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[PMID]: 25029617
[Au] Autor:Marinkovic G; Hamers AA; de Vries CJ; de Waard V
[Ad] Address:Department of Medical Biochemistry, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
[Ti] Title:6-Mercaptopurine Reduces Macrophage Activation and Gut Epithelium Proliferation Through Inhibition of GTPase Rac1.
[So] Source:Inflamm Bowel Dis;20(9):1487-95, 2014 Sep.
[Is] ISSN:1536-4844
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Inflammatory bowel disease is characterized by chronic intestinal inflammation. Azathioprine and its metabolite 6-mercaptopurine (6-MP) are effective immunosuppressive drugs that are widely used in patients with inflammatory bowel disease. However, established understanding of their immunosuppressive mechanism is limited. Azathioprine and 6-MP have been shown to affect small GTPase Rac1 in T cells and endothelial cells, whereas the effect on macrophages and gut epithelial cells is unknown. METHODS: Macrophages (RAW cells) and gut epithelial cells (Caco-2 cells) were activated by cytokines and the effect on Rac1 signaling was assessed in the presence or absence of 6-MP. RESULTS: Rac1 is activated in macrophages and epithelial cells, and treatment with 6-MP resulted in Rac1 inhibition. In macrophages, interferon-γ induced downstream signaling through c-Jun-N-terminal Kinase (JNK) resulting in inducible nitric oxide synthase (iNOS) expression. iNOS expression was reduced by 6-MP in a Rac1-dependent manner. In epithelial cells, 6-MP efficiently inhibited tumor necrosis factor-α-induced expression of the chemokines CCL2 and interleukin-8, although only interleukin-8 expression was inhibited in a Rac1-dependent manner. In addition, activation of the transcription factor STAT3 was suppressed in a Rac1-dependent fashion by 6-MP, resulting in reduced proliferation of the epithelial cells due to diminished cyclin D1 expression. CONCLUSIONS: These data demonstrate that 6-MP affects macrophages and gut epithelial cells beneficially, in addition to T cells and endothelial cells. Furthermore, mechanistic insight is provided to support development of Rac1-specific inhibitors for clinical use in inflammatory bowel disease.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1097/MIB.0000000000000122

  2 / 249738 MEDLINE  
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[PMID]: 25128495
[Au] Autor:Fukuda M; Mizutani T; Mochizuki W; Matsumoto T; Nozaki K; Sakamaki Y; Ichinose S; Okada Y; Tanaka T; Watanabe M; Nakamura T
[Ad] Address:Department of Gastroenterology and Hepatology....
[Ti] Title:Small intestinal stem cell identity is maintained with functional Paneth cells in heterotopically grafted epithelium onto the colon.
[So] Source:Genes Dev;28(16):1752-7, 2014 Aug 15.
[Is] ISSN:1549-5477
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:To develop stem cell therapy for small intestinal (SI) diseases, it is essential to determine whether SI stem cells in culture retain their tissue regeneration capabilities. By using a heterotopic transplantation approach, we show that cultured murine SI epithelial organoids are able to reconstitute self-renewing epithelia in the colon. When stably integrated, the SI-derived grafts show many features unique only to the SI but distinct from the colonic epithelium. Our study provides evidence that cultured adult SI stem cells could be a source for cell therapy of intestinal diseases, maintaining their identity along the gastrointestinal tract through an epithelium-intrinsic mechanism.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1101/gad.245233.114

  3 / 249738 MEDLINE  
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[PMID]: 25056732
[Au] Autor:Franceschini V; Bettini S; Pifferi S; Menini A; Siciliano G; Ognio E; Brini AT; Di Oto E; Revoltella RP
[Ad] Address:Department of Biological, Geological and Environmental Sciences, University of Bologna, and Foundation Onlus Stem Cells and Life, Via Selmi 3, 40126 Bologna, Italy, valeria.franceschini@unibo.it....
[Ti] Title:Transplanted human adipose tissue-derived stem cells engraft and induce regeneration in mice olfactory neuroepithelium in response to dichlobenil subministration.
[So] Source:Chem Senses;39(7):617-29, 2014 Sep.
[Is] ISSN:1464-3553
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:We used immunodeficient mice, whose dorsomedial olfactory region was permanently damaged by dichlobenil inoculation, to test the neuroregenerative properties of transplanted human adipose tissue-derived stem cells after 30 and 60 days. Analysis of polymerase chain reaction bands revealed that stem cells preferentially engrafted in the lesioned olfactory epithelium compared with undamaged mucosa of untreated transplanted mice. Although basal cell proliferation in untransplanted lesioned mice did not give rise to neuronal cells in the olfactory mucosa, we observed clusters of differentiating olfactory cells in transplanted mice. After 30 days, and even more at 60 days, epithelial thickness was partially recovered to normal values, as also the immunohistochemical properties. Functional reactivity to odorant stimulation was also confirmed through electro-olfactogram recording in the dorsomedial epithelium. Furthermore, we demonstrated that engrafted stem cells fused with mouse cells in the olfactory organ, even if heterokaryons detected were too rare to hypothesize they directly repopulated the lesioned epithelium. The data reported prove that the migrating transplanted stem cells were able to induce a neuroregenerative process in a specific lesioned sensory area, enforcing the perspective that they could become an available tool for stem cell therapy.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1093/chemse/bju035

