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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 angiogenic ability of endothelial progenitor cells.(A) Immunofluorescence assay showing the fluorescence intensity of CD31 labeling in the Notch signaling pathway activation groups. The fluorescence intensity of CD31 is presented as a ratio to the vector (control) group. (B) Immunofluorescence assay showing the fluorescence intensity of CD31 labeling in the Notch signaling pathway inhibition groups. The fluorescence intensity of CD31 is presented as a ratio to the scrambled siRNA 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. vector group; #P < 0.05, vs. scrambled siRNA group. Notch1 OE: Notch1 overexpression group; Jagged1 OE: Jagged1 overexpression group; JAG1: Ligand for multipe 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 4: Activation of the Notch signaling pathway enhanced the angiogenic ability of endothelial progenitor cells.(A) Immunofluorescence assay showing the fluorescence intensity of CD31 labeling in the Notch signaling pathway activation groups. The fluorescence intensity of CD31 is presented as a ratio to the vector (control) group. (B) Immunofluorescence assay showing the fluorescence intensity of CD31 labeling in the Notch signaling pathway inhibition groups. The fluorescence intensity of CD31 is presented as a ratio to the scrambled siRNA 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. vector group; #P < 0.05, vs. scrambled siRNA group. Notch1 OE: Notch1 overexpression group; Jagged1 OE: Jagged1 overexpression group; JAG1: Ligand for multipe Notch receptors and involved in the mediation of Notch signaling; siNotch1: Notch1 knockdown group; siJagged1: Jagged1 knockdown group; DAPT: γ-secretase inhibitor IX.

Mentions: CD31, also known as platelet endothelial cell adhesion molecule, is a marker of endothelial cells and can be used to examine the formation of blood vessels (Shim et al., 2015). Compared with the control group (vector group), the fluorescence intensity of CD31 was significantly enhanced in EPCs transfected with Notch1 or Jagged1 overexpression constructs (P < 0.05). This effect was similar to that produced by Jagged1 (P > 0.05; Figure 4A). Compared with the scrambled siRNA group, Notch1 or Jagged1 knockdown significantly diminished the fluorescence intensity of CD31 in EPCs (P < 0.05). This effect is similar to that produced by DAPT, which blocks the Notch signaling pathway (P > 0.05; Figure 4B). These data show that the Notch signaling pathway enhances the angiogenic ability of EPCs.


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 angiogenic ability of endothelial progenitor cells.(A) Immunofluorescence assay showing the fluorescence intensity of CD31 labeling in the Notch signaling pathway activation groups. The fluorescence intensity of CD31 is presented as a ratio to the vector (control) group. (B) Immunofluorescence assay showing the fluorescence intensity of CD31 labeling in the Notch signaling pathway inhibition groups. The fluorescence intensity of CD31 is presented as a ratio to the scrambled siRNA 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. vector group; #P < 0.05, vs. scrambled siRNA group. Notch1 OE: Notch1 overexpression group; Jagged1 OE: Jagged1 overexpression group; JAG1: Ligand for multipe 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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Figure 4: Activation of the Notch signaling pathway enhanced the angiogenic ability of endothelial progenitor cells.(A) Immunofluorescence assay showing the fluorescence intensity of CD31 labeling in the Notch signaling pathway activation groups. The fluorescence intensity of CD31 is presented as a ratio to the vector (control) group. (B) Immunofluorescence assay showing the fluorescence intensity of CD31 labeling in the Notch signaling pathway inhibition groups. The fluorescence intensity of CD31 is presented as a ratio to the scrambled siRNA 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. vector group; #P < 0.05, vs. scrambled siRNA group. Notch1 OE: Notch1 overexpression group; Jagged1 OE: Jagged1 overexpression group; JAG1: Ligand for multipe Notch receptors and involved in the mediation of Notch signaling; siNotch1: Notch1 knockdown group; siJagged1: Jagged1 knockdown group; DAPT: γ-secretase inhibitor IX.
Mentions: CD31, also known as platelet endothelial cell adhesion molecule, is a marker of endothelial cells and can be used to examine the formation of blood vessels (Shim et al., 2015). Compared with the control group (vector group), the fluorescence intensity of CD31 was significantly enhanced in EPCs transfected with Notch1 or Jagged1 overexpression constructs (P < 0.05). This effect was similar to that produced by Jagged1 (P > 0.05; Figure 4A). Compared with the scrambled siRNA group, Notch1 or Jagged1 knockdown significantly diminished the fluorescence intensity of CD31 in EPCs (P < 0.05). This effect is similar to that produced by DAPT, which blocks the Notch signaling pathway (P > 0.05; Figure 4B). These data show that the Notch signaling pathway enhances the angiogenic ability of EPCs.

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