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  • 1.
    Ibarra, Cristian
    et al.
    Karolinska Inst, Dept Med Biochem & Biophys, SE-17177 Stockholm, Sweden.
    Karlsson, Marie
    Karolinska Inst, Dept Med Biochem & Biophys, SE-17177 Stockholm, Sweden.
    Codeluppi, Simone
    Karolinska Inst, Dept Med Biochem & Biophys, SE-17177 Stockholm, Sweden;Karolinska Inst, Dept Physiol & Pharmacol, Stockholm, Sweden.
    Varas-Godoy, Manuel
    Karolinska Inst, Dept Med Biochem & Biophys, SE-17177 Stockholm, Sweden;Univ Los Andes, Ctr Invest Biomed, Fac Med, Santiago, Chile.
    Zhang, Songbai
    Karolinska Inst, Dept Med Biochem & Biophys, SE-17177 Stockholm, Sweden.
    Louhivuori, Lauri
    Karolinska Inst, Dept Med Biochem & Biophys, SE-17177 Stockholm, Sweden.
    Mangsbo, Sara
    Uppsala University, Science for Life Laboratory, SciLifeLab. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences.
    Hosseini, Arad
    Karolinska Univ Hosp, Dept Mol Med & Surg, Stockholm, Sweden.
    Soltani, Navid
    Karolinska Inst, Dept Med Biochem & Biophys, SE-17177 Stockholm, Sweden.
    Kaba, Rahim
    Karolinska Inst, Dept Med Biochem & Biophys, SE-17177 Stockholm, Sweden.
    Lundgren, T. Kalle
    Karolinska Inst, Dept Med Biochem & Biophys, SE-17177 Stockholm, Sweden.
    Hosseini, Abolfazl
    Karolinska Univ Hosp, Dept Mol Med & Surg, Stockholm, Sweden.
    Tanaka, Nobuyuki
    Karolinska Inst, Dept Med Biochem & Biophys, SE-17177 Stockholm, Sweden;Keio Univ, Sch Med, Dept Urol, Tokyo, Japan.
    Oya, Mototsugu
    Keio Univ, Sch Med, Dept Urol, Tokyo, Japan.
    Wiklund, Peter
    Karolinska Univ Hosp, Dept Mol Med & Surg, Stockholm, Sweden.
    Miyakawa, Ayako
    Karolinska Inst, Dept Med Biochem & Biophys, SE-17177 Stockholm, Sweden;Karolinska Univ Hosp, Dept Mol Med & Surg, Stockholm, Sweden.
    Uhlen, Per
    Karolinska Inst, Dept Med Biochem & Biophys, SE-17177 Stockholm, Sweden;Keio Univ, Grad Sch Med, Tokyo, Japan.
    BCG-induced cytokine release in bladder cancer cells is regulated by Ca2+ signaling2019In: Molecular Oncology, ISSN 1574-7891, E-ISSN 1878-0261, Vol. 13, no 2, p. 202-211Article in journal (Refereed)
    Abstract [en]

    Bacillus Calmette-Guerin (BCG) is widely used in the clinic to effectively treat superficial urinary bladder cancer. However, a significant proportion of patients who fail to respond to BCG risk cystectomy or death. Though more than 3 million cancer treatments with BCG occur annually, surprisingly little is known about the initial signaling cascades activated by BCG. Here, we report that BCG induces a rapid intracellular Ca2+ (calcium ion) signal in bladder cancer cells that is essential for activating the transcription factor nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappa B) and for synthesizing and secreting proinflammatory cytokines, including interleukin 8 (IL-8). A similar Ca2+ response was observed when cells were exposed to the supernatant of BCG. Studying cellular molecular mechanisms involved in the BCG signaling event, we found pivotal roles for phospholipase C and the Toll-like receptor 4. Further assessment revealed that this signaling pathway induces synthesis of IL-8, whereas exocytosis appeared to be controlled by global Ca2+ signaling. These results shed new light on the molecular mechanisms underlying BCG treatment of bladder cancer, which can help in improving therapeutic efficacy and reducing adverse side effects.

  • 2.
    Lam, Matti
    et al.
    Karolinska Inst, Dept Neurosci, Stockholm, Sweden.
    Moslem, Mohsen
    Karolinska Inst, Dept Neurosci, Stockholm, Sweden.
    Bryois, Julien
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
    Pronk, Robin J.
    Karolinska Inst, Dept Neurosci, Stockholm, Sweden.
    Uhlin, Elias
    Karolinska Inst, Dept Neurosci, Stockholm, Sweden.
    Ellström, Ivar Dehnisch
    Karolinska Inst, Dept Med Biochem & Biophys, Stockholm, Sweden.
    Laan, Loora
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Medicinsk genetik och genomik. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Olive, Jessica
    Karolinska Inst, Dept Neurosci, Stockholm, Sweden.
    Morse, Rebecca
    Karolinska Inst, Dept Neurosci, Stockholm, Sweden.
    Rönnholm, Harriet
    Karolinska Inst, Dept Neurosci, Stockholm, Sweden.
    Louhivuori, Lauri
    Karolinska Inst, Dept Med Biochem & Biophys, Stockholm, Sweden.
    Korol, Sergiy V.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Birnir: Molecular Physiology and Neuroscience.
    Dahl, Niklas
    Uppsala University, Science for Life Laboratory, SciLifeLab. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Medicinsk genetik och genomik.
    Uhlén, Per
    Karolinska Inst, Dept Med Biochem & Biophys, Stockholm, Sweden.
    Anderlid, Britt-Marie
    Karolinska Inst, Dept Mol Med & Surg, Stockholm, Sweden.
    Kele, Malin
    Karolinska Inst, Dept Neurosci, Stockholm, Sweden.
    Sullivan, Patrick F.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
    Falk, Anna
    Karolinska Inst, Dept Neurosci, Stockholm, Sweden.
    Single cell analysis of autism patient with bi-allelic NRXN1-alpha deletion reveals skewed fate choice in neural progenitors and impaired neuronal functionality2019In: Experimental Cell Research, ISSN 0014-4827, E-ISSN 1090-2422, Vol. 383, no 1, article id UNSP 111469Article in journal (Refereed)
    Abstract [en]

    We generated human iPS derived neural stem cells and differentiated cells from healthy control individuals and an individual with autism spectrum disorder carrying bi-allelic NRXN1-alpha deletion. We investigated the expression of NRXN1-alpha during neural induction and neural differentiation and observed a pivotal role for NRXN1-alpha during early neural induction and neuronal differentiation. Single cell RNA-seq pinpointed neural stem cells carrying NRXN1-alpha deletion shifting towards radial glia-like cell identity and revealed higher proportion of differentiated astroglia. Furthermore, neuronal cells carrying NRXN1-alpha deletion were identified as immature by single cell RNA-seq analysis, displayed significant depression in calcium signaling activity and presented impaired maturation action potential profile in neurons investigated with electrophysiology. Our observations propose NRXN1-alpha plays an important role for the efficient establishment of neural stem cells, in neuronal differentiation and in maturation of functional excitatory neuronal cells.

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