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Activation of the Notch signaling pathway promotes neurovascular repair after traumatic brain injury.

Ran QS, Yu YH, Fu XH, Wen YC - Neural Regen Res (2015)

Bottom Line: Therefore, in the present study, we controlled the Notch signaling pathway using overexpression and knockdown constructs.Activation of the Notch signaling pathway by Notch1 or Jagged1 overexpression enhanced the migration, invasiveness and angiogenic ability of endothelial progenitor cells.Suppression of the Notch signaling pathway with Notch1 or Jagged1 siRNAs reduced the migratory capacity, invasiveness and angiogenic ability of endothelial progenitor cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurosurgery, the First People's Hospital of ZunYi/the Third Affiliated Hospital of ZunYi Medical College, Zunyi, Guizhou Province, China.

ABSTRACT
The Notch signaling pathway plays a key role in angiogenesis and endothelial cell formation, but it remains unclear whether it is involved in vascular repair by endothelial progenitor cells after traumatic brain injury. Therefore, in the present study, we controlled the Notch signaling pathway using overexpression and knockdown constructs. Activation of the Notch signaling pathway by Notch1 or Jagged1 overexpression enhanced the migration, invasiveness and angiogenic ability of endothelial progenitor cells. Suppression of the Notch signaling pathway with Notch1 or Jagged1 siRNAs reduced the migratory capacity, invasiveness and angiogenic ability of endothelial progenitor cells. Activation of the Notch signaling pathway in vivo in a rat model of mild traumatic brain injury promoted neurovascular repair. These findings suggest that the activation of the Notch signaling pathway promotes blood vessel formation and tissue repair after brain trauma.

No MeSH data available.


Related in: MedlinePlus

Specific activation or inhibition of the Notch signaling pathway in endothelial progenitor cells.(A) Left: Western blot assay showing the overexpression of Notch1 and Jagged1. Con: Control group; Notch1 OE: Notch1 overexpression group; Jagged1 OE: Jagged1 overexpression group. Right: Hes1 promoter activity measured with luciferase reporter assay. (B) Left: Western blot assay showing knockdown of Notch1 and Jagged1. siNC: Control group; siNotch1: Notch1 knockdown group; siJagged1: Jagged1 knockdown group. Right: Hes1 promoter activity measured with luciferase reporter assay. Hes1 promoter activity is presented as a ratio to the control group. Data are expressed as the mean ± SD. Differences between groups were compared using one-way analysis of variance and nonparametric Mann-Whitney U test. Experiments were performed in triplicate. *P < 0.05, vs. control group.
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Figure 1: Specific activation or inhibition of the Notch signaling pathway in endothelial progenitor cells.(A) Left: Western blot assay showing the overexpression of Notch1 and Jagged1. Con: Control group; Notch1 OE: Notch1 overexpression group; Jagged1 OE: Jagged1 overexpression group. Right: Hes1 promoter activity measured with luciferase reporter assay. (B) Left: Western blot assay showing knockdown of Notch1 and Jagged1. siNC: Control group; siNotch1: Notch1 knockdown group; siJagged1: Jagged1 knockdown group. Right: Hes1 promoter activity measured with luciferase reporter assay. Hes1 promoter activity is presented as a ratio to the control group. Data are expressed as the mean ± SD. Differences between groups were compared using one-way analysis of variance and nonparametric Mann-Whitney U test. Experiments were performed in triplicate. *P < 0.05, vs. control group.

Mentions: Notch1 and Jagged1 plasmids were transfected into EPCs in vitro. Western blot assay demonstrated that expression levels of Notch1 and Jagged1 were significantly increased in the transfected EPCs (P < 0.05). Luciferase reporter assay revealed that the Notch signaling pathway was activated after overexpression of Notch1 and Jagged1 (Figure 1A). Notch1 and Jagged1 protein levels were knocked down after Notch1 and Jagged1 siRNAs were transfected into cells (P < 0.05). Luciferase reporter assay showed that Hes1 promoter activity was significantly inhibited when the Notch signaling pathway was suppressed by transfecting the siRNAs (Figure 1B). These data suggest that the Notch signaling pathway was specifically activated or suppressed.


