Changes in endothelial cell proliferation and vascular permeability after systemic lipopolysaccharide administration in the subfornical organ.
The subfornical organ (SFO) has highly permeable fenestrated vasculature and is a key site for immune-to-brain communications. Recently, we showed the occurrence of continuous angiogenesis in the SFO. In the present study, we found that systemic administration of bacterial lipopolysaccharide (LPS) reduced the vascular permeability and endothelial cell proliferation. In LPS-administered mice, the SFO vasculature showed a significant decrease in the immunoreactivity of plasmalemma vesicle associated protein-1, a marker of endothelial fenestral diaphragms. These data suggest that vasculature undergoes structural change to decrease vascular permeability in response to systemic LPS administration.
Department of Anatomy & Neuroscience, Faculty of Medicine, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan. Electronic address: morita@naramed-u.ac.jp.
Shoko
S
Morita-Takemura
Department of Anatomy & Neuroscience, Faculty of Medicine, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan.
Kazuki
K
Nakahara
Department of Anatomy & Neuroscience, Faculty of Medicine, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan.
Kouko
K
Tatsumi
Department of Anatomy & Neuroscience, Faculty of Medicine, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan; Department of Functional Anatomy, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan.
Hiroaki
H
Okuda
Department of Anatomy & Neuroscience, Faculty of Medicine, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan.
Tatsuhide
T
Tanaka
Department of Anatomy & Neuroscience, Faculty of Medicine, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan.
Ayami
A
Isonishi
Department of Anatomy & Neuroscience, Faculty of Medicine, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan.
Akio
A
Wanaka
D000818:Animals; D001973:Bromodeoxyuridine / Q000378:metabolism; D002199:Capillary Permeability / Q000187:drug effects*; D002352:Carrier Proteins / Q000378:metabolism; D049109:Cell Proliferation / Q000187:drug effects*; D042783:Endothelial Cells / Q000187:drug effects*; D049452:Green Fluorescent Proteins / Q000235:genetics / Q000378:metabolism; D008070:Lipopolysaccharides / Q000633:toxicity*; D008297:Male; D008565:Membrane Proteins / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D018613:Microscopy, Confocal; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D013356:Subfornical Organ / Q000187:drug effects* / Q000473:pathology; D013997:Time Factors
D002352:Carrier Proteins; D008070:Lipopolysaccharides; D008565:Membrane Proteins; D019408:Platelet Endothelial Cell Adhesion Molecule-1; C486772:Plvap protein, mouse; D049452:Green Fluorescent Proteins; D001973:Bromodeoxyuridine
Angiogenesis; Blood–brain barrier; Fenestrated endothelial cells; Inflammation