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Venalis P Maurer B Akhmetshina A Busch N Dees C Stürzl M Zwerina J Jüngel A Gay S Schett G Distler O Distler JH 《Journal of cellular and molecular medicine》2009,13(10):4185-4191
Systemic sclerosis (SSc) is a systemic autoimmune disease that is characterized by microangiopathy with progressive loss of capillaries and tissue fibrosis. Imatinib exerts potent anti-fibrotic effects and is currently evaluated in clinical trials. The aim of the present study was to exclude that the anti-fibrotic effects of imatinib are complicated by inhibitory effects on endothelial cell functions, which might augment vascular disease in SSc. Endothelial cells and mice were treated with pharmacologically relevant concentrations of imatinib. The expression of markers of vascular activation was assessed with real-time PCR. Proliferation was analysed with the cell counting experiments and the MTT assay. Apoptosis was quantified with caspase 3 assays, annexin V in vitro and with TUNEL staining in vivo. Migration was studied with scratch and transwell assays. Tube forming was investigated with the matrigel assay. Imatinib did not alter the expression of markers of vascular activation. Imatinib did not increase the percentage of annexin V positive cells or the activity of caspase 3. No reduction in proliferation or metabolic activity of endothelial cells was observed. Imatinib did not affect migration of endothelial cells and did not reduce the formation of capillary tubes. Consistent with the in vitro data, no difference in the number of apoptotic endothelial cells was observed in vivo in mice treated with imatinib. Imatinib does not inhibit activation, viability, proliferation, migration or tube forming of endothelial cells in vitro and in vivo. Thus, treatment with imatinib might not augment further endothelial cell damage in SSc. 相似文献
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Vilma Kaškonienė Paulius Kaškonas Audrius Maruška Ona Ragažinskienė 《Acta Physiologiae Plantarum》2011,33(6):2377-2385
The variation in the content and composition of essential oils of Bidens tripartita L. grown in Lithuania has been studied using supercritical CO2 extraction followed by GC–MS. Extraction of essential oils was performed at two different pressures (9.1 and 15.1 MPa). Plant
material has been harvested at different phenological stages (from June to September). A total of 26 different compounds were
identified in the essential oils. The highest content and diversity of compounds was determined during the full-flowering
stage. Identified substances were mainly monoterpene hydrocarbons and sesquiterpene hydrocarbons. The main components were
α-pinene, p-cymene, trans-β-ocimene, and β-elemene. Chemometric analysis, including principal component and hierarchical cluster analyses, showed the
dependence of the essential oils qualitative as well as quantitative composition on the phenological stage the plant was collected
at. It also revealed that there was no correlation between age of the plant and quantity of the identified compounds. 相似文献
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Sandra Münch Stefanie Weidtkamp-Peters Karolin Klement Paulius Grigaravicius Shamci Monajembashi Paolo Salomoni Pier Paolo Pandolfi Klaus Wei?hart Peter Hemmerich 《Molecular and cellular biology》2014,34(10):1733-1746
The PML tumor suppressor has been functionally implicated in DNA damage response and cellular senescence. Direct evidence for such a role based on PML knockdown or knockout approaches is still lacking. We have therefore analyzed the irradiation-induced DNA damage response and cellular senescence in human and mouse fibroblasts lacking PML. Our data show that PML nuclear bodies (NBs) nonrandomly associate with persistent DNA damage foci in unperturbed human skin and in high-dose-irradiated cell culture systems. PML bodies do not associate with transient γH2AX foci after low-dose gamma irradiation. Superresolution microscopy reveals that all PML bodies within a nucleus are engaged at Rad51- and RPA-containing repair foci during ongoing DNA repair. The lack of PML (i) does not majorly affect the DNA damage response, (ii) does not alter the efficiency of senescence induction after DNA damage, and (iii) does not affect the proliferative potential of primary mouse embryonic fibroblasts during serial passaging. Thus, while PML NBs specifically accumulate at Rad51/RPA-containing lesions and senescence-derived persistent DNA damage foci, they are not essential for DNA damage-induced and replicative senescence of human and murine fibroblasts. 相似文献
