Limits...
CCL2 induces neural stem cell proliferation and neuronal differentiation in Niemann-Pick type C mice.

Hong YR, Lee H, Park MH, Lee JK, Lee JY, Suh HD, Jeong MS, Bae JS, Jin HK - J. Vet. Med. Sci. (2015)

Bottom Line: Targeting of neuronal cells in the brain therefore represents a potential clinical intervention strategy to reduce the rate of disease progression and improve the quality of life.However, the direct effect of CCL2 on neurogenesis has not been ascertained.CCL2-treated NSCs showed significantly increased capacity for self-renewal, proliferation and neuronal differentiation.

View Article: PubMed Central - PubMed

Affiliation: Stem Cell Neuroplasticity Research Group, Kyungpook National University, Daegu, Korea.

ABSTRACT
Niemann-Pick type C disease (NP-C) is a rare and ultimately fatal lysosomal storage disorder with variable neurologic symptoms. Loss of neuronal function and neuronal cell death occur in the NP-C brain, similar to the findings for other neurodegenerative diseases. Targeting of neuronal cells in the brain therefore represents a potential clinical intervention strategy to reduce the rate of disease progression and improve the quality of life. We previously reported that bone marrow stem cells show a neurogenic effect through CCL2 (also known as monocyte chemoattractant protein-1, MCP-1) secretion in the brains of NP-C mice. However, the direct effect of CCL2 on neurogenesis has not been ascertained. Here, to define neurogenic effects of CCL2 in NP-C, we applied human recombinant CCL2 to neural stem cells (NSCs) derived from NP-C mice. CCL2-treated NSCs showed significantly increased capacity for self-renewal, proliferation and neuronal differentiation. Similar results were observed in the subventricular zone of NP-C mice after CCL2 treatment. Furthermore, infusion of CCL2 into the NP-C mouse brain resulted in reduction of neuroinflammation. Taken together, our results demonstrate that CCL2 is a potential new therapeutic agent for NP-C.

No MeSH data available.


Related in: MedlinePlus

CCL2 elicited functional improvement in NP-C mice. Rota-rod scores of mice wereaveraged and plotted beginning 3 days after CCL2 treatment (WT and NP-C, n=15;CCL2-treated NP-C, n=9). All data are given as mean ± SEM.#P<0.05, ##P<0.01,###P<0.005 compared to non-treated NP-C mice.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4488406&req=5

fig_005: CCL2 elicited functional improvement in NP-C mice. Rota-rod scores of mice wereaveraged and plotted beginning 3 days after CCL2 treatment (WT and NP-C, n=15;CCL2-treated NP-C, n=9). All data are given as mean ± SEM.#P<0.05, ##P<0.01,###P<0.005 compared to non-treated NP-C mice.

Mentions: There were also slight improvements in the rota-rod score of CCL2-treated NP-C micecompared to those of non-treated NP-C mice, although this difference did not reachstatistical significance (Fig. 5Fig. 5.


CCL2 induces neural stem cell proliferation and neuronal differentiation in Niemann-Pick type C mice.

Hong YR, Lee H, Park MH, Lee JK, Lee JY, Suh HD, Jeong MS, Bae JS, Jin HK - J. Vet. Med. Sci. (2015)

CCL2 elicited functional improvement in NP-C mice. Rota-rod scores of mice wereaveraged and plotted beginning 3 days after CCL2 treatment (WT and NP-C, n=15;CCL2-treated NP-C, n=9). All data are given as mean ± SEM.#P<0.05, ##P<0.01,###P<0.005 compared to non-treated NP-C mice.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4488406&req=5

fig_005: CCL2 elicited functional improvement in NP-C mice. Rota-rod scores of mice wereaveraged and plotted beginning 3 days after CCL2 treatment (WT and NP-C, n=15;CCL2-treated NP-C, n=9). All data are given as mean ± SEM.#P<0.05, ##P<0.01,###P<0.005 compared to non-treated NP-C mice.
Mentions: There were also slight improvements in the rota-rod score of CCL2-treated NP-C micecompared to those of non-treated NP-C mice, although this difference did not reachstatistical significance (Fig. 5Fig. 5.

Bottom Line: Targeting of neuronal cells in the brain therefore represents a potential clinical intervention strategy to reduce the rate of disease progression and improve the quality of life.However, the direct effect of CCL2 on neurogenesis has not been ascertained.CCL2-treated NSCs showed significantly increased capacity for self-renewal, proliferation and neuronal differentiation.

View Article: PubMed Central - PubMed

Affiliation: Stem Cell Neuroplasticity Research Group, Kyungpook National University, Daegu, Korea.

ABSTRACT
Niemann-Pick type C disease (NP-C) is a rare and ultimately fatal lysosomal storage disorder with variable neurologic symptoms. Loss of neuronal function and neuronal cell death occur in the NP-C brain, similar to the findings for other neurodegenerative diseases. Targeting of neuronal cells in the brain therefore represents a potential clinical intervention strategy to reduce the rate of disease progression and improve the quality of life. We previously reported that bone marrow stem cells show a neurogenic effect through CCL2 (also known as monocyte chemoattractant protein-1, MCP-1) secretion in the brains of NP-C mice. However, the direct effect of CCL2 on neurogenesis has not been ascertained. Here, to define neurogenic effects of CCL2 in NP-C, we applied human recombinant CCL2 to neural stem cells (NSCs) derived from NP-C mice. CCL2-treated NSCs showed significantly increased capacity for self-renewal, proliferation and neuronal differentiation. Similar results were observed in the subventricular zone of NP-C mice after CCL2 treatment. Furthermore, infusion of CCL2 into the NP-C mouse brain resulted in reduction of neuroinflammation. Taken together, our results demonstrate that CCL2 is a potential new therapeutic agent for NP-C.

No MeSH data available.


Related in: MedlinePlus