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[PMID]: 25126792
[Au] Autor:Morris SA; Cahan P; Li H; Zhao AM; San Roman AK; Shivdasani RA; Collins JJ; Daley GQ
[Ad] Address:Stem Cell Transplantation Program, Division of Pediatric Hematology and Oncology, Manton Center for Orphan Disease Research, Howard Hughes Medical Institute, Boston Children's Hospital and Dana Farber Cancer Institute, Boston, MA 02115, USA; Department of Biological Chemistry and Molecular Pharmacol...
[Ti] Title:Dissecting Engineered Cell Types and Enhancing Cell Fate Conversion via CellNet.
[So] Source:Cell;158(4):889-902, 2014 Aug 14.
[Is] ISSN:1097-4172
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Engineering clinically relevant cells in vitro holds promise for regenerative medicine, but most protocols fail to faithfully recapitulate target cell properties. To address this, we developed CellNet, a network biology platform that determines whether engineered cells are equivalent to their target tissues, diagnoses aberrant gene regulatory networks, and prioritizes candidate transcriptional regulators to enhance engineered conversions. Using CellNet, we improved B cell to macrophage conversion, transcriptionally and functionally, by knocking down predicted B cell regulators. Analyzing conversion of fibroblasts to induced hepatocytes (iHeps), CellNet revealed an unexpected intestinal program regulated by the master regulator Cdx2. We observed long-term functional engraftment of mouse colon by iHeps, thereby establishing their broader potential as endoderm progenitors and demonstrating direct conversion of fibroblasts into intestinal epithelium. Our studies illustrate how CellNet can be employed to improve direct conversion and to uncover unappreciated properties of engineered cells.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review

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[PMID]: 25063195
[Au] Autor:Seppala M; Xavier GM; Fan CM; Cobourne MT
[Ad] Address:Department of Craniofacial Development and Stem Cell Biology, King's College London Dental Institute, Guy's Hospital, London SE1 9RT, UK Department of Orthodontics, King's College London Dental Institute, Guy's Hospital, London SE1 9RT, UK....
[Ti] Title:Boc modifies the spectrum of holoprosencephaly in the absence of Gas1 function.
[So] Source:Biol Open;3(8):728-40, 2014.
[Is] ISSN:2046-6390
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Holoprosencephaly is a heterogeneous developmental malformation of the central nervous system characterized by impaired forebrain cleavage, midline facial anomalies and wide phenotypic variation. Indeed, microforms represent the mildest manifestation, associated with facial anomalies but an intact central nervous system. In many cases, perturbations in sonic hedgehog signaling are responsible for holoprosencephaly. Here, we have elucidated the contribution of Gas1 and an additional hedgehog co-receptor, Boc during early development of the craniofacial midline, by generating single and compound mutant mice. Significantly, we find Boc has an essential role in the etiology of a unique form of lobar holoprosencephaly that only occurs in conjunction with combined loss of Gas1. Whilst Gas1(-/-) mice have microform holoprosencephaly characterized by a single median maxillary central incisor, cleft palate and pituitary anomalies, Boc(-/-) mice have a normal facial midline. However, Gas1(-/-); Boc(-/-) mutants have lobar holoprosencephaly associated with clefting of the lip, palate and tongue, secondary to reduced sonic hedgehog transduction in the central nervous system and face. Moreover, maxillary incisor development is severely disrupted in these mice, arresting prior to cellular differentiation as a result of apoptosis in the odontogenic epithelium. Thus, Boc and Gas1 retain an essential function in these tooth germs, independent of their role in midline development of the central nervous system and face. Collectively, this phenotype demonstrates both redundancy and individual requirements for Gas1 and Boc during sonic hedgehog transduction in the craniofacial midline and suggests BOC as a potential digenic locus for lobar holoprosencephaly in human populations.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Da] Date of entry for processing:140816
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.1242/bio.20147989

