Search

Your search keyword '"Hermanson, Ola"' showing total 208 results
Start Over Author "Hermanson, Ola" Language english
208 results on '"Hermanson, Ola"'

9. Irradiation-induced changes in neural progenitor cells are reversed by lithium: Immature newborn dentate granule neurons display dendritic processes that are either tangential or parallel to the granule cell layer of the dentate gyrus of the hippocampus

Author

Zanni, Giulia, Goto, Shinobu, Fragopoulou, Adamantia F., Gaudenzi, Giulia, Naidoo, Vinogran, Di Martino, Elena, Levy, Gabriel, Dominguez, Cecilia A., Dethlefsen, Olga, Cedazo-Minguez, Angel, Merino-Serrais, Paula, Stamatakis, Antonios, Hermanson, Ola, and Blomgren, Klas

Published
2021
Full Text
View/download PDF

24. Autologous Peripheral Blood Mononuclear Cells as Treatment in Refractory Acute Respiratory Distress Syndrome

Author

Jungebluth, Philipp, Holzgraefe, Bernhard, Lim, Mei Ling, Duru, Adil Doganay, Lundin, Vanessa, Heldring, Nina, Wiklander, Oscar P.B., Nordin, Joel Z., Chrobok, Michael, Roderburg, Christoph, Sjöqvist, Sebastian, Anderstam, Björn, Rodríguez, Antonio Beltrán, Haag, Johannes C., Gustafsson, Ylva, Roddewig, Katharina G., Jones, Petra, Wood, Matthew J.A., Luedde, Tom, Teixeira, Ana I., Hermanson, Ola, Winqvist, Ola, Kalzén, Håkan, El Andaloussi, Samir, Alici, Evren, and Macchiarini, Paolo

Published
2015
Full Text
View/download PDF

27. The histone H4 lysine 16 acetyltransferase hMOF regulates the outcome of autophagy

Author

Fullgrabe, Jens, Lynch-Day, Melinda A., Heldring, Nina, Li, Wenbo, Struijk, Robert B., Ma, Qi, Hermanson, Ola, Rosenfeld, Michael G., Klionsky, Daniel J., and Joseph, Bertrand

Subjects
Observations, Research, Properties, Cell regulation -- Observations, Autophagy (Cytology) -- Research, Histones -- Properties, Cellular control mechanisms -- Observations
Abstract

Autophagy is a catabolic process that results in the autophagosome-dependent lysosomal degradation of bulk cytoplasmic contents, abnormal protein aggregates and excess or damaged organelles (1,2). This process involves a series [...], Autophagy is an evolutionarily conserved catabolic process involved in several physiological and pathological processes (1,2).Although primarily cytoprotective, autophagy can also contribute to cell death; it is thus important to understand what distinguishes the life or death decision in autophagic cells (3). Here we report that induction of autophagy is coupled to reduction of histone H4 lysine 16 acetylation (H4K16ac) through downregulation of the histone acetyltransferase hMOF (also called KAT8 or MYST1), and demonstrate that this histone modification regulates the outcome of autophagy. At a genome-wide level, we find that H4K16 deacetylation is associated predominantly with the downregulation of autophagy-related genes. Antagonizing H4K16ac downregulation upon autophagy induction results in the promotion of cell death. Our findings establish that alteration in a specific histone post-translational modification during autophagy affects the transcriptional regulation of autophagy-related genes and initiates a regulatory feedbackloop, which serves as a key determinant of survival versus death responses upon autophagy induction.

Published
2013

29. Recombinant Spider Silk Protein Matrices Facilitate Differentiation of Neural Stem Cells Into Mature and Functional Neurons

Author

Lewicka, Michalina, Rebellato, Paola, Lewicki, Jakub, Uhlen, Per, Rising, Anna, and Hermanson, Ola

Subjects
nervous system, Materials Science (miscellaneous), Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy)
Abstract