Activation of the Notch signaling pathway promotes neurovascular repair after traumatic brain injury.

Ran QS, Yu YH, Fu XH, Wen YC - Neural Regen Res (2015)

Specific activation or inhibition of the Notch signaling pathway in endothelial progenitor cells.(A) Left: Western blot assay showing the overexpression of Notch1 and Jagged1. Con: Control group; Notch1 OE: Notch1 overexpression group; Jagged1 OE: Jagged1 overexpression group. Right: Hes1 promoter activity measured with luciferase reporter assay. (B) Left: Western blot assay showing knockdown of Notch1 and Jagged1. siNC: Control group; siNotch1: Notch1 knockdown group; siJagged1: Jagged1 knockdown group. Right: Hes1 promoter activity measured with luciferase reporter assay. Hes1 promoter activity is presented as a ratio to the control group. Data are expressed as the mean ± SD. Differences between groups were compared using one-way analysis of variance and nonparametric Mann-Whitney U test. Experiments were performed in triplicate. *P < 0.05, vs. control group.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
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getmorefigures.php?uid=PMC4590238&req=5

Figure 1: Specific activation or inhibition of the Notch signaling pathway in endothelial progenitor cells.(A) Left: Western blot assay showing the overexpression of Notch1 and Jagged1. Con: Control group; Notch1 OE: Notch1 overexpression group; Jagged1 OE: Jagged1 overexpression group. Right: Hes1 promoter activity measured with luciferase reporter assay. (B) Left: Western blot assay showing knockdown of Notch1 and Jagged1. siNC: Control group; siNotch1: Notch1 knockdown group; siJagged1: Jagged1 knockdown group. Right: Hes1 promoter activity measured with luciferase reporter assay. Hes1 promoter activity is presented as a ratio to the control group. Data are expressed as the mean ± SD. Differences between groups were compared using one-way analysis of variance and nonparametric Mann-Whitney U test. Experiments were performed in triplicate. *P < 0.05, vs. control group.
Mentions: Notch1 and Jagged1 plasmids were transfected into EPCs in vitro. Western blot assay demonstrated that expression levels of Notch1 and Jagged1 were significantly increased in the transfected EPCs (P < 0.05). Luciferase reporter assay revealed that the Notch signaling pathway was activated after overexpression of Notch1 and Jagged1 (Figure 1A). Notch1 and Jagged1 protein levels were knocked down after Notch1 and Jagged1 siRNAs were transfected into cells (P < 0.05). Luciferase reporter assay showed that Hes1 promoter activity was significantly inhibited when the Notch signaling pathway was suppressed by transfecting the siRNAs (Figure 1B). These data suggest that the Notch signaling pathway was specifically activated or suppressed.

Bottom Line: Therefore, in the present study, we controlled the Notch signaling pathway using overexpression and knockdown constructs.Activation of the Notch signaling pathway by Notch1 or Jagged1 overexpression enhanced the migration, invasiveness and angiogenic ability of endothelial progenitor cells.Suppression of the Notch signaling pathway with Notch1 or Jagged1 siRNAs reduced the migratory capacity, invasiveness and angiogenic ability of endothelial progenitor cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurosurgery, the First People's Hospital of ZunYi/the Third Affiliated Hospital of ZunYi Medical College, Zunyi, Guizhou Province, China.

ABSTRACT
The Notch signaling pathway plays a key role in angiogenesis and endothelial cell formation, but it remains unclear whether it is involved in vascular repair by endothelial progenitor cells after traumatic brain injury. Therefore, in the present study, we controlled the Notch signaling pathway using overexpression and knockdown constructs. Activation of the Notch signaling pathway by Notch1 or Jagged1 overexpression enhanced the migration, invasiveness and angiogenic ability of endothelial progenitor cells. Suppression of the Notch signaling pathway with Notch1 or Jagged1 siRNAs reduced the migratory capacity, invasiveness and angiogenic ability of endothelial progenitor cells. Activation of the Notch signaling pathway in vivo in a rat model of mild traumatic brain injury promoted neurovascular repair. These findings suggest that the activation of the Notch signaling pathway promotes blood vessel formation and tissue repair after brain trauma.

No MeSH data available.


Related in: MedlinePlus