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  • 1.
    Gallio, Marco
    et al.
    Södertörns högskola, Avdelning Naturvetenskap. Karolinska Institute.
    Sturgill, G
    Case Western Reserve University School of Medicine, Cleveland, USA.
    Rather, P
    Case Western Reserve University School of Medicine, Cleveland, USA.
    Kylsten, Per
    Södertörns högskola, Avdelning Naturvetenskap.
    A conserved mechanism for extracellular signaling in eukaryotes and prokaryotes2002Ingår i: Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, E-ISSN 1091-6490, Vol. 99, nr 19, s. 12208-12213Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Epidermal growth factor receptor (EGFr) is a key mediator of cell communication during animal development and homeostasis. In Drosophila, the signaling event is commonly regulated by the polytopic membrane protein Rhomboid (RHO), which mediates the proteolytic activation of EGFr ligands, allowing the secretion of the active signal. Until very recently, the biochemical function of RHO had remained elusive. It is now believed that Drosophila RHO is the founder member of a previously undescribed family of serine proteases, and that it could be directly responsible for the unusual, intramembranous cleavage of EGFr ligands. Here we show that the function of RHO is conserved in Gram-negative bacteria. AarA, a Providencia stuartii RHO-related protein, is active in Drosophila on the fly EGFr ligands. Vice versa, Drosophila RHO-1 can effectively rescue the bacterium's ability to produce or release the signal that activates density-dependent gene regulation (or quorum sensing). This study provides the first evidence that prokaryotic and eukaryotic RHOs could have a conserved role in cell communication and that their biochemical properties could be more similar than previously anticipated.

  • 2. Jensen, Lasse Dahl Ejby
    et al.
    Cao, Renhai
    Hedlund, Eva-Maria
    Söll, Iris
    Södertörns högskola, Institutionen för livsvetenskaper, Molekylärbiologi.
    Lundberg, Jon O.
    Hauptmann, Giselbert
    Södertörns högskola, Institutionen för livsvetenskaper, Molekylärbiologi.
    Steffensen, John Fleng
    Cao, Yihai
    Nitric oxide permits hypoxia-induced lymphatic perfusion by controlling arterial-lymphatic conduits in zebrafish and glass catfish2009Ingår i: Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, E-ISSN 1091-6490, Vol. 106, nr 43, s. 18408-18413Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The blood and lymphatic vasculatures are structurally and functionally coupled in controlling tissue perfusion, extracellular interstitial fluids, and immune surveillance. Little is known, however, about the molecular mechanisms that underlie the regulation of bloodlymphatic vessel connections and lymphatic perfusion. Here we show in the adult zebrafish and glass catfish (Kryptopterus bicirrhis) that blood-lymphatic conduits directly connect arterial vessels to the lymphatic system. Under hypoxic conditions, arterial-lymphatic conduits (ALCs) became highly dilated and linearized by NO-induced vascular relaxation, which led to blood perfusion into the lymphatic system. NO blockage almost completely abrogated hypoxia-induced ALC relaxation and lymphatic perfusion. These findings uncover mechanisms underlying hypoxia-induced oxygen compensation by perfusion of existing lymphatics in fish. Our results might also imply that the hypoxia-induced NO pathway contributes to development of progression of pathologies, including promotion of lymphatic metastasis by modulating arterial-lymphatic conduits, in the mammalian system.

