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Prolonged systemic hyperglycemia does not cause pericyte loss and permeability at the mouse blood-brain barrier
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Vascular Biology. (Rudbecklaboratoriet)
Karolinska Inst, Dept Med, Integrated Cardiometab Ctr, Huddinge, Sweden.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology. Univ Oxford, Physiol Anat & Genet, Sherrington Bldg,Pk Rd, Oxford, England. (Rudbecklaboratoriet)
Karolinska Inst, Dept Med, Integrated Cardiometab Ctr, Huddinge, Sweden.
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2018 (English)In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 8, article id 17462Article in journal (Refereed) Published
Abstract [en]

Diabetes mellitus is associated with cognitive impairment and various central nervous system pathologies such as stroke, vascular dementia, or Alzheimer's disease. The exact pathophysiology of these conditions is poorly understood. Recent reports suggest that hyperglycemia causes cerebral microcirculation pathology and blood-brain barrier (BBB) dysfunction and leakage. The majority of these reports, however, are based on methods including in vitro BBB modeling or streptozotocininduced diabetes in rodents, opening questions regarding the translation of the in vitro findings to the in vivo situation, and possible direct effects of streptozotocin on the brain vasculature. Here we used a genetic mouse model of hyperglycemia (Ins2(AKITA)) to address whether prolonged systemic hyperglycemia induces BBB dysfunction and leakage. We applied a variety of methodologies to carefully evaluate BBB function and cellular integrity in vivo, including the quantification and visualization of specific tracers and evaluation of transcriptional and morphological changes in the BBB and its supporting cellular components. These experiments did neither reveal altered BBB permeability nor morphological changes of the brain vasculature in hyperglycemic mice. We conclude that prolonged hyperglycemia does not lead to BBB dysfunction, and thus the cognitive impairment observed in diabetes may have other causes.

Place, publisher, year, edition, pages
NATURE PUBLISHING GROUP , 2018. Vol. 8, article id 17462
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Neurosciences
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URN: urn:nbn:se:uu:diva-372388DOI: 10.1038/s41598-018-35576-0ISI: 000451619100004PubMedID: 30498224OAI: oai:DiVA.org:uu-372388DiVA, id: diva2:1275816
Funder
Swedish Research Council, 2015-00550EU, European Research Council, AdG294556Knut and Alice Wallenberg Foundation, 2015.0030Swedish Cancer Society, CAN-2016-0777Swedish Cancer Society, 150735Available from: 2019-01-07 Created: 2019-01-07 Last updated: 2019-01-07Bibliographically approved

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Mäe, Maarja AndaloussiVanlandewijck, MichaelHe, LiqunNahar, KhayrunHofmann, Jennifer J.Betsholtz, Christer

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Mäe, Maarja AndaloussiVanlandewijck, MichaelHe, LiqunNahar, KhayrunHofmann, Jennifer J.Keller, AnnikaBetsholtz, Christer
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