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Wavelength and solvent independent photochemistry: the electrocyclic ring-closure of indolylfulgides
Cordes, Thorben,Herzog, Teja T.,Malkmus, Stephan,Draxler, Simone,Brust, Thomas,Digirolamo, Jessica A.,Lees, Watson J.,Braun, Markus Korean Society of Photoscience 2009 Photochemical & photobiological sciences Vol.8 No.4
A wavelength and solvent dependent study of a photochromic indolylfulgide is presented. The ring-closure reaction is characterized using stationary and time-resolved spectroscopy with femtosecond time resolution. After excitation into the first excited singlet state ($S_1$) the photoprocesses proceed on ultrafast timescales (0.3-0.45 ps) in both polar and non-polar solvents. Excitation into higher electronic states results in similar reaction kinetics as found for $S_1$ excitation. A simple kinetic scheme can be established for the photoprocesses under all different experimental conditions: as expected from organic textbooks neither the solvent surroundings nor the excitation wavelength strongly alter the reaction scheme. The experimental study demonstrates that the ring-closure reaction of photochromic indolylfulgides can be considered as a very robust photoprocess: this fact may lead to a great variety of different applications where the reaction dynamics of the molecular switch are not disturbed by any surrounding effects.
Follicular stimulating hormone enhances Notch 1 expression in SK-OV-3 ovarian cancer cells
박영한,김수진,정병훈,Thomas J Herzog,Jason Wright,Jan Kitajewski,임채춘,장봉림,강정배,김성주 대한부인종양학회 2010 Journal of Gynecologic Oncology Vol.21 No.2
Objective: Notch is known as a transmembranous receptor family with four homologous forms - Notch 1, Notch 2,Notch 3, and Notch 4 and related to cell fate regulation and angiogenesis. The purpose is to investigate the effect of follicular stimulating hormone (FSH) on the Notch 1 expression and proliferation in ovarian cancer cells. Methods: Human ovarian cancer cell line, SK-OV-3 and FSH were used. XTT cell proliferation and cell migration assay were carried out with FSH 100 mIU/mL and Notch 1 siRNA. Western blots and reverse transcriptase-polymerase chain reactions (RT-PCR) were carried out to determine the expression level of the Notch 1 protein and mRNA with FSH treatment in 0, 1, 5, 10, 100, 200, 300 mIU/mL concentrations. Immunofluorescent (IF) stains were performed in SK-OV-3 cell cultures with FSH 100 mIU/mL. Student-t tests were used in statistical analyses. Results: The SK-OV-3 have Notch 1 receptors in their natural status. FSH stimulated SK-OV-3 cells in XTT cell proliferation and cell migration assays and notch 1 siRNA inhibited. The expression level of Notch 1 protein and mRNA were increased in a dose dependent pattern according to FSH concentrations compared to untreated cells. IF stains also showed brighter Notch1 expressions in the FSH treated cells compared to the control cells. Conclusion: FSH enhances proliferation & migration and Notch 1 signaling in SK-OV-3 cells. The Notch signaling probably supports one of the cell proliferating mechanisms of FSH in ovarian cancer cells.
Syndecan-4 regulates ADAMTS-5 activation and cartilage breakdown in osteoarthritis
Echtermeyer, Frank,Bertrand, Jessica,Dreier, Rita,Meinecke, Ingmar,Neugebauer, Katja,Fuerst, Martin,Lee, Yun Jong,Song, Yeong Wook,Herzog, Christine,Theilmeier, Gregor,Pap, Thomas Nature Publishing Group 2009 Nature medicine Vol.15 No.9
Aggrecan cleavage by a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 5 (ADAMTS-5) is crucial for the breakdown of cartilage matrix during osteoarthritis, a degenerative joint disease that leads to the progressive destruction of articular structures. The mechanisms of ADAMTS-5 activation and their links to the pathogenesis of osteoarthritis remain poorly understood, but syndecans have been shown to be involved in the activation of ADAMTS-4 (ref. 3). Here we show that syndecan-4 is specifically induced in type X collagen–producing chondrocytes both in human osteoarthritis and in murine models of the disease. The loss of syndecan-4 in genetically modified mice and intra-articular injections of syndecan-4–specific antibodies into wild-type mice protect from proteoglycan loss and thereby prevent osteoarthritic cartilage damage in a surgically induced model of osteoarthritis. The occurrence of less severe osteoarthritis-like cartilage destruction in both syndecan-4–deficient mice and syndecan-4–specific antibody–treated wild-type mice results from a marked decrease in ADAMTS-5 activity. Syndecan-4 controls the activation of ADAMTS-5 through direct interaction with the protease and through regulating mitogen-activated protein kinase (MAPK)-dependent synthesis of matrix metalloproteinase-3 (MMP-3). Our data suggest that strategies aimed at the inhibition of syndecan-4 will be of great value for the treatment of cartilage damage in osteoarthritis.