Neural stem cells (NSCs) show great promise in drug discovery and clinical application. Yet few efforts have been made to optimize biocompatible materials for such cells to be expanded and used in clinical conditions. We have previously demonstrated that NSCs are readily cultured on substrates of certain recombinant spider silk protein without addition of animal- or human-derived components. The question remains however whether this material allows differentiation into functional neurons, and whether such differentiation can take place also when the NSCs are cultured not only upon but also within the biodegradable material. Here we demonstrate that "foam"-like structures generated from recombinant spider silk protein (4RepCT) provided excellent matrices for the generation and multicellular analysis of functional excitatory neurons from NSCs without addition of animal- or human-derived components. NSCs isolated from the cerebral cortices of rat embryos were cultured at either 4RepCT matrices shaped as foam-like structures without coating, or on conventional polystyrene plates coated with poly-L-ornithine and fibronectin. Upon treatment with recombinant proteins including the extracellular signaling factor BMP4 or a combination of BMP4 and the signaling factor Wnt3a, the cortical NSCs cultured in 4RepCT foam-like structures differentiated efficiently into neurons that responded to glutamate receptor agonists, such as AMPA, to the same extent as control cultures. Matrices derived from recombinant spider silk proteins thus provide a functional microenvironment for neural stem cells with little or no animal- or human-derived components and can be employed in the development of new strategies in stem cell research and tissue engineering.

Published
2021
Full Text
View/download PDF

32. Nuclear Receptor Binding Protein 2 Is Downregulated in Medulloblastoma, and Reduces Tumor Cell Survival upon Overexpression

Author

Xiong, Anqi, Roy, Ananya, Spyrou, Argyris, Weishaupt, Holger, Marinescu, Voichita D., Olofsson, Tommie, Hermanson, Ola, Swartling, Fredrik J., and Forsberg-Nilsson, Karin

Subjects
Cell- och molekylärbiologi, apoptosis, pseudokinase, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, NRBP, lcsh:RC254-282, Article, Cell and Molecular Biology, brain tumor, pediatric cancer
Abstract

Pseudokinases, comprising 10% of the human kinome, are emerging as regulators of canonical kinases and their functions are starting to be defined. We previously identified the pseudokinase Nuclear Receptor Binding Protein 2 (NRBP2) in a screen for genes regulated during neural differentiation. During mouse brain development, NRBP2 is expressed in the cerebellum, and in the adult brain, mainly confined to specific neuronal populations. To study the role of NRBP2 in brain tumors, we stained a brain tumor tissue array for NRPB2, and find its expression to be low, or absent, in a majority of the tumors. This includes medulloblastoma (MB), a pediatric tumor of the cerebellum. Using database mining of published MB data sets, we also find that NRBP2 is expressed at a lower level in MB than in the normal cerebellum. Recent studies indicate that MB exhibits frequent epigenetic alternations and we therefore treated MB cell lines with drugs inhibiting DNA methylation or histone deacetylation, which leads to an upregulation of NRBP2 mRNA expression, showing that it is under epigenetic regulation in cultured MB cells. Furthermore, forced overexpression of NRBP2 in MB cell lines causes a dramatic decrease in cell numbers, increased cell death, impaired cell migration and inhibited cell invasion in vitro. Taken together, our data indicate that downregulation of NRBP2 may be a feature by which MB cells escape growth regulation.

Published
2020

33. Corrigendum: The histone H4 lysine 16 acetyltransferase hMOF regulates the outcome of autophagy

Author

Fllgrabe, Jens, Lynch-Day, Melinda A., Heldring, Nina, Li, Wenbo, Struijk, Robert B., Ma, Qi, Hermanson, Ola, Rosenfeld, Michael G., Klionsky, Daniel J., and Joseph, Bertrand

Abstract

Author(s): Jens Fllgrabe; Melinda A. Lynch-Day; Nina Heldring; Wenbo Li; Robert B. Struijk; Qi Ma; Ola Hermanson; Michael G. Rosenfeld; Daniel J. Klionsky; Bertrand Joseph Nature 500, 468471 (2013); doi:10.1038/nature12313 [...]

Published
2017
Full Text
View/download PDF

44. NRXN1 Deletion and Exposure to Methylmercury Increase Astrocyte Differentiation by Different Notch-Dependent Transcriptional Mechanisms.

Author

Raciti, Marilena, Salma, Jahan, Spulber, Stefan, Gaudenzi, Giulia, Khalajzeyqami, Zahra, Conti, Mirko, Anderlid, Britt-Marie, Falk, Anna, Hermanson, Ola, and Ceccatelli, Sandra

Subjects
AUTISM spectrum disorders, METHYLMERCURY, HUMAN stem cells, NOTCH signaling pathway
Abstract

