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Astaxanthin improves stem cell potency via an increase in the proliferation of neural progenitor cells.

Kim JH, Nam SW, Kim BW, Choi W, Lee JH, Kim WJ, Choi YH - Int J Mol Sci (2010)

Bottom Line: Treatment with astaxanthin significantly increased proliferation and colony formation of NPCs.In Western blot analysis, astaxanthin induced significant activation of phosphatidylinositol 3-kinase (PI3K) and its downstream mediators in a time-dependent manner.These results clearly showed that astaxanthin induces proliferation of NPCs via activation of the PI3K and MEK signaling pathways and improves stem cell potency via stemness acting signals.

View Article: PubMed Central - PubMed

Affiliation: Department of Biomaterial Control, Dong-Eui University, Busan, 614-714, Korea; E-Mails: 12845@deu.ac.kr (J.-H.K.); bwkim@deu.ac.kr (B.-W.K.); wbchoi@deu.ac.kr (W.C.); jonghwanlee@deu.ac.kr (J.-H.L.).

ABSTRACT
The present study was designed to investigate the question of whether or not astaxanthin improves stem cell potency via an increase in proliferation of neural progenitor cells (NPCs). Treatment with astaxanthin significantly increased proliferation and colony formation of NPCs. For identification of possible activated signaling molecules involved in active cell proliferation occurring after astaxanthin treatment, total protein levels of several proliferation-related proteins, and expression levels of proliferation-related transcription factors, were assessed in NPCs. In Western blot analysis, astaxanthin induced significant activation of phosphatidylinositol 3-kinase (PI3K) and its downstream mediators in a time-dependent manner. Results of RT-PCR analysis showed upregulation of proliferation-related transcription factors and stemness genes. To estimate the relevance of PI3K and mitogen-activated protein, or extracellular signal-regulated kinase kinase (MEK) signaling pathways in cell growth of astaxanthin-treated NPCs, inhibition assays were performed with LY294002, a specific inhibitor of PI3K, and PD98059, a specific inhibitor of MEK, respectively. These results clearly showed that astaxanthin induces proliferation of NPCs via activation of the PI3K and MEK signaling pathways and improves stem cell potency via stemness acting signals.

Show MeSH
Astaxanthin induces proliferation of NPCs via the PI3K and MEK signaling pathways. To estimate the relevance of the PI3K and MEK signaling pathways in cell growth in astaxanthin-treated NPCs, inhibition assays were performed with LY294002 (10 μM) and PD98059 (10 μM). (A) Inhibition of PI3K and MEK has been shown to cause inhibition of cell growth in astaxanthin-treated NPCs in vitro; (B) LY294002 induced downregulation of PI3K, p-Rac, p-c-Raf, p-MEK, p-ERK, p-Akt, p-mTOR, and p-Stat3 proteins; (C) PD98059 significantly induced reduction of p-MEK, p-ERK, and p-Stat3; (D) PD98059 caused downregulation of proliferation-related transcription factors and stemness genes.
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f3-ijms-11-05109: Astaxanthin induces proliferation of NPCs via the PI3K and MEK signaling pathways. To estimate the relevance of the PI3K and MEK signaling pathways in cell growth in astaxanthin-treated NPCs, inhibition assays were performed with LY294002 (10 μM) and PD98059 (10 μM). (A) Inhibition of PI3K and MEK has been shown to cause inhibition of cell growth in astaxanthin-treated NPCs in vitro; (B) LY294002 induced downregulation of PI3K, p-Rac, p-c-Raf, p-MEK, p-ERK, p-Akt, p-mTOR, and p-Stat3 proteins; (C) PD98059 significantly induced reduction of p-MEK, p-ERK, and p-Stat3; (D) PD98059 caused downregulation of proliferation-related transcription factors and stemness genes.

Mentions: For identification of possible activated signaling molecules involved in active cell proliferation occurring after astaxanthin treatment, total protein levels of several proliferation-related proteins were assessed in NPCs by Western blot analysis. Figure 2B shows the results of Western blot in astaxanthin-treated NPCs for different lengths of time (0, 6, and 12 h). In Western blot analysis, astaxanthin induced significant activation of PI3K and its downstream mediators, p-Rac, p-c-Raf, p-MEK, p-ERK, p-Akt, p-mTOR, and p-Stat3 [29] in a time-dependent manner. This study then examined the relevance of the PI3K and MEK signaling pathways in cell growth in astaxanthin-treated NPCs. For these studies, inhibition assays were performed with specific inhibitors, LY294002 (a specific inhibitor of PI3K) and PD98059 (a specific inhibitor of MEK). Astaxanthin-treated NPCs were treated with LY294002 or PD98059, or were left untreated. After LY294002 and PD98059 treatment respectively, the relative cell proliferation rate of astaxanthin-treated NPCs was assessed by trypan blue exclusion: Results are shown in Figure 3A. PI3K and MEK inhibition have been shown to cause inhibition of cell growth in astaxanthin-treated NPCs in vitro. As shown in Figure 3B, the results of Western blot analysis indicated that LY294002 significantly induced downregulation of PI3K, p-Rac, p-c-Raf, p-MEK, p-ERK, p-Akt, p-mTOR, and p-Stat3 proteins.


