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  • Nature Publishing Group (NPG)  (93)
  • The American Physiological Society (APS)  (62)
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  • 1
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    Ginkgolide B inhibits renal cyst development in in vitro and in vivo cyst models (2012)
    The American Physiological Society (APS)
    Details
    Publication Date: 2012-05-16
    Description: Autosomal dominant polycystic kidney disease (ADPKD) is a common inherited disease characterized by massive enlargement of fluid-filled cysts in the kidney. However, there is no effective therapy yet for this disease. To examine whether ginkgolide B, a natural compound, inhibits cyst development, a Madin-Darby canine kidney (MDCK) cyst model, an embryonic kidney cyst model, and a PKD mouse model were used. Interestingly, ginkgolide B significantly inhibited MDCK cyst formation dose dependently, with up to 69% reduction by 2 μM ginkgolide B. Ginkgolide B also significantly inhibited cyst enlargement in the MDCK cyst model, embryonic kidney cyst model, and PKD mouse model. To determine the underlying mechanisms, the effect of ginkgolide B on MDCK cell viability, proliferation, apoptosis, chloride transporter CFTR activity, and intracellular signaling pathways were also studied. Ginkgolide B did not affect cell viability, proliferation, and expression and activity of the chloride transporter CFTR that mediates cyst fluid secretion. Ginkgolide B induced cyst cell differentiation and altered the Ras/MAPK signaling pathway. Taken together, our results demonstrate that ginkgolide B inhibits renal cyst formation and enlargement, suggesting that ginkgolide B might be developed into a novel candidate drug for ADPKD.
    Print ISSN: 1931-857X
    Electronic ISSN: 1522-1466
    Topics: Medicine
    Published by The American Physiological Society (APS)
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  • 2
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    Post-translational modifications as key regulators of TNF-induced necroptosis (2016)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2016-07-08
    Description: Post-translational modifications as key regulators of TNF-induced necroptosis Cell Death and Disease 7, e2293 (July 2016). doi:10.1038/cddis.2016.197 Authors: X Liu, F Shi, Y Li, X Yu, S Peng, W Li, X Luo & Y Cao
    Electronic ISSN: 2041-4889
    Topics: Biology , Medicine
    Published by Nature Publishing Group (NPG)
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  • 3
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    Inhibition of Notch signaling pathway attenuates sympathetic hyperinnervation together with the augmentation of M2 macrophages in rats post-myocardial infarction (2016)
    The American Physiological Society (APS)
    Details
    Publication Date: 2016-01-02
    Description: Inflammation-dominated sympathetic sprouting adjacent to the necrotic region following myocardial infarction (MI) has been implicated in the etiology of arrhythmias resulting in sudden cardiac death; however, the mechanisms responsible remain to be elucidated. Although being a key immune mediator, the role of Notch has yet to be explored. We investigated whether Notch regulates macrophage responses to inflammation and affects cardiac sympathetic reinnervation in rats undergoing MI. MI was induced by coronary artery ligation. A high level of Notch intracellular domain was observed in the macrophages that infiltrated the infarct area at 3 days post-MI. The administration of the Notch inhibitor N-N-(3,5-difluorophenacetyl- l -alanyl)-S-phenylglycine-t-butyl ester (DAPT) (intravenously 30 min before MI and then daily until death) decreased the number of macrophages and significantly increased the M2 macrophage activation profile in the early stages and attenuated the expression of nerve growth factor (NGF). Eventually, NGF-induced sympathetic hyperinnervation was blunted, as assessed by the immunofluorescence of tyrosine hydroxylase. At 7 days post-MI, the arrhythmia score of programmed electric stimulation in the vehicle-treated infarcted rats was higher than that in rats treated with DAPT. Further deterioration in cardiac function and decreases in the plasma levels of TNF-α and IL-1β were also detected. In vitro studies revealed that LPS/IFN- upregulated the surface expression of NGF in M1 macrophages in a Notch-dependent manner. We concluded that Notch inhibition during the acute inflammatory response phase is associated with the downregulation of NGF, probably through a macrophage-dependent pathway, thus preventing the process of sympathetic hyperinnervation.
