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UXT potentiates angiogenesis by attenuating Notch signaling.

Zhou Y, Ge R, Wang R, Liu F, Huang Y, Liu H, Hao Y, Zhou Q, Wang C - Development (2015)

Bottom Line: This prevents RBP-Jκ/CSL from activation and thus inhibits the consequent gene inductions.Furthermore, blockade of Notch signaling rescues the angiogenesis defect caused by UXT knockdown both in vitro and in vivo.Taken together, the data presented in this study characterize UXT as a novel repressor of Notch signaling, shedding new light on the molecular regulation of angiogenesis.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China State Key Laboratory of Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.

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UXT is essential for zebrafish angiogenesis. (A-C) RT-PCR verification of angiogenesis markers in 18 hpf, 24 hpf or 30 hpf zebrafish embryos injected with 4 ng of control morpholino (Ctrl MO) or with 4 ng of UXT morpholino (UXT MO). Data shown are the mean±s.e.m. (at least three independent experiments); *P<0.05, **P<0.01 versus the corresponding control. (D) Whole-mount in situ hybridization of embryos injected with 4 ng of control morpholino (Ctrl MO) or 4 ng of UXT morpholino (UXT MO). Riboprobes against the angiogenesis marker kdrl, the pronephric marker pax2.1 and the erythroid marker gata1 were visualized at 22 hpf. The red arrowhead indicates the decreased expression of kdrl in UXT-deficient embryos.
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DEV112532F2: UXT is essential for zebrafish angiogenesis. (A-C) RT-PCR verification of angiogenesis markers in 18 hpf, 24 hpf or 30 hpf zebrafish embryos injected with 4 ng of control morpholino (Ctrl MO) or with 4 ng of UXT morpholino (UXT MO). Data shown are the mean±s.e.m. (at least three independent experiments); *P<0.05, **P<0.01 versus the corresponding control. (D) Whole-mount in situ hybridization of embryos injected with 4 ng of control morpholino (Ctrl MO) or 4 ng of UXT morpholino (UXT MO). Riboprobes against the angiogenesis marker kdrl, the pronephric marker pax2.1 and the erythroid marker gata1 were visualized at 22 hpf. The red arrowhead indicates the decreased expression of kdrl in UXT-deficient embryos.

Mentions: It has been well established that the angiogenesis of intersegmental vessels (ISVs) mainly takes place at the time window from 18 hpf to 30 hpf in zebrafish (Fouquet et al., 1997). This led us to speculate that UXT might play a role in ISV development. To explore this possibility, we investigated mRNA expression of the angiogenesis markers, including cox2, nestin1, angpt1, flt1 and kdrl (Albini et al., 1996; Amoh et al., 2005; Kim et al., 2006; Luttun et al., 2002; Stefater et al., 2011; Wu et al., 2006), and of the somite marker myod, at 18 hpf, 24 hpf and 30 hpf. When the expression of UXT was knocked down, these angiogenesis markers were expressed at slightly lower levels at 18 hpf and 24 hpf (Fig. 2A,B), but were strikingly decreased at 30 hpf (Fig. 2C; supplementary material Fig. S5).Fig. 2.


UXT potentiates angiogenesis by attenuating Notch signaling.

Zhou Y, Ge R, Wang R, Liu F, Huang Y, Liu H, Hao Y, Zhou Q, Wang C - Development (2015)

UXT is essential for zebrafish angiogenesis. (A-C) RT-PCR verification of angiogenesis markers in 18 hpf, 24 hpf or 30 hpf zebrafish embryos injected with 4 ng of control morpholino (Ctrl MO) or with 4 ng of UXT morpholino (UXT MO). Data shown are the mean±s.e.m. (at least three independent experiments); *P<0.05, **P<0.01 versus the corresponding control. (D) Whole-mount in situ hybridization of embryos injected with 4 ng of control morpholino (Ctrl MO) or 4 ng of UXT morpholino (UXT MO). Riboprobes against the angiogenesis marker kdrl, the pronephric marker pax2.1 and the erythroid marker gata1 were visualized at 22 hpf. The red arrowhead indicates the decreased expression of kdrl in UXT-deficient embryos.
© Copyright Policy - open-access
Related In: Results  -  Collection

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DEV112532F2: UXT is essential for zebrafish angiogenesis. (A-C) RT-PCR verification of angiogenesis markers in 18 hpf, 24 hpf or 30 hpf zebrafish embryos injected with 4 ng of control morpholino (Ctrl MO) or with 4 ng of UXT morpholino (UXT MO). Data shown are the mean±s.e.m. (at least three independent experiments); *P<0.05, **P<0.01 versus the corresponding control. (D) Whole-mount in situ hybridization of embryos injected with 4 ng of control morpholino (Ctrl MO) or 4 ng of UXT morpholino (UXT MO). Riboprobes against the angiogenesis marker kdrl, the pronephric marker pax2.1 and the erythroid marker gata1 were visualized at 22 hpf. The red arrowhead indicates the decreased expression of kdrl in UXT-deficient embryos.
Mentions: It has been well established that the angiogenesis of intersegmental vessels (ISVs) mainly takes place at the time window from 18 hpf to 30 hpf in zebrafish (Fouquet et al., 1997). This led us to speculate that UXT might play a role in ISV development. To explore this possibility, we investigated mRNA expression of the angiogenesis markers, including cox2, nestin1, angpt1, flt1 and kdrl (Albini et al., 1996; Amoh et al., 2005; Kim et al., 2006; Luttun et al., 2002; Stefater et al., 2011; Wu et al., 2006), and of the somite marker myod, at 18 hpf, 24 hpf and 30 hpf. When the expression of UXT was knocked down, these angiogenesis markers were expressed at slightly lower levels at 18 hpf and 24 hpf (Fig. 2A,B), but were strikingly decreased at 30 hpf (Fig. 2C; supplementary material Fig. S5).Fig. 2.

Bottom Line: This prevents RBP-Jκ/CSL from activation and thus inhibits the consequent gene inductions.Furthermore, blockade of Notch signaling rescues the angiogenesis defect caused by UXT knockdown both in vitro and in vivo.Taken together, the data presented in this study characterize UXT as a novel repressor of Notch signaling, shedding new light on the molecular regulation of angiogenesis.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China State Key Laboratory of Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.

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