrocarbon receptor (AHR), blocked eyelid closure in genetic mutants in which MAP3K1 signaling was attenuated but did not disturb this developmental program in either wild type or mutant mice with attenuated epidermal growth factor receptor or WNT signaling. Exposure also markedly inhibited c-Jun phosphorylation in Map3k1(+/-) embryonic eyelid epithelium, suggesting that dioxin-induced AHR pathways can synergize with gene mutations to inhibit MAP3K1 signaling. Our studies uncover a novel mechanism through which the dioxin-AHR axis interacts with the MAP3K1 signaling pathways during fetal development and provide strong empirical evidence that specific gene alterations can increase the risk of developmental abnormalities driven by environmental pollutant exposure.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1508
[Cu] Class update date: 150815
[Lr] Last revision date:150815
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1074/jbc.M115.665729

  7 / 258443 MEDLINE  
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[PMID]: 26195794
[Au] Autor:Murata Y; Kotani T; Supriatna Y; Kitamura Y; Imada S; Kawahara K; Nishio M; Daniwijaya EW; Sadakata H; Kusakari S; Mori M; Kanazawa Y; Saito Y; Okawa K; Takeda-Morishita M; Okazawa H; Ohnishi H; Azuma T; Suzuki A; Matozaki T
[Ad] Address:Division of Molecular and Cellular Signaling, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan;...
[Ti] Title:Protein tyrosine phosphatase SAP-1 protects against colitis through regulation of CEACAM20 in the intestinal epithelium.
[So] Source:Proc Natl Acad Sci U S A;112(31):E4264-71, 2015 Aug 4.
[Is] ISSN:1091-6490
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Intestinal epithelial cells contribute to regulation of intestinal immunity in mammals, but the detailed molecular mechanisms of such regulation have remained largely unknown. Stomach-cancer-associated protein tyrosine phosphatase 1 (SAP-1, also known as PTPRH) is a receptor-type protein tyrosine phosphatase that is localized specifically at microvilli of the brush border in gastrointestinal epithelial cells. Here we show that SAP-1 ablation in interleukin (IL)-10-deficient mice, a model of inflammatory bowel disease, resulted in a marked increase in the severity of colitis in association with up-regulation of mRNAs for various cytokines and chemokines in the colon. Tyrosine phosphorylation of carcinoembryonic antigen-related cell adhesion molecule (CEACAM) 20, an intestinal microvillus-specific transmembrane protein of the Ig superfamily, was greatly increased in the intestinal epithelium of the SAP-1-deficient animals, suggesting that this protein is a substrate for SAP-1. Tyrosine phosphorylation of CEACAM20 by the protein tyrosine kinase c-Src and the consequent association of CEACAM20 with spleen tyrosine kinase (Syk) promoted the production of IL-8 in cultured cells through the activation of nuclear factor-κB (NF-κB). In addition, SAP-1 and CEACAM20 were found to form a complex through interaction of their ectodomains. SAP-1 and CEACAM20 thus constitute a regulatory system through which the intestinal epithelium contributes to intestinal immunity.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1508
[Cu] Class update date: 150815
[Lr] Last revision date:150815
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1073/pnas.1510167112

  8 / 258443 MEDLINE  
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[PMID]: 25979994
[Au] Autor:Jansen F; Kalbe B; Scholz P; Frnzel B; Osterloh M; Wolters D; Hatt H; Neuhaus EM; Osterloh S
[Ad] Address:From the Department of Cell Physiology, Faculty for Biology and Biotechnology....
[Ti] Title:Biochemical Large-Scale Interaction Analysis of Murine Olfactory Receptors and Associated Signaling Proteins with Post-Synaptic Density 95, Drosophila Discs Large, Zona-Occludens 1 (PDZ) Domains.
[So] Source:Mol Cell Proteomics;14(8):2072-84, 2015 Aug.
[Is] ISSN:1535-9484
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:G protein-coupled receptors (GPCRs) constitute the largest family among mammalian membrane proteins and are capable of initiating numerous essential signaling cascades. Various GPCR-mediated pathways are organized into protein microdomains that can be orchestrated and regulated through scaffolding proteins, such as PSD-95/discs-large/ZO1 (PDZ) domain proteins. However, detailed binding characteristics of PDZ-GPCR interactions remain elusive because these interactions seem to be more complex than previously thought. To address this issue, we analyzed binding modalities using our established model system. This system includes the 13 individual PDZ domains of the multiple PDZ domain protein 1 (MUPP1; the largest PDZ protein), a broad range of murine olfactory receptors (a multifaceted gene cluster within the family of GPCRs), and associated olfactory signaling proteins. These proteins were analyzed in a large-scale peptide microarray approach and continuative interaction studies. As a result, we demonstrate that canonical binding motifs were not overrepresented among the interaction partners of MUPP1. Furthermore, C-terminal phosphorylation and distinct amino acid replacements abolished PDZ binding promiscuity. In addition to the described in vitro experiments, we identified new interaction partners within the murine olfactory epithelium using pull-down-based interactomics and could verify the partners through co-immunoprecipitation. In summary, the present study provides important insight into the complexity of the binding characteristics of PDZ-GPCR interactions based on olfactory signaling proteins, which could identify novel clinical targets for GPCR-associated diseases in the future.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1508
[Cu] Class update date: 150815
[Lr] Last revision date:150815
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1074/mcp.M114.045997

