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  • 1.
    Fontana, Jacopo
    et al.
    KTH, Skolan för teknikvetenskap (SCI), Tillämpad fysik, Cellens fysik. KTH, Centra, Science for Life Laboratory, SciLifeLab.
    Fritz, Nicolas
    KTH, Skolan för teknikvetenskap (SCI), Tillämpad fysik, Cellens fysik. KTH, Centra, Science for Life Laboratory, SciLifeLab.
    Brismar, Hjalmar
    KTH, Skolan för teknikvetenskap (SCI), Tillämpad fysik, Cellens fysik. KTH, Centra, Science for Life Laboratory, SciLifeLab.
    Aperia, Anita
    KTH, Centra, Science for Life Laboratory, SciLifeLab.
    Apoptosis caused by excessive mitochondrial albumin uptake in renal cells is initiated by increased mitochondrial calcium concentration2015Inngår i: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 29Artikkel i tidsskrift (Annet vitenskapelig)
  • 2.
    Fritz, Nicolas
    et al.
    KTH, Skolan för teknikvetenskap (SCI), Tillämpad fysik, Cellens fysik. KTH, Centra, Science for Life Laboratory, SciLifeLab.
    Akkuratov, Evgeny
    KTH.
    Liebmann, Thomas
    KTH, Centra, Science for Life Laboratory, SciLifeLab.
    Lindskog, Maria
    Brismar, Hjalmar
    KTH, Skolan för teknikvetenskap (SCI), Tillämpad fysik, Cellens fysik. KTH, Centra, Science for Life Laboratory, SciLifeLab.
    Aperia, Anita
    KTH, Centra, Science for Life Laboratory, SciLifeLab.
    Functional consequences of the disease-causing T613M mutation of NKAalpha3 for hippocampal neurons2015Inngår i: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 29Artikkel i tidsskrift (Annet vitenskapelig)
  • 3.
    Gunnarson, E
    et al.
    Department of Woman and Child Health, Karolinska Institutet, Stockholm, Sweden.
    Zelenina, Marina
    Department of Woman and Child Health, Karolinska Institutet, Stockholm, Sweden.
    Aperia, Anita
    Department of Woman and Child Health, Karolinska Institutet, Stockholm, Sweden.
    Regulation of brain aquaporins2004Inngår i: Neuroscience, ISSN 0306-4522, E-ISSN 1873-7544, Vol. 129, nr 4, s. 947-955Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Emerging evidence suggests that brain aquaporins (AQP) play important roles for the dynamic regulation of brain water homeostasis and for the regulation of cerebrospinal fluid production. This review deals with the short- and long-term regulation of AQP4 and AQP9, both expressed in astrocytes, and of AQP1, expressed in the choroid plexus. AQP1 and 4 have in other cell types been shown to be regulated by phosphorylation. Phosphorylation affects the gating of AQP4 and the trafficking and insertion into membrane of AQP1. Mercury inhibits the water permeability of AQP1 and AQP9, but not AQP4. The permeability of AQP4 is increased by lead. AQP4 is also regulated by protein-protein interaction. The assembly between AQP4 and syntrophin is required for the proper localization of AQP4 in the astrocyte plasma membrane that faces capillaries. There is evidence from studies on peripheral tissues that steroid hormones regulate the expression of AQP1, AQP4 and AQP9. There is also evidence that the expression of AQP1 can be regulated by ubiquitination, and that osmolality can regulate the expression of AQP1, AQP4 and AQP9. Further insight into the mechanisms by which brain AQPs are regulated will be of utmost clinical importance, since perturbed water flow via brain AQPs has been implicated in many neurological diseases and since, in brain edema, water flow via AQP4 may have a harmful effect.

