Morphological differentiation of endothelial cells co-cultured with astrocytes on type-I or type-IV collagen

Tagami, Motoki; Yamagata, Kazuo; Fujino, Hideaki; Kubota, Akiyoshi; Nara, Yasuo; Yamori, Yukio

doi:10.1007/bf00318790

Cited by 42 publications

(22 citation statements)

References 22 publications

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“…Downregulated genes included Type I, Type III, and Type IV procollagens (Fig. 7A), which are thought to be essential for endothelial cell-astrocyte interactions (Tagami et al, 1992). TaqMan real-time RT-PCR confirmed the results of the GeneChip analysis (Fig.…”

Section: Glial Bmpria Plays a Critical Role In Formation Of The Bbbsupporting

confidence: 58%

BMP signaling through BMPRIA in astrocytes is essential for proper cerebral angiogenesis and formation of the blood–brain-barrier

Araya

Kudo

Kawano

et al. 2008

Molecular and Cellular Neuroscience

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Bone morphogenetic protein (BMP) signaling is involved in differentiation of neural precursor cells into astrocytes, but its contribution to angiogenesis is not well characterized. This study examines the role of BMP signaling through BMP type IA receptor (BMPRIA) in early neural development using a conditional knockout mouse model, in which Bmpr1a is selectively disrupted in telencephalic neural stem cells. The conditional mutant mice show a significant increase in the number of cerebral blood vessels and the level of vascular endothelial growth factor (VEGF) is significantly upregulated in the mutant astrocytes. The mutant mice also show leakage of immunoglobulin around cerebral microvessels in neonatal mice, suggesting a defect in formation of the blood-brain-barrier. In addition, astrocytic endfeet fail to encircle cortical blood vessels in the mutant mice. These results suggest that BMPRIA signaling in astrocytes regulates the expression of VEGF for proper cerebrovascular angiogenesis and has a role on in the formation of the blood-brain-barrier.

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Section: Glial Bmpria Plays a Critical Role In Formation Of The Bbbsupporting

confidence: 58%

BMP signaling through BMPRIA in astrocytes is essential for proper cerebral angiogenesis and formation of the blood–brain-barrier

Araya

Kudo

Kawano

et al. 2008

Molecular and Cellular Neuroscience

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“…These primary astrocytes were maintained in Dulbecco's modified Eagle's medium (DMEM; Nissui Pharmaceutical, Tokyo, Japan) supplemented with 10% fetal bovine serum (FBS; Gibco-BRL Life Technologies, Tokyo, Japan) at 37°C in a CO 2 incubator (95% air and 5% CO 2 ). Cultures with a homogeneous cell population, consisting of Ͼ95% astrocytes as determined by glial fibriary acidic protein (GFAP) staining, were used in these experiments (Tagami et al, 1992).…”

Section: Materials and Methods Astrocyte Culturesmentioning

confidence: 99%

Differential regulation of glial cell line‐derived neurotrophic factor (GDNF) mRNA expression during hypoxia and reoxygenation in astrocytes isolated from stroke‐prone spontaneously hypertensive rats

Yamagata

Tagami

Ikeda

et al. 2001

Glia

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Glial cell line-derived neurotrophic factor (GDNF) plays several important roles in the survival and recovery of mature neurons during ischemia. We examined the possibility that the expression of GDNF mRNA and the release of GDNF protein are regulated differentially in cultured astrocytes from the stroke-prone spontaneously hypertensive rat (SHRSP) compared with those from Wistar Kyoto rats (WKY) during hypoxia and reoxygenation (H/R) and after exposure to glutamate and hydrogen peroxide (H(2)O(2)). The mRNA expression was quantitated by reverse transcription-polymerase chain reaction (RT-PCR) based on the fluorescent TaqMan methodology. A new instrument capable of measuring fluorescence in real-time was used to quantify gene amplification in astrocytes. GDNF protein was investigated by enzyme-linked immunosorbent assay (ELISA). GDNF mRNA expression and GDNF protein release at normoxia were greater in SHRSP than in WKY astrocytes. During H/R, however, the mRNA expression and protein release tended to be reduced in SHRSP compared with WKY. Glutamate and H(2)O(2) induced the expression of GDNF mRNA and the release of GDNF protein in both WKY and SHRSP in a dose-dependent manner. Levels of GDNF mRNA and protein in SHRSP were significantly lower than in WKY. These findings indicate that GDNF production in SHRSP astrocytes was low in response to H/R, glutamate, and H(2)O(2), compared with that observed in WKY. We conclude that the attenuated production of GDNF in astrocytes is involved in neuronal vulnerability in SHRSP during H/R, as GDNF production, which is stimulated by glutamate and H(2)O(2), is closely related to the protective effect against H/R-mediated neurotoxicity.

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“…Generated by endothelial cells and astrocytes in concert during development, the basal lamina forms a biologically active connection between the two cell components, which requires their juxtaposition (Bernstein et al, 1985;Kusaka et al, 1985). In culture, astrocytes secrete laminin, fibronectin, and chondroitin sulfate proteoglycan, while collagens stimulate astrocyte-induced endothelial cell maturation (Ard and Faissner, 1991;Tagami et al, 1992;Webersinke et al, 1992). Conversely, endothelial cell-derived ECM components stimulate astrocyte growth and function (e.g., glutamine synthetase activity) (Nagano et al, 1993;Kozlova et al, 1993).…”

Section: Integrin-matrix Interactions and Microvessel Integritymentioning

confidence: 99%

Cerebral Microvessel Responses to Focal Ischemia

Zoppo

Mabuchi

2003

J Cereb Blood Flow Metab

539

449

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Summary:Cerebral microvessels have a unique ultrastructure form, which allows for the close relationship of the endothelium and blood elements to the neurons they serve, via intervening astrocytes. To focal ischemia, the cerebral microvasculature rapidly displays multiple dynamic responses. Immediate events include breakdown of the primary endothelial cell permeability barrier, with transudation of plasma, expression of endothelial cell-leukocyte adhesion receptors, loss of endothelial cell and astrocyte integrin receptors, loss of their matrix ligands, expression of members of several matrix-degrading protease families, and the appearance of receptors associated with angiogenesis and neovascularization. These events occur pari passu with neuron injury. Alterations in the microvessel matrix after the onset of ischemia also suggest links to changes in nonvascular cell viability. Microvascular obstruction within the ischemic territory occurs after occlusion and reperfusion of the feeding arteries ("focal no-reflow" phenomenon). This can result from extrinsic compression and intravascular events, including leukocyte(-platelet) adhesion, platelet-fibrin interactions, and activation of coagulation. All of these events occur in microvessels heterogeneously distributed within the ischemic core. The panorama of acute microvessel responses to focal cerebral ischemia provide opportunities to understand interrelationships between neurons and their microvascular supply and changes that underlie a number of central nervous system neurodegenerative disorders.

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Morphological differentiation of endothelial cells co-cultured with astrocytes on type-I or type-IV collagen

Cited by 42 publications

References 22 publications

BMP signaling through BMPRIA in astrocytes is essential for proper cerebral angiogenesis and formation of the blood–brain-barrier

BMP signaling through BMPRIA in astrocytes is essential for proper cerebral angiogenesis and formation of the blood–brain-barrier

Differential regulation of glial cell line‐derived neurotrophic factor (GDNF) mRNA expression during hypoxia and reoxygenation in astrocytes isolated from stroke‐prone spontaneously hypertensive rats

Cerebral Microvessel Responses to Focal Ischemia

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