  9 / 258443 MEDLINE  
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[PMID]: 26063583
[Au] Autor:Malta M; Ribeiro J; Monteiro P; Loureiro J; Medeiros R; Sousa H
[Ad] Address:Faculty of Science, University of Porto, Rua do Campo Alegre, Porto, 4169-007, Portugal.
[Ti] Title:Let-7c is a Candidate Biomarker for Cervical Intraepithelial Lesions: A Pilot Study.
[So] Source:Mol Diagn Ther;19(3):191-6, 2015 Jun.
[Is] ISSN:1179-2000
[Cp] Country of publication:New Zealand
[La] Language:eng
[Ab] Abstract:BACKGROUND: Numerous studies have been performed to discover predictive/prognostic biomarkers for human papillomavirus (HPV) infection and cervical cancer development. More recently, microRNAs were suggested as possible biomarkers of HPV-associated cancers and our aim was to characterize the expression of let-7c in exfoliated cervical cells from women with cervical intraepithelial lesions. METHODS: Let-7c expression was evaluated by quantitative reverse transcription-polymerase chain reaction in 73 women with normal or cervical intraepithelial lesions: normal epithelium with (n = 17) and without (n = 21) HPV infection; low-grade squamous intraepithelial lesions (n = 14); and high-grade squamous intraepithelial lesions (n = 21). RESULTS: Data showed a trend to down-regulation in women with low-grade squamous intraepithelial lesions (2(-ΔΔCt) = 0.38, p = 0.06) and a significant decreased expression of let-7c in women with low-grade squamous intraepithelial lesions (2(-ΔΔCt) = 0.21; p = 0.004). The combined analysis of all cervical intraepithelial lesions revealed a down-regulation of let-7c expression (2(-ΔΔCt) = 0.27; p = 0.011). CONCLUSION: Our results showed that let-7c expression is significantly changed in the different cervical intraepithelial lesions and its levels should be further investigated as a possible biomarker for cervical intraepithelial lesions using exfoliated cervical cells as the sample source.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1007/s40291-015-0145-4

  10 / 258443 MEDLINE  
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[PMID]: 26080254
[Au] Autor:Durmaz A; Yildizoglu ; Polat B; Binar M
[Ad] Address:Department of Otolaryngology, Gulhane Military Medical Academy, Etlik, Ankara, Turkey.
[Ti] Title:A Middle Cranial Fossa Dermoid Cyst Treated by an Endonasal Endoscopic Approach.
[So] Source:J Craniofac Surg;26(4):e333-5, 2015 Jun.
[Is] ISSN:1536-3732
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Dermoid cysts are rare, benign, congenital ectodermal inclusion cysts in the skull base, comprising skin supplements surrounded by squamous epithelium. In the period of embryological development, the cysts originate from ectodermal cells left behind in the cranial region by the closure of the neural tube and are primarily located at the midline, especially in the subarachnoid spaces. These lesions are usually asymptomatic and diagnosed incidentally. When the cysts reach large sizes, they can be symptomatic due to infection, rupture, or mass effect around neurovascular tissue. The cysts typically demonstrate accurate radiological diagnostic features. In this case report, we present a rare dermoid cyst in the middle cranial fossa, treated by an endonasal endoscopic approach. The endonasal endoscopic management of appropriate middle cranial fossa is discussed as a recent advance in the extended applications of endoscopic sinus surgery.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Js] Journal subset:D
[St] Status:In-Process
[do] DOI:10.1097/SCS.0000000000001737


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