  • 4. Gunnarson, E.
    et al.
    Zelenina, Marina
    KTH, Skolan för teknikvetenskap (SCI), Tillämpad fysik, Cellens fysik.
    Song, Yutong
    Illarionova, N.
    Brismar, Hjalmar
    KTH, Skolan för teknikvetenskap (SCI), Tillämpad fysik, Cellens fysik.
    Andersson, Ulf
    Zelenin, S.
    Aperia, Anita
    Effect of the brain protecting agent erythropoietin on astrocyte function2009Konferansepaper (Fagfellevurdert)
  • 5. Gunnarson, Eli
    et al.
    Zelenina, Marina
    Karolinska Institutet.
    Song, Yutong
    Kowalewski, Jacob M.
    KTH, Skolan för teknikvetenskap (SCI), Tillämpad fysik, Cellens fysik.
    Brismar, Hjalmar
    KTH, Skolan för teknikvetenskap (SCI), Tillämpad fysik, Cellens fysik.
    Brines, Michael
    Cerami, Antony
    Andersson, Ulf
    Aperia, Anita
    Kvinnor och barns hälsa, Karolinska Institutet.
    Erythropoietin modulation of astrocyte water permeability: a potential component of neuroprotection2008Inngår i: Neuroscience 2008, 2008Konferansepaper (Fagfellevurdert)
  • 6.
    Kamali-Zare, Padideh
    et al.
    KTH, Skolan för teknikvetenskap (SCI), Tillämpad fysik, Cellens fysik.
    Kowalewski, Jacob M.
    KTH, Skolan för teknikvetenskap (SCI), Tillämpad fysik, Cellens fysik.
    Aperia, Anita
    Kvinnor och barns hälsa, Karolinska Institutet.
    Brismar, Hjalmar
    KTH, Skolan för teknikvetenskap (SCI), Tillämpad fysik, Cellens fysik.
    Diffusion Limited Space (DLS) and its impact on water and K+ homeostasis in kidney principal cells and astrocytes2008Inngår i: 9th International Conference on Systems Biology, 2008Konferansepaper (Fagfellevurdert)
  • 7. Liu, Xiao
    et al.
    Spicarova, Zuzana
    Rydholm, Susanna
    KTH, Skolan för teknikvetenskap (SCI), Tillämpad fysik, Cellens fysik.
    Li, Juan
    Brismar, Hjalmar
    KTH, Skolan för teknikvetenskap (SCI), Tillämpad fysik, Cellens fysik.
    Aperia, Anita
    Ankyrin B Modulates the Function of Na,K-ATPase/Inositol 1,4,5-Trisphosphate Receptor Signaling Microdomain2008Inngår i: Journal of Biological Chemistry, ISSN 0021-9258, E-ISSN 1083-351X, Vol. 283, nr 17, s. 11461-11468Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Na, K-ATPase and inositol 1,4,5-trisphosphate (IP3) receptor (IP3R) can form a signaling microdomain that in the presence of ouabain triggers highly regular calcium oscillations. Downstream effects include NF-kappa B activation. Here we report that ankyrin B (Ank-B), expressed in most mammalian cells, plays a pivotal role in the function of the Na, K-ATPase/ IP3R signaling microdomain. In studies performed on a monkey kidney cell line, we show that Ank-B co-precipitates with both Na, K-ATPase and IP3R. We identify the N terminus tail of the Na, K-ATPase catalytic subunit and the N-terminal portion 1-604 of the IP3R as novel binding sites for Ank-B. Knockdown of Ank-B with small interfering RNA reduced the expression of Ank-B to 15-30%. This down-regulation of Ank-B attenuated the interaction between Na, K-ATPase and IP3R, reduced the number of cells responding to pM doses of ouabain with calcium oscillations, altered the calcium oscillatory pattern, and abolished the ouabain effect on NF-kappa B. In contrast, Ank-B down-regulation had no effect on the ion transporting function of Na, K-ATPase and no effect on the distribution and apparent mobility of Na, K-ATPase in the plasma membrane.

  • 8.
    Nilsson, Linnea
    et al.
    KTH, Skolan för teknikvetenskap (SCI), Tillämpad fysik, Cellens fysik.
    Burlaka, Ievgeniiya
    Brismar, Hjalmar
    KTH, Skolan för teknikvetenskap (SCI), Tillämpad fysik, Cellens fysik. Karolinska Inst, Sweden.
    Aperia, Anita
    Scott, Lena
    Glucose activation of the mitochondrial apoptotic pathway in proximal tubular cells and protective effect of ouabain signaling2015Inngår i: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 29Artikkel i tidsskrift (Annet vitenskapelig)
  • 9. Ringman, Andreas
    et al.
    Zelenina, Marina
    Department of Woman and Child Health, Astrid Lindgren Children's Hospital Research Laboratory Q2:09, Karolinska Institutet.
    Eklöf, Ann-Christine
    Aperia, Anita
    Department of Woman and Child Health, Astrid Lindgren Children's Hospital Research Laboratory Q2:09, Karolinska Institutet.
    Frenckner, Björn
    NKCC-1 and ENaC are down-regulated in nitrofen-induced hypoplastic lungs with congenital diaphragmatic hernia2008Inngår i: Pediatric surgery international (Print), ISSN 0179-0358, E-ISSN 1437-9813, Vol. 24, nr 9, s. 993-1000Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Congenital diaphragmatic hernia (CDH) is accompanied by pulmonary hypoplasia and pulmonary hypertension. Fetal lung growth is dependent on the secretion of lung liquid, which normally is absorbed at partus. The ion channel NKCC-1 is involved in this secretory process, but has recently also been reported to be implicated in absorption. CDH patients show a disturbed transition from secretion to absorption. alpha- and beta-ENaC are essential for lung liquid absorption. Common for all transcellular ion transport is the need for Na/K-ATPase as a primary driving force. The aim of the study was first to map the normal pulmonary expression of the above proteins during late gestation and secondly to see if the expression was affected in a CDH rat model. Pregnant Sprague-Dawley rat dams were given nitrofen on gestational day 9.5 to induce CDH. The fetuses were removed on gestational days E18 and E21. In addition, newborn rats were harvested postpartum on day P2. The fetuses were put into one of two groups: hypoplastic lungs without CDH (N-CDH) and hypoplastic lungs with CDH (N+CDH). The pulmonary expression of NKCC-1, alpha-/beta-ENaC and Na/K-ATPase was then analyzed using Western blot. We found that the protein levels of NKCC-1 on gestational days E18 and E21 were significantly lower among fetuses with N+CDH as well as N-CDH compared to controls. The expression of beta-ENaC was also significantly down-regulated in both the groups on E18 and E21. The protein levels of alpha-ENaC and Na/K-ATPase were not found to be significantly decreased, but both showed a tendency towards down-regulation. The marked down-regulation of NKCC-1 in fetal hypoplastic lungs with CDH indicates a possibly decreased lung liquid production. This may be one of the mechanisms behind the disturbed pulmonary development in CDH. We also show that beta-ENaC is down-regulated. Down-regulation of beta-ENaC may result in abnormal lung liquid absorption, which could be one of the mechanisms behind the respiratory distress seen in CDH patients postpartum.