    Print ISSN: 0363-6143
    Electronic ISSN: 1522-1563
    Topics: Medicine
    Published by The American Physiological Society (APS)
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  • 4
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    Differential effects of bisphenol A diglicydyl ether on bone quality and marrow adiposity in ovary-intact and ovariectomized rats (2016)
    The American Physiological Society (APS)
    Details
    Publication Date: 2016-12-03
    Description: Bisphenol A diglycidyl ether (BADGE), a PPAR2 antagonist, has been shown to inhibit marrow adipogenesis and promote bone formation in intact animals. We investigated the impact of BADGE on a new and more clinically relevant physiological model, the ovariectomized (OVX) rat model. Forty female Wistar rats were divided into four treatment groups for 12 wk ( n = 10/group): sham+vehicle, sham+BADGE, OVX+vehicle, and OVX+BADGE. Postmortem analyses included MRI, micro-CT, serological test, histomorphometry, biomechanical tests, RT-PCR, and Western blot. Overall, OVX induced a sequential marrow fat expansion accompanied by bone deterioration. Compared with OVX controls, BADGE reduced fat fraction of the distal femur by 36.3%, adipocyte density by 33.0%, adipocyte size by 28.6%, adipocyte volume percentage by 57.8%, and adipogenic markers PPAR2 and C/EBPα by ~50% in OVX rats. Similar results were observed in sham rats vs. vehicle. BADGE could promote bone quality in sham rats; however, BADGE did not significantly improve trabecular microarchitecture, biomechanical strength, and dynamic histomorphometric parameters except for trabecular separation in OVX rats. We concluded that early BADGE treatment at a dose of 30 mg/kg attenuates marrow adiposity in ovary-intact and OVX rats and stimulates bone formation in ovary-intact rats but does not significantly rescue bone quality in OVX rats.
    Print ISSN: 0193-1849
    Electronic ISSN: 1522-1555
    Topics: Medicine
    Published by The American Physiological Society (APS)
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  • 5
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    Correction: eEF-2 kinase is a critical regulator of Warbrug effect through controlling PP2A-A synthesis (2018)
    Nature Publishing Group (NPG)
    In: Oncogene
    Details
    Publication Date: 2018-07-05
    Description: Correction: eEF-2 kinase is a critical regulator of Warbrug effect through controlling PP2A-A synthesis Correction: eEF-2 kinase is a critical regulator of Warbrug effect through controlling PP2A-A synthesis, Published online: 04 July 2018; doi:10.1038/s41388-018-0322-0 Correction: eEF-2 kinase is a critical regulator of Warbrug effect through controlling PP2A-A synthesis
    Print ISSN: 0950-9232
    Topics: Medicine
    Published by Nature Publishing Group (NPG)
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  • 6
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    Sleeping beauty: awakening urothelium from its slumber (2017)
    The American Physiological Society (APS)
    Details
    Publication Date: 2017-04-08
    Description: The bladder urothelium is essentially quiescent but regenerates readily upon injury. The process of urothelial regeneration harkens back to the process of urothelial development whereby urothelial stem/progenitor cells must proliferate and terminally differentiate to establish all three urothelial layers. How the urothelium regulates the level of proliferation and the timing of differentiation to ensure the precise degree of regeneration is of significant interest in the field. Without a carefully-orchestrated process, urothelial regeneration may be inadequate, thereby exposing the host to toxins or pathogens. Alternatively, regeneration may be excessive, thereby setting the stage for tumor development. This review describes our current understanding of urothelial regeneration. The current controversies surrounding the identity and location of urothelial progenitor cells that mediate urothelial regeneration are discussed and evidence for each model is provided. We emphasize the factors that have been shown to be crucial for urothelial regeneration, including local growth factors that stimulate repair, and epithelial-mesenchymal cross talk, which ensures feedback regulation. Also highlighted is the emerging concept of epigenetic regulation of urothelial regeneration, which additionally fine tunes the process through transcriptional regulation of cell cycle genes and growth and differentiation factors. Finally, we emphasize how several of these pathways and/or programs are often dysregulated during malignant transformation, further corroborating their importance in directing normal urothelial regeneration. Together, evidence in the field suggests that any attempt to exploit regenerative programs for the purposes of enhanced urothelial repair or replacement must take into account this delicate balance.
