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  • 1.
    Akanda, Nesar
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi.
    Tofighi, Roshan
    Karolinska Inst, Dept Neurosci, SE-17177 Stockholm, Sweden .
    Brask, Johan
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi.
    Tamm, Christoffer
    Karolinska Inst, Dept Neurosci, SE-17177 Stockholm, Sweden .
    Elinder, Fredrik
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Ceccatelli, Sandra
    Karolinska Inst, Dept Neurosci, SE-17177 Stockholm, Sweden .
    Voltage-dependent anion channels (VDAC) in the plasma membrane play a critical role in apoptosis in differentiated hippocampal neurons but not in neural stem cells2008Ingår i: Cell Cycle, ISSN 1538-4101, E-ISSN 1551-4005, Vol. 7, nr 20, s. 3225-3234Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    microRNAs (miRNAs) are small non-coding RNAs that regulate a large variety of cellular processes including differentiation, apoptosis and proliferation. Several miRNAs display defective expression patterns in human tumors with the consequent alteration of target oncogene or tumor suppressor genes. Many of these miRNAs modulate the major proliferation pathways through direct interaction with critical regulators such as RAS, PI3K/PTEN or ABL, as well as members of the retinoblastoma pathway, Cyclin-CDK complexes or cell cycle inhibitors of the INK4 or Cip/Kip families. A complex interplay between miRNAs and MYC or E2F family members also exists to modulate cell cycle-dependent transcription during normal or tumoral proliferation. The ability of miRNAs to modulate these proliferation pathways may have relevant implications not only in physiological or developmental processes but also in tumor progression or cancer therapy.

  • 2.
    Danielsson, Bengt
    et al.
    Pharmaneti3, Sweden Uppsala University, Sweden .
    Danielsson, Christian
    Karolinska Institute, Sweden .
    Brask, Johan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Skold, Anna-Carin
    AstraZeneca RandD, Sweden .
    Pehrson, Richard
    AstraZeneca RandD, Sweden .
    Stockling, Kenneth
    AstraZeneca RandD, Sweden .
    Hellmold, Heike
    AstraZeneca RandD, Sweden .
    Elinder, Fredrik
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Sylven, Christer
    Karolinska Institute, Sweden .
    Drug induced embryonic cardiac arrhythmia: A teratogenic mechanism of human relevance in TOXICOLOGY LETTERS, vol 211, issue , pp S186-S1862012Ingår i: TOXICOLOGY LETTERS, Elsevier , 2012, Vol. 211, s. S186-S186Konferensbidrag (Refereegranskat)
    Abstract [en]

    n/a

  • 3.
    Danielsson, C
    et al.
    Karolinska Institutet, Stoclholm.
    Brask, Johan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Sköld, A-C
    AstraZeneca R&D, Södertälje.
    Andersson, A
    Karolinska Institutet, Stockholm.
    Pehrson, R
    AstraZeneca R&D, Södertälje.
    Stockling, K
    AstraZeneca R&D, Södertälje.
    Elinder, Fredrik
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Hellmold, H
    AstraZeneca R&D, Södertälje.
    Sylven, C
    Karolinska Institutet, Stockholm.
    Danielsson, B. R.
    Pharmanet Development, Stockholm.
    Is Cardiac Arrhythmia in the Human Embryo a Possible Mechanism for Cardiovascular Defects by I-Kr Blocking Antidepressants? in BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY, vol 91, issue 5, pp 345-3452011Ingår i: BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY, WILEY-BLACKWELL, COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA , 2011, Vol. 91, nr 5, s. 345-345Konferensbidrag (Refereegranskat)
    Abstract [en]