  6 / 249738 MEDLINE  
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[PMID]: 25029666
[Au] Autor:Birket SE; Chu KK; Liu L; Houser GH; Diephuis BJ; Wilsterman EJ; Dierksen G; Mazur M; Shastry S; Li Y; Watson JD; Smith AT; Schuster BS; Hanes J; Grizzle WE; Sorscher EJ; Tearney GJ; Rowe SM
[Ad] Address:1 Department of Medicine.
[Ti] Title:A functional anatomic defect of the cystic fibrosis airway.
[So] Source:Am J Respir Crit Care Med;190(4):421-32, 2014 Aug 15.
[Is] ISSN:1535-4970
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:RATIONALE: The mechanisms underlying cystic fibrosis (CF) lung disease pathogenesis are unknown. OBJECTIVES: To establish mechanisms linking anion transport with the functional microanatomy, we evaluated normal and CF piglet trachea as well as adult swine trachea in the presence of selective anion inhibitors. METHODS: We investigated airway functional microanatomy using microoptical coherence tomography, a new imaging modality that concurrently quantifies multiple functional parameters of airway epithelium in a colocalized fashion. MEASUREMENTS AND MAIN RESULTS: Tracheal explants from wild-type swine demonstrated a direct link between periciliary liquid (PCL) hydration and mucociliary transport (MCT) rates, a relationship frequently invoked but never experimentally confirmed. However, in CF airways this relationship was completely disrupted, with greater PCL depths associated with slowest transport rates. This disrupted relationship was recapitulated by selectively inhibiting bicarbonate transport in vitro and ex vivo. CF mucus exhibited increased viscosity in situ due to the absence of bicarbonate transport, explaining defective MCT that occurs even in the presence of adequate PCL hydration. CONCLUSIONS: An inherent defect in CF airway surface liquid contributes to delayed MCT beyond that caused by airway dehydration alone and identifies a fundamental mechanism underlying the pathogenesis of CF lung disease in the absence of antecedent infection or inflammation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.1164/rccm.201404-0670OC

  7 / 249738 MEDLINE  
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[PMID]: 25114863
[Au] Autor:De Sibio MT; de Oliveira M; Moretto FC; Olimpio RM; Conde SJ; Luvizon AC; Nogueira CR
[Ad] Address:Maria Teresa De Sibio, Miriane de Oliveira, Fernanda Cristina Fontes Moretto, Regiane Marques Castro Olimpio, Sandro José Conde, Célia Regina Nogueira, Department of Internal Medicine, Botucatu Medical School, Univ Estadual Paulista-UNESP, Botucatu, SP 18618-970, Brazil....
[Ti] Title:Triiodothyronine and breast cancer.
[So] Source:World J Clin Oncol;5(3):503-8, 2014 Aug 10.
[Is] ISSN:2218-4333
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The thyroid hormones (THs), triiodothyronine (T3) and thyroxine (T4), are essential for survival; they are involved in the processes of development, growth, and metabolism. In addition to hyperthyroidism or hypothyroidism, THs are involved in other diseases. The role of THs in the development and differentiation of mammary epithelium is well established; however, their specific role in the pathogenesis of breast cancer (BC) is controversial. Steroid hormones affect many human cancers and the abnormal responsiveness of the mammary epithelial cells to estradiol (E2) in particular is known to be an important cause for the development and progression of BC. The proliferative effect of T3 has been demonstrated in various types of cancer. In BC cell lines, T3 may foster the conditions for tumor proliferation and increase the effect of cell proliferation by E2; thus, T3 may play a role in the development and progression of BC. Studies show that T3 has effects similar to E2 in BC cell lines. Despite controversy regarding the relationship between thyroid disturbances and the incidence of BC, studies show that thyroid status may influence the development of tumor, proliferation and metastasis.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1408
[Cu] Class update date: 140815
[Lr] Last revision date:140815
[Da] Date of entry for processing:140812
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.5306/wjco.v5.i3.503

