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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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Nox4 is required for transforming growth factor-β1 (TGF-β1)-induced wound healing. Adv-Nox4i blunted the stimulatory effect of TGF-β1 (10 ng/ml) on wound healing response of (A and B) HUVECs and (C) HMECs. Similarly, TGF-β1 (10 ng/ml) induced wound healing response in wild-type mouse cells (WT), and this response was blunted in Nox4 KO MHEC (C and D). Representative high magnification images of a single wound-scratched healing assay performed on (A) HUVECs and (D) MHEC (scale bar represents 100 μm). Quantitative measures (mean ± SEM from n = 3–6) of wound healing responses are expressed as a percentage of cells infected with Adv-GFP controls or WT without TGF-β1 treatment. *P < 0.05 from Adv-GFP without TGF-β1 treatment; †P < 0.05 from Adv-GFP or WT treatment in the presence of TGF-β1.
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fig06: Nox4 is required for transforming growth factor-β1 (TGF-β1)-induced wound healing. Adv-Nox4i blunted the stimulatory effect of TGF-β1 (10 ng/ml) on wound healing response of (A and B) HUVECs and (C) HMECs. Similarly, TGF-β1 (10 ng/ml) induced wound healing response in wild-type mouse cells (WT), and this response was blunted in Nox4 KO MHEC (C and D). Representative high magnification images of a single wound-scratched healing assay performed on (A) HUVECs and (D) MHEC (scale bar represents 100 μm). Quantitative measures (mean ± SEM from n = 3–6) of wound healing responses are expressed as a percentage of cells infected with Adv-GFP controls or WT without TGF-β1 treatment. *P < 0.05 from Adv-GFP without TGF-β1 treatment; †P < 0.05 from Adv-GFP or WT treatment in the presence of TGF-β1.

Mentions: Disruption of the intact layer of endothelial cells by using a scratch assay model causes migration and proliferation of adjacent cells to fill in the wounded areas. As expected, TGF-β1 accelerated the wound closure in Adv-GFP infected HUVEC and HMECs (Fig.6A–C). Importantly, TGF-β1-induced wound recovery was abolished by Adv-Nox4i (Fig.6A–C). Similarly, TGF-β1 increased the wound closure in wild-type MHEC when compared with untreated endothelial cells (Fig.6D and E), and this wound recovery response was decreased in Nox4 KO-derived mouse MHEC (Fig.6D and E). These data suggest that TGF-β1 promoted migration and wound closure responses of endothelial cells depend on Nox4.


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)

Nox4 is required for transforming growth factor-β1 (TGF-β1)-induced wound healing. Adv-Nox4i blunted the stimulatory effect of TGF-β1 (10 ng/ml) on wound healing response of (A and B) HUVECs and (C) HMECs. Similarly, TGF-β1 (10 ng/ml) induced wound healing response in wild-type mouse cells (WT), and this response was blunted in Nox4 KO MHEC (C and D). Representative high magnification images of a single wound-scratched healing assay performed on (A) HUVECs and (D) MHEC (scale bar represents 100 μm). Quantitative measures (mean ± SEM from n = 3–6) of wound healing responses are expressed as a percentage of cells infected with Adv-GFP controls or WT without TGF-β1 treatment. *P < 0.05 from Adv-GFP without TGF-β1 treatment; †P < 0.05 from Adv-GFP or WT treatment in the presence of TGF-β1.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig06: Nox4 is required for transforming growth factor-β1 (TGF-β1)-induced wound healing. Adv-Nox4i blunted the stimulatory effect of TGF-β1 (10 ng/ml) on wound healing response of (A and B) HUVECs and (C) HMECs. Similarly, TGF-β1 (10 ng/ml) induced wound healing response in wild-type mouse cells (WT), and this response was blunted in Nox4 KO MHEC (C and D). Representative high magnification images of a single wound-scratched healing assay performed on (A) HUVECs and (D) MHEC (scale bar represents 100 μm). Quantitative measures (mean ± SEM from n = 3–6) of wound healing responses are expressed as a percentage of cells infected with Adv-GFP controls or WT without TGF-β1 treatment. *P < 0.05 from Adv-GFP without TGF-β1 treatment; †P < 0.05 from Adv-GFP or WT treatment in the presence of TGF-β1.
Mentions: Disruption of the intact layer of endothelial cells by using a scratch assay model causes migration and proliferation of adjacent cells to fill in the wounded areas. As expected, TGF-β1 accelerated the wound closure in Adv-GFP infected HUVEC and HMECs (Fig.6A–C). Importantly, TGF-β1-induced wound recovery was abolished by Adv-Nox4i (Fig.6A–C). Similarly, TGF-β1 increased the wound closure in wild-type MHEC when compared with untreated endothelial cells (Fig.6D and E), and this wound recovery response was decreased in Nox4 KO-derived mouse MHEC (Fig.6D and E). These data suggest that TGF-β1 promoted migration and wound closure responses of endothelial cells depend on Nox4.

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