Controversial evidence points to a possible involvement of methylmercury (MeHg) in the etiopathogenesis of autism spectrum disorders (ASD). In the present study, we used human neuroepithelial stem cells from healthy donors and from an autistic patient bearing a bi-allelic deletion in the gene encoding for NRXN1 to evaluate whether MeHg would induce cellular changes comparable to those seen in cells derived from the ASD patient. In healthy cells, a subcytotoxic concentration of MeHg enhanced astroglial differentiation similarly to what observed in the diseased cells (N1), as shown by the number of GFAP positive cells and immunofluorescence signal intensity. In both healthy MeHg-treated and N1 untreated cells, aberrations in Notch pathway activity seemed to play a critical role in promoting the differentiation toward glia. Accordingly, treatment with the established Notch inhibitor DAPT reversed the altered differentiation. Although our data are not conclusive since only one of the genes involved in ASD is considered, the results provide novel evidence suggesting that developmental exposure to MeHg, even at subcytotoxic concentrations, induces alterations in astroglial differentiation similar to those observed in ASD. [ABSTRACT FROM AUTHOR]

Published
2019
Full Text
View/download PDF

47. RETRACTED: Tracheobronchial transplantation with a stem-cell-seeded bioartificial nanocomposite: a proof-of-concept study

Author

Jungebluth, Philipp, Alici, Evren, Baiguera, Silvia, Blomberg, Pontus, Bozóky, Béla, Crowley, Claire, Einarsson, Oskar, Gudbjartsson, Tomas, Le Guyader, Sylvie, Henriksson, Gert, Hermanson, Ola, Juto, Jan Erik, Leidner, Bertil, Lilja, Tobias, Liska, Jan, Luedde, Tom, Lundin, Vanessa, Moll, Guido, Roderburg, Christoph, Strömblad, Staffan, Sutlu, Tolga, Watz, Emma, Seifalian, Alexander, and Macchiarini, Paolo

Published
2011
Full Text
View/download PDF

49. Post-Translational Modifications of Histones in Vertebrate Neurogenesis.

Author

Mitrousis, Nikolaos, Tropepe, Vincent, Hermanson, Ola, Represa, Alfonso, Cremer, Harold, and Hoekman, Marco

Subjects
POST-translational modification, DEVELOPMENTAL neurobiology, HISTONES
Abstract

The process of neurogenesis, through which the entire nervous system of an organism is formed, has attracted immense scientific attention for decades. How can a single neural stem cell give rise to astrocytes, oligodendrocytes, and neurons? Furthermore, how is a neuron led to choose between the hundreds of different neuronal subtypes that the vertebrate CNS contains? Traditionally, niche signals and transcription factors have been on the spotlight. Recent research is increasingly demonstrating that the answer may partially lie in epigenetic regulation of gene expression. In this article, we comprehensively review the role of post-translational histone modifications in neurogenesis in both the embryonic and adult CNS. [ABSTRACT FROM AUTHOR]

Published
2015
Full Text
View/download PDF

50. A SNP in the HTT promoter alters NF-κB binding and is a bidirectional genetic modifier of Huntington disease.

Author

Bečanović, Kristina, Nørremølle, Anne, Neal, Scott J, Kay, Chris, Collins, Jennifer A, Arenillas, David, Lilja, Tobias, Gaudenzi, Giulia, Manoharan, Shiana, Doty, Crystal N, Beck, Jessalyn, Lahiri, Nayana, Portales-Casamar, Elodie, Warby, Simon C, Connolly, Colúm, De Souza, Rebecca A G, Tabrizi, Sarah J, Hermanson, Ola, Langbehn, Douglas R, and Hayden, Michael R

Subjects
HUNTINGTON'S chorea diagnosis, HUNTINGTON'S chorea treatment, GENE expression, HUNTINGTON disease, NEUROSCIENCES, PATIENTS
Abstract

Cis-regulatory variants that alter gene expression can modify disease expressivity, but none have previously been identified in Huntington disease (HD). Here we provide in vivo evidence in HD patients that cis-regulatory variants in the HTT promoter are bidirectional modifiers of HD age of onset. HTT promoter analysis identified a NF-κB binding site that regulates HTT promoter transcriptional activity. A non-coding SNP, rs13102260:G > A, in this binding site impaired NF-κB binding and reduced HTT transcriptional activity and HTT protein expression. The presence of the rs13102260 minor (A) variant on the HD disease allele was associated with delayed age of onset in familial cases, whereas the presence of the rs13102260 (A) variant on the wild-type HTT allele was associated with earlier age of onset in HD patients in an extreme case-based cohort. Our findings suggest a previously unknown mechanism linking allele-specific effects of rs13102260 on HTT expression to HD age of onset and have implications for HTT silencing treatments that are currently in development. [ABSTRACT FROM AUTHOR]

Published
2015
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results