  8 / 249738 MEDLINE  
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[PMID]: 25114495
[Au] Autor:Mazzotta C; Ramovecchi V
[Ad] Address:Unità Operativa Complessa di Oculistica, Siena University Hospital, Siena, Italy.
[Ti] Title:Customized epithelial debridement for thin ectatic corneas undergoing corneal cross-linking: epithelial island cross-linking technique.
[So] Source:Clin Ophthalmol;8:1337-43, 2014.
[Is] ISSN:1177-5467
[Cp] Country of publication:New Zealand
[La] Language:eng
[Ab] Abstract:Thin corneas with a minimum corneal thickness less than 400 µm after epithelial removal represent a contraindication to standard epithelium-off cross-linking (CXL) treatment due to a significant endothelial cell density decrease and potentiality of permanent haze development. Preoperative swelling of the cornea with hypoosmolar riboflavin solutions broadens the spectrum of CXL indications to thin corneas. However the iatrogenic swelling effect might not be durable throughout the CXL procedure increasing the risk of postoperative complications. The transepithelial CXL technique proposed for thin corneas demonstrated poor clinical results and mid- to long-term keratoconus instability. The epithelial island CXL technique with customized pachymetry-guided epithelial debridement was evaluated by means of in vivo laser scanning confocal microscopy, corneal topography, and clinical examination in a 1-year follow-up, in order to assess if it may be considered an alternative surgical option for keratoconic patients with thin corneas undergoing corneal collagen CXL. According to our clinical and in-vivo micro-morphological results the technique results safe, and efficacious in stabilizing progressive keratoconus and may be considered a valid option in the treatment of thin ectatic corneas alone or in combination with hypoosmolar or dextran-free riboflavin solutions.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Cu] Class update date: 140815
[Lr] Last revision date:140815
[Da] Date of entry for processing:140812
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.2147/OPTH.S66372

  9 / 249738 MEDLINE  
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[PMID]: 25114809
[Au] Autor:Borgonovo AE; Bernardini L; Francinetti P; Rizza F; Re D
[Ad] Address:Department of Oral Surgery, Fondazione IRCCS Ca' Granda, Ospedale Maggiore Policlinico, Via Commenda 10, 20122 Milan, Italy....
[Ti] Title:Odontogenic keratocyst mimicking paradental cyst.
[So] Source:Case Rep Dent;2014:974241, 2014.
[Is] ISSN:2090-6447
[Cp] Country of publication:Egypt
[La] Language:eng
[Ab] Abstract:Objective. The aim of this paper is to present an uncommon clinical and radiographic aspect of odontogenic keratocyst (OKC) mimicking paradental cyst. Methods. A 32-year-old female patient showed a well-delimited radiolucent lesion connected with the root of the left third molar with close anatomical relationship with the mandibular canal. The clinical, radiographic, and anamnestic features lead us to diagnose a paradental cyst that was treated by enucleation after extraction of the partially impacted tooth. Results. Histological analysis showed typical histological features of PKC such as the presence of a lining of stratified squamous epithelium with a well-defined basal layer of palisading columnar of cuboidal cells. Conclusion. Initial X-ray analysis and the position of the lesion related to the third mandibular tooth caused us to mistakenly diagnose a paradental cyst. We were only able to identify the cyst as an PKC rather than a paradental cyst after histological analysis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Cu] Class update date: 140815
[Lr] Last revision date:140815
[Da] Date of entry for processing:140812
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.1155/2014/974241

  10 / 249738 MEDLINE  
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[PMID]: 25114926
[Au] Autor:Wang XP; Cheng ZY; Schmid KL
[Ad] Address:The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, Qilu Hospital, Shandong University, Jinan, Shandong 250012, China.
[Ti] Title:GABAB Receptors Expressed in Human Aortic Endothelial Cells Mediate Intracellular Calcium Concentration Regulation and Endothelial Nitric Oxide Synthase Translocation.
[So] Source:Biomed Res Int;2014:871735, 2014.
[Is] ISSN:2314-6141
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:GABAB receptors regulate the intracellular Ca(2+) concentration ([Ca(2+)]i) in a number of cells (e.g., retina, airway epithelium and smooth muscle), but whether they are expressed in vascular endothelial cells and similarly regulate the [Ca(2+)]i is not known. The purpose of this study was to investigate the expression of GABAB receptors, a subclass of receptors to the inhibitory neurotransmitter γ-aminobutyric acid (GABA), in cultured human aortic endothelial cells (HAECs), and to explore if altering receptor activation modified [Ca(2+)]i and endothelial nitric oxide synthase (eNOS) translocation. Real-time PCR, western blots and immunofluorescence were used to determine the expression of GABAB1 and GABAB2 in cultured HAECs. The effects of GABAB receptors on [Ca(2+)]i in cultured HAECs were demonstrated using fluo-3. The influence of GABAB receptors on eNOS translocation was assessed by immunocytochemistry. Both GABAB1 and GABAB2 mRNA and protein were expressed in cultured HAECs, and the GABAB1 and GABAB2 proteins were colocated in the cell membrane and cytoplasm. One hundred µM baclofen caused a transient increase of [Ca(2+)]i and eNOS translocation in cultured HAECs, and the effects were attenuated by pretreatment with the selective GABAB receptor antagonists CGP46381 and CGP55845. GABAB receptors are expressed in HAECs and regulate the [Ca(2+)]i and eNOS translocation. Cultures of HAECs may be a useful in vitro model for the study of GABAB receptors and vascular biology.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1155/2014/871735


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