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Paulius Gibiea Eric Peterman Huxley K. Hoffman Schuyler Van Engeleburg Vytenis Arvydas Skeberdis Rytis Prekeris 《Molecular biology of the cell》2021,32(7):554
Abscission is a complex cellular process that is required for mitotic division. It is well established that coordinated and localized changes in actin and microtubule dynamics are vital for cytokinetic ring formation, as well as establishment of the abscission site. Actin cytoskeleton reorganization during abscission would not be possible without the interplay between Rab11- and Rab35-containing endosomes and their effector proteins, whose roles in regulating endocytic pathways at the cleavage furrow have now been studied extensively. Here, we identified Rab14 as a novel regulator of cytokinesis. We demonstrate that depletion of Rab14 causes either cytokinesis failure or significantly prolongs division time. We show that Rab14 contributes to the efficiency of recruiting Rab11-endosomes to the thin intracellular bridge (ICB) microtubules and that Rab14 knockout leads to inhibition of actin clearance at the abscission site. Finally, we demonstrate that Rab14 binds to microtubule minus-end interacting MACF2/CAMSAP3 complex and that this binding affects targeting of endosomes to the ICB microtubules. Collectively, our data identified Rab14 and MACF2/CAMSAP3 as proteins that regulate actin depolymerization and endosome targeting during cytokinesis. 相似文献
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Visual processing in the brain seems to provide fast but coarse information before information about fine details. Such dynamics occur also in single neurons at several levels of the visual system. In the dorsal lateral geniculate nucleus (LGN), neurons have a receptive field (RF) with antagonistic center-surround organization, and temporal changes in center-surround organization are generally assumed to be due to a time-lag of the surround activity relative to center activity. Spatial resolution may be measured as the inverse of center size, and in LGN neurons RF-center width changes during static stimulation with durations in the range of normal fixation periods (250-500 ms) between saccadic eye-movements. The RF-center is initially large, but rapidly shrinks during the first ~100 ms to a rather sustained size. We studied such dynamics in anesthetized cats during presentation (250 ms) of static spots centered on the RF with main focus on the transition from the first transient and highly dynamic component to the second more sustained component. The results suggest that the two components depend on different neuronal mechanisms that operate in parallel and with partial temporal overlap rather than on a continuously changing center-surround balance. Results from mathematical modeling further supported this conclusion. We found that existing models for the spatiotemporal RF of LGN neurons failed to account for our experimental results. The modeling demonstrated that a new model, in which the response is given by a sum of an early transient component and a partially overlapping sustained component, adequately accounts for our experimental data. 相似文献
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Paulo M. G. Rodrigues Paulius Grigaravicius Martina Remus Gabriel R. Cavalheiro Anielle L. Gomes Mauricio R. Martins Lucien Frappart David Reuss Peter J. McKinnon Andreas von Deimling Rodrigo A. P. Martins Pierre-Olivier Frappart 《PloS one》2013,8(7)
Nibrin (NBN or NBS1) and ATM are key factors for DNA Double Strand Break (DSB) signaling and repair. Mutations in NBN or ATM result in Nijmegen Breakage Syndrome and Ataxia telangiectasia. These syndromes share common features such as radiosensitivity, neurological developmental defects and cancer predisposition. However, the functional synergy of Nbn and Atm in different tissues and developmental stages is not yet understood. Here, we show in vivo consequences of conditional inactivation of both genes in neural stem/progenitor cells using Nestin-Cre mice. Genetic inactivation of Atm in the central nervous system of Nbn-deficient mice led to reduced life span and increased DSBs, resulting in increased apoptosis during neural development. Surprisingly, the increase of DSBs and apoptosis was found only in few tissues including cerebellum, ganglionic eminences and lens. In sharp contrast, we showed that apoptosis associated with Nbn deletion was prevented by simultaneous inactivation of Atm in developing retina. Therefore, we propose that Nbn and Atm collaborate to prevent DSB accumulation and apoptosis during development in a tissue- and developmental stage-specific manner. 相似文献