    Print ISSN: 1931-857X
    Electronic ISSN: 1522-1466
    Topics: Medicine
    Published by The American Physiological Society (APS)
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  • 7
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    CGI-99 promotes breast cancer metastasis via autocrine interleukin-6 signaling (2017)
    Nature Publishing Group (NPG)
    In: Oncogene
    Details
    Publication Date: 2017-06-30
    Description: CGI-99 promotes breast cancer metastasis via autocrine interleukin-6 signaling Oncogene 36, 3695 (29 June 2017). doi:10.1038/onc.2016.525 Authors: C Lin, W Liao, Y Jian, Y Peng, X Zhang, L Ye, Y Cui, B Wang, X Wu, Z Xiong, S Wu, J Li, X Wang & L Song
    Print ISSN: 0950-9232
    Topics: Medicine
    Published by Nature Publishing Group (NPG)
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  • 8
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    FOXA1 inhibits prostate cancer neuroendocrine differentiation (2017)
    Nature Publishing Group (NPG)
    In: Oncogene
    Details
    Publication Date: 2017-07-14
    Description: FOXA1 inhibits prostate cancer neuroendocrine differentiation Oncogene 36, 4072 (13 July 2017). doi:10.1038/onc.2017.50 Authors: J Kim, H Jin, J C Zhao, Y A Yang, Y Li, X Yang, X Dong & J Yu
    Print ISSN: 0950-9232
    Topics: Medicine
    Published by Nature Publishing Group (NPG)
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  • 9
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    Calmodulin-dependent binding to the NHE1 cytosolic tail mediates activation of the Na+/H+ exchanger by Ca2+ and endothelin (2013)
    The American Physiological Society (APS)
    Details
    Publication Date: 2013-12-02
    Description: The mammalian Na + /H + exchanger isoform 1 (NHE1) is a ubiquitous plasma membrane protein that regulates intracellular pH by removing a single proton (H + ) in exchange for one extracellular Na + . The human protein contains a ~500-amino acid membrane domain and a regulatory, ~315-amino acid cytosolic domain. NHE1 is activated by a number of hormones including endothelin (ET) and by Ca 2+ . The regulatory tail possesses an inhibitory calmodulin (CaM)-binding domain, and inhibition of NHE1 is relieved by binding of a Ca 2+ -CaM complex. We examined the dynamics of ET-1 and Ca 2+ regulation of binding to NHE1 in vivo. CFP was linked to the NHE1 protein cytoplasmic COOH terminus. This was stably transfected into AP-1 cells that are devoid of their own NHE1 protein. The protein was expressed and targeted properly and retained NHE1 activity comparable to the wild-type protein. We examined the in vivo coupling of NHE1 to CaM by Förster resonance energy transfer using CaM linked to the fluorescent protein Venus. CaM interaction with NHE1 was dynamic. Removal of serum reduced CaM interaction with NHE1. Addition of the Ca 2+ ionophore ionomycin increased the interaction between CaM and NHE1. We expressed an ET receptor in AP-1 cells and also found a time-dependent association of NHE1 with CaM in vivo that was dependent on ET treatment. The results are the first demonstration of the in vivo association of NHE1 and CaM through ET-dependent signaling pathways.
    Print ISSN: 0363-6143
    Electronic ISSN: 1522-1563
    Topics: Medicine
    Published by The American Physiological Society (APS)
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  • 10
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    MicroRNA-100/99a, deregulated in acute lymphoblastic leukaemia, suppress proliferation and promote apoptosis by regulating the FKBP51 and IGF1R/mTOR signalling pathways (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-10-17
    Description: MicroRNA-100/99a, deregulated in acute lymphoblastic leukaemia, suppress proliferation and promote apoptosis by regulating the FKBP51 and IGF1R/mTOR signalling pathways British Journal of Cancer 109, 2189 (15 October 2013). doi:10.1038/bjc.2013.562 Authors: X-J Li, X-Q Luo, B-W Han, F-T Duan, P-P Wei & Y-Q Chen
    Keywords: acute lymphoblastic leukaemiamiRNAFKBP51 signallingIGF1R/mTOR signalling pathwayapoptosisproliferation
    Print ISSN: 0007-0920
    Electronic ISSN: 1532-1827
    Topics: Medicine
    Published by Nature Publishing Group (NPG)
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