    n/a

  • 4.
    Danielsson, Christian
    et al.
    Karolinska University Hospital, Sweden .
    Brask, Johan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Skold, Anna-Carin
    AstraZeneca RandD Sodertalje, Sweden .
    Genead, Rami
    Karolinska University Hospital, Sweden .
    Andersson, Agneta
    Karolinska University Hospital, Sweden .
    Andersson, Ulf
    AstraZeneca RandD Sodertalje, Sweden .
    Stockling, Kenneth
    AstraZeneca RandD Sodertalje, Sweden .
    Pehrson, Rickard
    AstraZeneca RandD Sodertalje, Sweden .
    Grinnemo, Karl-Henrik
    Karolinska University Hospital, Sweden .
    Salari, Sajjad
    Linköpings universitet, Institutionen för klinisk och experimentell medicin. Linköpings universitet, Hälsouniversitetet.
    Hellmold, Heike
    AstraZeneca RandD Sodertalje, Sweden .
    Danielsson, Bengt
    Pharmanet Dev Grp, Sweden Uppsala University, Sweden .
    Sylven, Christer
    Karolinska University Hospital, Sweden .
    Elinder, Fredrik
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Exploration of human, rat, and rabbit embryonic cardiomyocytes suggests K-channel block as a common teratogenic mechanism2013Ingår i: Cardiovascular Research, ISSN 0008-6363, E-ISSN 1755-3245, Vol. 97, nr 1, s. 23-32Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Several drugs blocking the rapidly activating potassium (K-r) channel cause malformations (including cardiac defects) and embryonic death in animal teratology studies. In humans, these drugs have an established risk for acquired long-QT syndrome and arrhythmia. Recently, associations between cardiac defects and spontaneous abortions have been reported for drugs widely used in pregnancy (e.g. antidepressants), with long-QT syndrome risk. To investigate whether a common embryonic adverse-effect mechanism exists in the human, rat, and rabbit embryos, we made a comparative study of embryonic cardiomyocytes from all three species. less thanbrgreater than less thanbrgreater thanPatch-clamp and quantitative-mRNA measurements of K-r and slowly activating K (K-s) channels were performed on human, rat, and rabbit primary cardiomyocytes and cardiac samples from different embryo-foetal stages. The K-r channel was present when the heart started to beat in all species, but was, in contrast to human and rabbit, lost in rats in late organogenesis. The specific K-r-channel blocker E-4031 prolonged the action potential in a species- and development-dependent fashion, consistent with the observed K-r-channel expression pattern and reported sensitive periods of developmental toxicity. E-4031 also increased the QT interval and induced 2:1 atrio-ventricular block in multi-electrode array electrographic recordings of rat embryos. The K-s channel was expressed in human and rat throughout the embryo-foetal period but not in rabbit. less thanbrgreater than less thanbrgreater thanThis first comparison of mRNA expression, potassium currents, and action-potential characteristics, with and without a specific K-r-channel blocker in human, rat, and rabbit embryos provides evidence of K-r-channel inhibition as a common mechanism for embryonic malformations and death.

  • 5.
    Englund, Ulrika
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Brask, Johan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Elinder, Fredrik
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Inhibition of SCN2A ortholog upregulation in Xenopus laevis oocytes prevents cell death2014Manuskript (preprint) (Övrigt vetenskapligt)
    Abstract [en]

    Transport of ions across the cell membrane is essential for the regulation of cell death and tissue homeostasis, and alterations in the function of voltage-gated ion channels and of the intracellular ionic compositions interfere with these processes. Opening of K, Na , or Cl channels have been linked to the apoptotic process and in many cases, opening of these channels precede caspase-3 activation and are thus early events in the apoptotic process. Consistent with the role of these channels in apoptosis, inhibition of these channels prevents or delays the apoptotic process. However, the role of ion channels during apoptosis has been difficult to explore, mainly due to unspecific/non-selective ion channe blockers. In the present investigation, the molecular identity of a  voltage-gated Na channel in oocytes from Xenopus laevis, which is crucial for the apoptotic response to mechanical stress, was identified. Specific down regulation of SCN2A Na channel expression by miRNA prevented apoptosis, suggesting that Na+ influx is essential for apoptosis in Xenopus oocytes.

  • 6.
    Johansson, Anne-Sofie
    et al.
    Karolinska Institute.
    Brask, Johan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Owe-Larsson, Bjorn
    Karolinska University.
    Hetta, Jerker
    Karolinska University.
    Lundkvist, Gabriella B. S.
    Karolinska Institute.
    Valproic Acid Phase Shifts the Rhythmic Expression of PERIOD2::LUCIFERASE2011Ingår i: Journal of Biological Rhythms, ISSN 0748-7304, E-ISSN 1552-4531, Vol. 26, nr 6, s. 541-551Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Valproic acid (VPA) is an anticonvulsant used to treat bipolar disorder, a psychiatric disease associated with disturbances in circadian rhythmicity. Little is known about how VPA affects circadian rhythms. The authors cultured tissues containing the master brain pacemaker for circadian rhythmicity, the suprachiasmatic nuclei (SCN), and skin fibroblasts from transgenic PERIOD2::LUCIFERASE (PER2::LUC) mice and studied the effect of VPA on the circadian PER2::LUC rhythm by measuring bioluminescence. VPA (1 mM) significantly phase advanced the PER2::LUC rhythm when applied at a time point corresponding to the lowest (trough, similar to ZT 0) PER2::LUC expression but phase delayed the PER2::LUC rhythm when the drug was administered at the time of highest (peak, similar to ZT 12) protein expression. In addition, it significantly increased the overall amplitude of PER2::LUC oscillations at time points at or close to ZT 12 but had no effect on period. Real-time PCR analyses on mouse and human fibroblasts revealed that expressions of other clock genes were increased after 2 h treatment with VPA. Because VPA is known to inhibit histone deacetylation, the authors treated cultures with an established histone deacetylation inhibitor, trichostatin A (TSA; 20 ng/mL), to compare the effect of VPA and TSA on molecular rhythmicity. They found that TSA had similar effects on the PER2::LUC rhythm as VPA. Furthermore, VPA and TSA significantly increased acetylation on histone H3 but in comparison little on histone H4. Lithium is another commonly used treatment for bipolar disorder. Therefore, the authors also studied the impact of lithium chloride (LiCl; 10 mM) on the PER2::LUC rhythm. LiCl delayed the phase, but in contrast to VPA and TSA, LiCl lengthened the PER2::LUC period and had no effect on histone acetylation. These results demonstrate that VPA can delay or advance the phase, as well as increase the amplitude, of the PERIOD2::LUCIFERASE rhythm depending on the circadian time of application. Furthermore, the authors show that LiCl delays the phase and lengthens the period of the PER2::LUC rhythm, confirming previous reports on circadian lithium effects. These different molecular effects may underlie differential chronotherapeutic effects of VPA and lithium.

