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Transforming growth factor-β1 requires NADPH oxidase 4 for angiogenesis in vitro and in vivo.

Peshavariya HM, Chan EC, Liu GS, Jiang F, Dusting GJ - J. Cell. Mol. Med. (2014)

Bottom Line: In cells from Nox4-deficient mice, TGF-β1-induced cell proliferation, migration and tube formation were abolished.In vivo, TGF-β1 stimulated growth of blood vessels into sponges implanted subcutaneously, and this angiogenesis was markedly reduced in Nox4 knockout mice.Thus, endothelial cells are regulated by a TGF-β1 signalling pathway involving Nox4-derived ROS to promote angiogenesis.

View Article: PubMed Central - PubMed

Affiliation: Centre for Eye Research Australia, Department of Ophthalmology, University of Melbourne, East Melbourne, Victoria, Australia; O'Brien Institute, Fitzroy, Victoria, Australia.

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A diagram showing the potential mechanism of transforming growth factor-β1-induced Smad2/3 signalling pathway which may be involved in Nox4 up-regulation and angiogenesis.
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fig08: A diagram showing the potential mechanism of transforming growth factor-β1-induced Smad2/3 signalling pathway which may be involved in Nox4 up-regulation and angiogenesis.

Mentions: In summary, we have shown that TGF-β1 stimulated Nox4 expression in endothelial cells, and demonstrated its significance for angiogenesis (Fig.8). Adaptation to hypoxia-induced secretion of different growth factors such as TGF-β1 and VEGF to increase neovascularization of ischaemic tissues is a hallmark of pathological angiogenesis in diabetic retinopathy and cancer. If several of these pro-angiogenic signalling pathways merge into Nox4, in such conditions of pathological angiogenesis Nox4 inhibition may be a superior therapeutic target than blocking TGF-β1 or VEGF individually.


Transforming growth factor-β1 requires NADPH oxidase 4 for angiogenesis in vitro and in vivo.

Peshavariya HM, Chan EC, Liu GS, Jiang F, Dusting GJ - J. Cell. Mol. Med. (2014)

A diagram showing the potential mechanism of transforming growth factor-β1-induced Smad2/3 signalling pathway which may be involved in Nox4 up-regulation and angiogenesis.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4508156&req=5

fig08: A diagram showing the potential mechanism of transforming growth factor-β1-induced Smad2/3 signalling pathway which may be involved in Nox4 up-regulation and angiogenesis.
Mentions: In summary, we have shown that TGF-β1 stimulated Nox4 expression in endothelial cells, and demonstrated its significance for angiogenesis (Fig.8). Adaptation to hypoxia-induced secretion of different growth factors such as TGF-β1 and VEGF to increase neovascularization of ischaemic tissues is a hallmark of pathological angiogenesis in diabetic retinopathy and cancer. If several of these pro-angiogenic signalling pathways merge into Nox4, in such conditions of pathological angiogenesis Nox4 inhibition may be a superior therapeutic target than blocking TGF-β1 or VEGF individually.

Bottom Line: In cells from Nox4-deficient mice, TGF-β1-induced cell proliferation, migration and tube formation were abolished.In vivo, TGF-β1 stimulated growth of blood vessels into sponges implanted subcutaneously, and this angiogenesis was markedly reduced in Nox4 knockout mice.Thus, endothelial cells are regulated by a TGF-β1 signalling pathway involving Nox4-derived ROS to promote angiogenesis.

View Article: PubMed Central - PubMed

Affiliation: Centre for Eye Research Australia, Department of Ophthalmology, University of Melbourne, East Melbourne, Victoria, Australia; O'Brien Institute, Fitzroy, Victoria, Australia.

Show MeSH
Related in: MedlinePlus