Astaxanthin improves stem cell potency via an increase in the proliferation of neural progenitor cells.

Kim JH, Nam SW, Kim BW, Choi W, Lee JH, Kim WJ, Choi YH - Int J Mol Sci (2010)

Astaxanthin induces proliferation of NPCs via the PI3K and MEK signaling pathways. To estimate the relevance of the PI3K and MEK signaling pathways in cell growth in astaxanthin-treated NPCs, inhibition assays were performed with LY294002 (10 μM) and PD98059 (10 μM). (A) Inhibition of PI3K and MEK has been shown to cause inhibition of cell growth in astaxanthin-treated NPCs in vitro; (B) LY294002 induced downregulation of PI3K, p-Rac, p-c-Raf, p-MEK, p-ERK, p-Akt, p-mTOR, and p-Stat3 proteins; (C) PD98059 significantly induced reduction of p-MEK, p-ERK, and p-Stat3; (D) PD98059 caused downregulation of proliferation-related transcription factors and stemness genes.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC3100832&req=5

f3-ijms-11-05109: Astaxanthin induces proliferation of NPCs via the PI3K and MEK signaling pathways. To estimate the relevance of the PI3K and MEK signaling pathways in cell growth in astaxanthin-treated NPCs, inhibition assays were performed with LY294002 (10 μM) and PD98059 (10 μM). (A) Inhibition of PI3K and MEK has been shown to cause inhibition of cell growth in astaxanthin-treated NPCs in vitro; (B) LY294002 induced downregulation of PI3K, p-Rac, p-c-Raf, p-MEK, p-ERK, p-Akt, p-mTOR, and p-Stat3 proteins; (C) PD98059 significantly induced reduction of p-MEK, p-ERK, and p-Stat3; (D) PD98059 caused downregulation of proliferation-related transcription factors and stemness genes.
Mentions: For identification of possible activated signaling molecules involved in active cell proliferation occurring after astaxanthin treatment, total protein levels of several proliferation-related proteins were assessed in NPCs by Western blot analysis. Figure 2B shows the results of Western blot in astaxanthin-treated NPCs for different lengths of time (0, 6, and 12 h). In Western blot analysis, astaxanthin induced significant activation of PI3K and its downstream mediators, p-Rac, p-c-Raf, p-MEK, p-ERK, p-Akt, p-mTOR, and p-Stat3 [29] in a time-dependent manner. This study then examined the relevance of the PI3K and MEK signaling pathways in cell growth in astaxanthin-treated NPCs. For these studies, inhibition assays were performed with specific inhibitors, LY294002 (a specific inhibitor of PI3K) and PD98059 (a specific inhibitor of MEK). Astaxanthin-treated NPCs were treated with LY294002 or PD98059, or were left untreated. After LY294002 and PD98059 treatment respectively, the relative cell proliferation rate of astaxanthin-treated NPCs was assessed by trypan blue exclusion: Results are shown in Figure 3A. PI3K and MEK inhibition have been shown to cause inhibition of cell growth in astaxanthin-treated NPCs in vitro. As shown in Figure 3B, the results of Western blot analysis indicated that LY294002 significantly induced downregulation of PI3K, p-Rac, p-c-Raf, p-MEK, p-ERK, p-Akt, p-mTOR, and p-Stat3 proteins.

Bottom Line: Treatment with astaxanthin significantly increased proliferation and colony formation of NPCs.In Western blot analysis, astaxanthin induced significant activation of phosphatidylinositol 3-kinase (PI3K) and its downstream mediators in a time-dependent manner.These results clearly showed that astaxanthin induces proliferation of NPCs via activation of the PI3K and MEK signaling pathways and improves stem cell potency via stemness acting signals.

View Article: PubMed Central - PubMed

Affiliation: Department of Biomaterial Control, Dong-Eui University, Busan, 614-714, Korea; E-Mails: 12845@deu.ac.kr (J.-H.K.); bwkim@deu.ac.kr (B.-W.K.); wbchoi@deu.ac.kr (W.C.); jonghwanlee@deu.ac.kr (J.-H.L.).

ABSTRACT
The present study was designed to investigate the question of whether or not astaxanthin improves stem cell potency via an increase in proliferation of neural progenitor cells (NPCs). Treatment with astaxanthin significantly increased proliferation and colony formation of NPCs. For identification of possible activated signaling molecules involved in active cell proliferation occurring after astaxanthin treatment, total protein levels of several proliferation-related proteins, and expression levels of proliferation-related transcription factors, were assessed in NPCs. In Western blot analysis, astaxanthin induced significant activation of phosphatidylinositol 3-kinase (PI3K) and its downstream mediators in a time-dependent manner. Results of RT-PCR analysis showed upregulation of proliferation-related transcription factors and stemness genes. To estimate the relevance of PI3K and mitogen-activated protein, or extracellular signal-regulated kinase kinase (MEK) signaling pathways in cell growth of astaxanthin-treated NPCs, inhibition assays were performed with LY294002, a specific inhibitor of PI3K, and PD98059, a specific inhibitor of MEK, respectively. These results clearly showed that astaxanthin induces proliferation of NPCs via activation of the PI3K and MEK signaling pathways and improves stem cell potency via stemness acting signals.

Show MeSH