  • 10. Ringman Uggla, Andreas
    et al.
    von Schewelov, Katarina
    Zelenina, Marina
    KTH, Skolan för teknikvetenskap (SCI), Tillämpad fysik, Cellens fysik.
    Aperia, Anita
    Nordic Centre of Excellence for Research in Water Imbalance Related Disorders (WIRED), Stockholm, Sweden.
    Frenckner, Björn
    Low pulmonary expression of epithelial Na(+) channel and Na(+), K(+)-ATPase in newborn infants with congenital diaphragmatic hernia2011Inngår i: Neonatology, ISSN 1661-7800, E-ISSN 1661-7819, Vol. 99, nr 1, s. 14-22Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: It has been suggested from several animal studies and clinical observations that congenital diaphragmatic hernia (CDH) with pulmonary hypoplasia is accompanied by a disturbed perinatal ion transport. This could lead to respiratory distress due to slower clearance of fetal lung fluid at birth.

    OBJECTIVES: The purpose of this study was to determine whether CDH is related to changes in the expression of three rate-limiting transporter proteins in lung epithelium at birth.

    METHODS: Tracheal aspirate was collected from 12 newborn infants with CDH and from 8 newborn control patients. Sampling was performed at postnatal age 18 and at 43 h in the CDH group and at 18 h in the control group. The protein abundance of α-, β- and γ-epithelial Na(+) channel (ENaC), aquaporin 5 and Na(+), K(+)-ATPase α(1) was analyzed using semiquantitative immunoblotting.

    RESULTS: The levels of β-ENaC, γ-ENaC and Na(+), K(+)-ATPase α(1) collected at 18 h postnatally were significantly lower in CDH infants compared to control infants. In the CDH group, no significant difference in the expression of the ENaC subunits, Na(+), K(+)-ATPase α(1) or aquaporin 5 could be detected between the two sampling time points.

    CONCLUSIONS: This downregulation may result in an abnormal lung fluid absorption which could be an important mechanism behind the respiratory distress seen in newborn CDH patients.

  • 11. Vieux, Rachel
    et al.
    Zelenina, Marina
    Nordic Center of Excellence for Research in Water Imbalance Related Disorders (WIRED), Karolinska Institutet, Stockholm, Sweden. Department of Women's and Children's Health, Karolinska Institutet.
    Aperia, Anita
    Nordic Center of Excellence for Research in Water Imbalance Related Disorders (WIRED), Karolinska Institutet, Stockholm, Sweden. Department of Women's and Children's Health, Karolinska Institutet.
    Hascoët, Jean-Michel
    The renal adverse effects of ibuprofen are not mediated by AQP2 water channels2010Inngår i: Pediatric nephrology (Berlin, West), ISSN 0931-041X, E-ISSN 1432-198X, Vol. 25, nr 7, s. 1277-1284Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The aim of this study was to determine (1) whether ibuprofen treatment in very preterm infants causes an increase in the renal water channel aquaporin-2 (AQP2) activity in the collecting duct via prostaglandin synthesis inhibition and (2) whether AQP2 activity remains disturbed long after ibuprofen treatment has ended. This was a prospective study involving premature infants with a gestation age of 27-31 weeks who received treatment between December 2005 and August 2006 in a tertiary Neonatal Intensive Care Unit. Each ibuprofen-treated infant was matched to two controls. Renal glomerular and tubular function were evaluated weekly for 1 month, and urinary AQP2 was measured by immuno-dotting. In total, 166 longitudinal samples were analyzed in 36 infants. Median [interquartile range] gestational age and birthweight were 28 [27.0-29.5] weeks and 1160 [1041-1242] g, respectively. Perinatal factors were similar in both groups. Urine output was significantly decreased in the ibuprofen-treated infants during the treatment. The urinary AQP2 level decreased significantly from day 2 to day 7 in both groups and was similar thereafter for the first month of life in ibuprofen-treated and control groups. Based on our results, we conclude that ibuprofen-induced oligo-anuria is not associated with a change in AQP2 activity and that ibuprofen does not affect AQP2 activity during the first month of life in very preterm neonates.

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