  • 3. Lee, Samantha Lin Chiou
    et al.
    Rouhi, Pegah
    Jensen, Lasse Dahl
    Zhang, Danfang
    Ji, Hong
    Hauptmann, Giselbert
    Södertörns högskola, Institutionen för livsvetenskaper, Molekylärbiologi.
    Ingham, Philip
    Cao, Yihai
    Hypoxia-induced pathological angiogenesis mediates tumor cell dissemination, invasion, and metastasis in a zebrafish tumor model2009Ingår i: Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, E-ISSN 1091-6490, Vol. 106, nr 46, s. 19485-19490Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Mechanisms underlying pathological angiogenesis in relation to hypoxia in tumor invasion and metastasis remain elusive. Here, we have developed a zebrafish tumor model that allows us to study the role of pathological angiogenesis under normoxia and hypoxia in arbitrating early events of the metastatic cascade at the single cell level. Under normoxia, implantation of a murine T241 fibrosarcoma into the perivitelline cavity of developing embryos of transgenic fli1:EGFP zebrafish did not result in significant dissemination, invasion, and metastasis. In marked contrast, under hypoxia substantial tumor cells disseminated from primary sites, invaded into neighboring tissues, and metastasized to distal parts of the fish body. Similarly, expression of the hypoxia-regulated angiogenic factor, vascular endothelial growth factor (VEGF) to a high level resulted in tumor cell dissemination and metastasis, which correlated with increased tumor neovascularization. Inhibition of VEGF receptor signaling pathways by sunitinib or VEGFR2 morpholinos virtually completely ablated VEGF-induced tumor cell dissemination and metastasis. To the best of our knowledge, hypoxia- and VEGF-induced pathological angiogenesis in promoting tumor dissemination, invasion, and metastasis has not been described perviously at the single cell level. Our findings also shed light on molecular mechanisms of beneficial effects of clinically available anti-VEGF drugs for cancer therapy.

  • 4.
    Mackenbach, Johan P
    et al.
    Erasmus University Medical Center, Rotterdam, The Netherlands.
    Valverde, José Rubio
    Erasmus University Medical Center, Rotterdam, The Netherlands.
    Artnik, Barbara
    Faculty of Medicine, Ljubljana, Slovenia.
    Bopp, Matthias
    University of Zürich, Zurich, Switzerland.
    Brønnum-Hansen, Henrik
    Copenhagen University, Copenhagen, Denmark.
    Deboosere, Patrick
    Vrije Universiteit Brussel, Ixelles, Belgium.
    Kalediene, Ramune
    Lithuanian University of Health Sciences, Kaunas, Lithuania;.
    Kovács, Katalin
    Demographic Research Institute, Budapest, Hungary.
    Leinsalu, Mall
    Södertörns högskola, Institutionen för samhällsvetenskaper, Sociologi. Södertörns högskola, Institutionen för samhällsvetenskaper, SCOHOST (Stockholm Centre for Health and Social Change). National Institute for Health Development, Tallinn, Estonia.
    Martikainen, Pekka
    University of Helsinki, Helsinki, Finland.
    Menvielle, Gwenn
    Sorbonne Universités, Paris, France.
    Regidor, Enrique
    Universidad Complutense de Madrid, Madrid, Spain.
    Rychtaříková, Jitka
    Charles University, Prague, Czech Republic.
    Rodriguez-Sanz, Maica
    Agència de Salut Pública de Barcelona, Barcelona, Spain.
    Vineis, Paolo
    Imperial College, London, United Kingdom.
    White, Chris
    Office of National Statistics, Newport, United Kingdom.
    Wojtyniak, Bogdan
    National Institute of Public Health-National Institute of Hygiene, Warsaw, Poland.
    Hu, Yannan
    Erasmus University Medical Center, Rotterdam, The Netherlands.
    Nusselder, Wilma J
    Erasmus University Medical Center, Rotterdam, The Netherlands.
    Trends in health inequalities in 27 European countries2018Ingår i: Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, E-ISSN 1091-6490, Vol. 115, nr 25, s. 6440-6445Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Unfavorable health trends among the lowly educated have recently been reported from the United States. We analyzed health trends by education in European countries, paying particular attention to the possibility of recent trend interruptions, including interruptions related to the impact of the 2008 financial crisis. We collected and harmonized data on mortality from <i>ca</i> 1980 to <i>ca</i> 2014 for 17 countries covering 9.8 million deaths and data on self-reported morbidity from <i>ca</i> 2002 to <i>ca</i> 2014 for 27 countries covering 350,000 survey respondents. We used interrupted time-series analyses to study changes over time and country-fixed effects analyses to study the impact of crisis-related economic conditions on health outcomes. Recent trends were more favorable than in previous decades, particularly in Eastern Europe, where mortality started to decline among lowly educated men and where the decline in less-than-good self-assessed health accelerated, resulting in some narrowing of health inequalities. In Western Europe, mortality has continued to decline among the lowly and highly educated, and although the decline of less-than-good self-assessed health slowed in countries severely hit by the financial crisis, this affected lowly and highly educated equally. Crisis-related economic conditions were not associated with widening health inequalities. Our results show that the unfavorable trends observed in the United States are not found in Europe. There has also been no discernible short-term impact of the crisis on health inequalities at the population level. Both findings suggest that European countries have been successful in avoiding an aggravation of health inequalities.

