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Stimulatory effects of thyroid hormone on brain angiogenesis in vivo and in vitro.

Artikel i vetenskaplig tidskrift
Författare Liqun Zhang
Christiana M Cooper-Kuhn
Ulf Nannmark
Klas Blomgren
Hans-Georg Kuhn
Publicerad i Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
Volym 30
Nummer/häfte 2
Sidor 323-35
ISSN 1559-7016
Publiceringsår 2010
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering
Institutionen för kliniska vetenskaper, Avdelningen för pediatrik
Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi
Sidor 323-35
Språk en
Länkar dx.doi.org/10.1038/jcbfm.2009.216
Ämnesord Animals, Antithyroid Agents, toxicity, Brain, blood supply, growth & development, Fluorescent Antibody Technique, Hypothyroidism, chemically induced, physiopathology, Immunohistochemistry, Microscopy, Electron, Transmission, Microvessels, pathology, Neovascularization, Physiologic, physiology, Propylthiouracil, toxicity, Rats, Rats, Wistar, Reverse Transcriptase Polymerase Chain Reaction, Thyroxine, metabolism, Triiodothyronine, metabolism
Ämneskategorier Neurovetenskap

Sammanfattning

Thyroid hormone is critical for the proper development of the central nervous system. However, the specific role of thyroid hormone on brain angiogenesis remains poorly understood. Treatment of rats from birth to postnatal day 21 (P21) with propylthiouracil (PTU), a reversible blocker of triiodothyronine (T3) synthesis, resulted in decreased brain angiogenesis, as indicated by reduced complexity and density of microvessels. However, when PTU was withdrawn at P22, these parameters were fully recovered by P90. These changes were paralleled by an altered expression of vascular endothelial growth factor A (Vegfa) and basic fibroblast growth factor (Fgf2). Physiologic concentrations of T3 and thyroxine (T4) stimulated proliferation and tubulogenesis of rat brain-derived endothelial (RBE4) cells in vitro. Protein and mRNA levels of VEGF-A and FGF-2 increased after T3 stimulation of RBE4 cells. The thyroid hormone receptor blocker NH-3 abolished T3-induced Fgf2 and Vegfa upregulation, indicating a receptor-mediated effect. Thyroid hormone inhibited the apoptosis in RBE4 cells and altered mRNA levels of apoptosis-related genes, namely Bcl2 and Bad. The present results show that thyroid hormone has a substantial impact on vasculature development in the brain. Pathologically altered vascularization could, therefore, be a contributing factor to the neurologic deficits induced by thyroid hormone deficiency.

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