  • 7.
    Salari, Sajjad
    et al.
    Linköpings universitet, Medicinska fakulteten. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi.
    Silverå Ejneby, Malin
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelning för neurobiologi. Linköpings universitet, Medicinska fakulteten.
    Brask, Johan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelning för neurobiologi. Linköpings universitet, Medicinska fakulteten.
    Elinder, Fredrik
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelning för neurobiologi. Linköpings universitet, Medicinska fakulteten.
    Isopimaric acid - a multi-targeting ion channel modulator reducing excitability and arrhythmicity in a spontaneously beating mouse atrial cell line2018Ingår i: Acta Physiologica, ISSN 1748-1708, E-ISSN 1748-1716, Vol. 222, nr 1, artikel-id e12895Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    AimAtrial fibrillation is the most common persistent cardiac arrhythmia, and it is not well controlled by present drugs. Because some resin acids open voltage-gated potassium channels and reduce neuronal excitability, we explored the effects of the resin acid isopimaric acid (IPA) on action potentials and ion currents in cardiomyocytes. MethodsSpontaneously beating mouse atrial HL-1 cells were investigated with the whole-cell patch-clamp technique. Results1-25 mol L-1 IPA reduced the action potential frequency by up to 50%. The effect of IPA on six different voltage-gated ion channels was investigated; most voltage-dependent parameters of ion channel gating were shifted in the negative direction along the voltage axis, consistent with a hypothesis that a lipophilic and negatively charged compound binds to the lipid membrane close to the positively charged voltage sensor of the ion channels. The major finding was that IPA inactivated sodium channels and L- and T-type calcium channels and activated the rapidly activating potassium channel and the transient outward potassium channel. Computer simulations of IPA effects on all of the ion currents were consistent with a reduced excitability, and they also showed that effects on the Na channel played the largest role to reduce the action potential frequency. Finally, induced arrhythmia in the HL-1 cells was reversed by IPA. ConclusionLow concentrations of IPA reduced the action potential frequency and restored regular firing by altering the voltage dependencies of several voltage-gated ion channels. These findings can form the basis for a new pharmacological strategy to treat atrial fibrillation.

  • 8.
    Skold, A C
    et al.
    AstraZeneca RandD Sodertalje.
    Danielsson, C
    Karolinska Institute.
    Brask, Johan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Salari, Sajjad
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Stockling, K
    AstraZeneca RandD Sodertalje.
    Andersson, A
    AstraZeneca RandD Sodertalje.
    Jalkesten, E
    AstraZeneca RandD Sodertalje.
    Grebius, M
    AstraZeneca RandD Sodertalje.
    Larsson, M
    AstraZeneca RandD Sodertalje.
    Lindstrom, A
    AstraZeneca RandD Sodertalje.
    Blomgren, B
    AstraZeneca RandD Sodertalje.
    Pehrson, R
    AstraZeneca RandD Sodertalje.
    Danielsson, B
    Pharmanet Dev Group.
    Hellmold, H
    AstraZeneca RandD Sodertalje.
    Sylven, C
    Karolinska Institute.
    Elinder, Fredrik
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Translational Research: Electrophysiological Development in the Embryonic Heart of Rats, Rabbits, and Humans in BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY, vol 91, issue 5, pp 357-3572011Ingår i: BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY, WILEY-BLACKWELL, COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA , 2011, Vol. 91, nr 5, s. 357-357Konferensbidrag (Refereegranskat)
    Abstract [en]

    n/a

1 - 8 av 8
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