Transforming Growth Factor-β2 Modulated Extracellular Matrix Component Expression in Cultured Human Optic Nerve Head Astrocytes

Fuchshofer, Rudolf; Birke, Marco T.; Welge–Lüßen, Ulrich; Kook, Daniel; Lütjen–Drecoll, Elke

doi:10.1167/iovs.04-0649

Cited by 139 publications

(111 citation statements)

References 34 publications

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“…It is reported that intracellular SMAD signaling induces expression of extracellular matrix (ECM) and basement membrane components in cultured astrocytes via Type IV pro-collagens (Fuchshofer et al, 2005;Gaussin, 2002;Jackson et al, 2003). ECM components regulated by SMAD signaling direct remodeling of blood vessels in some internal organs such as the lung or liver (Ng et al, 2005;Fernandez-L A, 2006).…”

Section: Discussionmentioning

confidence: 99%

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: Discussionmentioning

confidence: 99%

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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“…TGF-␤2 has been reported to induce fibronectin, collagen type I, and collagen type IV in both human retinal pigment epithelial cell line and cultured human optic nerve head astrocytes. 23,24 TGF-␤3 has also been reported to decrease matrix metalloproteinase-2 (MMP-2) and increase tissue inhibitor of metalloproteinase-1 (TIMP-1) and collagen type I in primary lung fibroblasts. 25 All three TGF-␤ isoforms have been reported to activate the TGF-␤ signaling pathway via Smad2 activation.…”

Section: Discussionmentioning

confidence: 99%

High Glucose-Induced Thioredoxin-Interacting Protein in Renal Proximal Tubule Cells Is Independent of Transforming Growth Factor-β1

Chen

Gilbert

et al. 2007

The American Journal of Pathology

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“…Biologically active CTGF is both secreted and expressed on the cell membrane (19,20). Conditioned medium prepared from 4F1 cells had prominent expression of CTGF compared with control 4V cells (Fig.…”

Section: Growth Inhibition Of Nsclc Cells By Ctgf Overexpressionmentioning

confidence: 97%

Suppression of Cell Proliferation and Signaling Transduction by Connective Tissue Growth Factor in Non–Small Cell Lung Cancer Cells

Chien¹,

Ding²,

Gui

et al. 2006

Molecular Cancer Research

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Connective tissue growth factor (CTGF) is a secreted protein that belongs to CCN family. The proteins in this family are implicated in various biological processes, such as angiogenesis, adhesion, migration, and apoptosis. In this study, we explored the roles of CTGF in lung tumorigenesis. The expression levels of CTGF in 58 lung cancer samples were reduced by >2 fold in 57% of the samples compared with matched normal samples using real-time reverse transcription-PCR. These results were confirmed by immunohistochemical staining for CTGF in normal lung epithelia and lung cancer. Cellular proliferation was inhibited in non -small cell lung cancer (NSCLC) cell lines NCI-H460, NCI-H520, NCI-H1299, and SK-MES-1 by CTGF overexpression. Partially purified CTGF suppressed lung cancer cell growth. The growth inhibition caused by CTGF overexpression was associated with growth arrest at G 0 -G 1 and prominent induction of p53 and ADP ribosylation factor. Most interestingly, overexpression of CTGF suppressed insulin-like growth factor-I -dependent Akt phosphorylation and epidermal growth factordependent extracellular signal-regulated kinase 1/2 phosphorylation. In summary, NSCLC cells expressed decreased levels of CTGF compared with normal lung cells; this lower expression has an effect on lung cancer cell proliferation and its cellular response to growth factors. Our data suggest that CTGF may behave as a secreted tumor suppressor protein in the normal lung, and its expression is suppressed in many NSCLCs.

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Transforming Growth Factor-β2 Modulated Extracellular Matrix Component Expression in Cultured Human Optic Nerve Head Astrocytes

Cited by 139 publications

References 34 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

High Glucose-Induced Thioredoxin-Interacting Protein in Renal Proximal Tubule Cells Is Independent of Transforming Growth Factor-β1

Suppression of Cell Proliferation and Signaling Transduction by Connective Tissue Growth Factor in Non–Small Cell Lung Cancer Cells

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