  • 5.
    Provost, P
    et al.
    Karolinska Institute.
    Silverstein, Rebecca A
    Södertörns högskola, Avdelning Naturvetenskap. Karolinska Institute.
    Dishart, D
    Karolinska Institute.
    Walfridsson, Julian
    Södertörns högskola, Avdelning Naturvetenskap. Karolinska Institute.
    Djupedal, Ingela
    Södertörns högskola, Avdelning Naturvetenskap. Karolinska Institute.
    Kniola, Barbara
    Södertörns högskola, Avdelning Naturvetenskap. Karolinska Institute.
    Wright, Anthony P H
    Södertörns högskola, Avdelning Naturvetenskap. Karolinska Institute.
    Samuelsson, B
    Karolinska Institute.
    Radmark, O
    Karolinska Institute.
    Ekwall, Karl
    Södertörns högskola, Avdelning Naturvetenskap. Karolinska Institute.
    Dicer is required for chromosome segregation and gene silencing in fission yeast cells2002Ingår i: Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, E-ISSN 1091-6490, Vol. 99, nr 26, s. 16648-16653Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    RNA interference is a form of gene silencing in which the nuclease Dicer cleaves double-stranded RNA into small interfering RNAs. Here we report a role for Dicer in chromosome segregation of fission yeast. Deletion of the Dicer (dcr1(+)) gene caused slow growth, sensitivity to thiabendazole, lagging chromosomes during anaphase, and abrogated silencing of centromeric repeats. As Dicer in other species, Dcr1p degraded double-stranded RNA into approximate to23 nucleotide fragments in vitro, and dcr1Delta cells were partially rescued by expression of human Dicer, indicating evolutionarily conserved functions. Expression profiling demonstrated that dcr1(+) was required for silencing of two genes containing a conserved motif.

  • 6. Stenvall, Jörgen
    et al.
    Fierro-Gonzalez, Juan Carlos
    Södertörns högskola, Institutionen för livsvetenskaper, Molekylärbiologi.
    Swoboda, Peter
    Södertörns högskola, Institutionen för livsvetenskaper, Molekylärbiologi.
    Saamarthy, Karunakar
    Cheng, Qing
    Cacho-Valadez, Briseida
    Arner, Elias S. J.
    Persson, Olof P.
    Miranda-Vizuete, Antonio
    Tuck, Simon
    Selenoprotein TRXR-1 and GSR-1 are essential for removal of old cuticle during molting in Caenorhabditis elegans2011Ingår i: Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, E-ISSN 1091-6490, Vol. 108, nr 3, s. 1064-1069Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Selenoproteins, in particular thioredoxin reductase, have been implicated in countering oxidative damage occurring during aging but the molecular functions of these proteins have not been extensively investigated in different animal models. Here we demonstrate that TRXR-1 thioredoxin reductase, the sole selenoprotein in Caenorhabditis elegans, does not protect against acute oxidative stress but functions instead together with GSR-1 glutathione reductase to promote the removal of old cuticle during molting. We show that the oxidation state of disulfide groups in the cuticle is tightly regulated during the molting cycle, and that when trxr-1 and gsr-1 function is reduced, disulfide groups in the cuticle remain oxidized. A selenocysteine-to-cysteine TRXR-1 mutant fails to rescue molting defects. Furthermore, worms lacking SELB-1, the C. elegans homolog of Escherichia coli SelB or mammalian EFsec, a translation elongation factor known to be specific for selenocysteine in E. coli, fail to incorporate selenocysteine, and display the same phenotype as those lacking trxr-1. Thus, TRXR-1 function in the reduction of old cuticle is strictly selenocysteine dependent in the nematode. Exogenously supplied reduced glutathione reduces disulfide groups in the cuticle and induces apolysis, the separation of old and new cuticle, strongly suggesting that molting involves the regulated reduction of cuticle components driven by TRXR-1 and GSR-1. Using dauer larvae, we demonstrate that aged worms have a decreased capacity to molt, and decreased expression of GSR-1. Together, our results establish a function for the selenoprotein TRXR-1 and GSR-1 in the removal of old cuticle from the surface of epidermal cells.

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