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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

Activation of the Notch signaling pathway enhanced the migration of endothelial progenitor cells.(A) Scratch test for evaluating the distance of cell migration in the Notch signaling pathway activation groups. The distance of cell migration is presented as a ratio to the vector group. (B) Scratch test for evaluating the distance of cell migration in the Notch signaling pathway inhibition groups. The distance of cell migration is presented as a ratio to the scrambled siRNA group. Data are expressed as the mean ± SD. The difference between groups was compared using one-way analysis of variance and nonparametric Mann-Whitney U test. Experiments were performed in triplicate. *P < 0.05, vs. vector group; #P < 0.05, vs. scrambled siRNA group. Notch1 OE: Notch1 overexpression group; Jagged1 OE: Jagged1 overexpression group; JAG1: Ligand for mulvipe Notch receptors and involved in the mediation of Notch signaling; siNotch1: Notch1 knockdown group; siJagged1: Jagged1 knockdown group; DAPT: γ-secretase inhibitor IX.
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Figure 2: Activation of the Notch signaling pathway enhanced the migration of endothelial progenitor cells.(A) Scratch test for evaluating the distance of cell migration in the Notch signaling pathway activation groups. The distance of cell migration is presented as a ratio to the vector group. (B) Scratch test for evaluating the distance of cell migration in the Notch signaling pathway inhibition groups. The distance of cell migration is presented as a ratio to the scrambled siRNA group. Data are expressed as the mean ± SD. The difference between groups was compared using one-way analysis of variance and nonparametric Mann-Whitney U test. Experiments were performed in triplicate. *P < 0.05, vs. vector group; #P < 0.05, vs. scrambled siRNA group. Notch1 OE: Notch1 overexpression group; Jagged1 OE: Jagged1 overexpression group; JAG1: Ligand for mulvipe Notch receptors and involved in the mediation of Notch signaling; siNotch1: Notch1 knockdown group; siJagged1: Jagged1 knockdown group; DAPT: γ-secretase inhibitor IX.

Mentions: The scratch test showed that compared with the empty plasmid control group (vector group), the distance migrated by the cells was greater after overexpression of Notch1 and Jagged1 (P < 0.05; Figure 2A). Compared with the scrambled siRNA group, migratory ability diminished after the Notch signaling pathway was inhibited by Notch1 and Jagged1 knockdown with siRNA (P < 0.05). These results are similar to those obtained using DAPT to block the Notch signaling pathway (P > 0.05; Figure 2B). These data indicate that the Notch signaling pathway promotes EPC migration.


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)

Activation of the Notch signaling pathway enhanced the migration of endothelial progenitor cells.(A) Scratch test for evaluating the distance of cell migration in the Notch signaling pathway activation groups. The distance of cell migration is presented as a ratio to the vector group. (B) Scratch test for evaluating the distance of cell migration in the Notch signaling pathway inhibition groups. The distance of cell migration is presented as a ratio to the scrambled siRNA group. Data are expressed as the mean ± SD. The difference between groups was compared using one-way analysis of variance and nonparametric Mann-Whitney U test. Experiments were performed in triplicate. *P < 0.05, vs. vector group; #P < 0.05, vs. scrambled siRNA group. Notch1 OE: Notch1 overexpression group; Jagged1 OE: Jagged1 overexpression group; JAG1: Ligand for mulvipe Notch receptors and involved in the mediation of Notch signaling; siNotch1: Notch1 knockdown group; siJagged1: Jagged1 knockdown group; DAPT: γ-secretase inhibitor IX.
© Copyright Policy - open-access
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4590238&req=5

Figure 2: Activation of the Notch signaling pathway enhanced the migration of endothelial progenitor cells.(A) Scratch test for evaluating the distance of cell migration in the Notch signaling pathway activation groups. The distance of cell migration is presented as a ratio to the vector group. (B) Scratch test for evaluating the distance of cell migration in the Notch signaling pathway inhibition groups. The distance of cell migration is presented as a ratio to the scrambled siRNA group. Data are expressed as the mean ± SD. The difference between groups was compared using one-way analysis of variance and nonparametric Mann-Whitney U test. Experiments were performed in triplicate. *P < 0.05, vs. vector group; #P < 0.05, vs. scrambled siRNA group. Notch1 OE: Notch1 overexpression group; Jagged1 OE: Jagged1 overexpression group; JAG1: Ligand for mulvipe Notch receptors and involved in the mediation of Notch signaling; siNotch1: Notch1 knockdown group; siJagged1: Jagged1 knockdown group; DAPT: γ-secretase inhibitor IX.
Mentions: The scratch test showed that compared with the empty plasmid control group (vector group), the distance migrated by the cells was greater after overexpression of Notch1 and Jagged1 (P < 0.05; Figure 2A). Compared with the scrambled siRNA group, migratory ability diminished after the Notch signaling pathway was inhibited by Notch1 and Jagged1 knockdown with siRNA (P < 0.05). These results are similar to those obtained using DAPT to block the Notch signaling pathway (P > 0.05; Figure 2B). These data indicate that the Notch signaling pathway promotes EPC migration.

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