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Profiling of Proteins Regulated by Venlafaxine during Neural Differentiation of Human Cells.

Doh MS, Han DM, Oh DH, Kim SH, Choi MR, Chai YG - Psychiatry Investig (2015)

Bottom Line: To study the effects of venlafaxine during neural differentiation at the cellular level, we looked at its effect on protein expression and regulation mechanisms during neural differentiation.Treatment with venlafaxine decreased expression of prolyl 4-hydroxylase (P4HB), ubiquitin-conjugating enzyme E2K (HIP2) and plastin 3 (T-plastin), and up-regulated expression of growth factor beta-3 (TGF-β3), dihydropyrimidinase-like 3 (DPYSL3), and pyruvate kinase (PKM) after differentiation for 1 and 7 days.Our findings may contribute to improve understanding of molecular mechanism of venlafaxine.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular and Life Sciences, Hanyang University, Ansan, Republic of Korea.

ABSTRACT

Objective: Antidepressants are known to positively influence several factors in patients with depressive disorders, resulting in increased neurogenesis and subsequent relief of depressive disorders. To study the effects of venlafaxine during neural differentiation at the cellular level, we looked at its effect on protein expression and regulation mechanisms during neural differentiation.

Methods: After exposing NCCIT cell-derived EBs to venlafaxine during differentiation (1 day and 7 days), changes in protein expression were analyzed by 2-DE and MALDI-TOF MS analysis. Gene levels of proteins regulated by venlafaxine were analyzed by real-time RT-PCR.

Results: Treatment with venlafaxine decreased expression of prolyl 4-hydroxylase (P4HB), ubiquitin-conjugating enzyme E2K (HIP2) and plastin 3 (T-plastin), and up-regulated expression of growth factor beta-3 (TGF-β3), dihydropyrimidinase-like 3 (DPYSL3), and pyruvate kinase (PKM) after differentiation for 1 and 7 days. In cells exposed to venlafaxine, the mRNA expression patterns of HIP2 and PKM, which function as negative and positive regulators of differentiation and neuronal survival, respectively, were consistent with the observed changes in protein expression.

Conclusion: Our findings may contribute to improve understanding of molecular mechanism of venlafaxine.

No MeSH data available.


Related in: MedlinePlus

Induction of differentiation of embryonic bodies derived from NCCIT cells. A: Experimental scheme. Human embryonic carcinoma (NCCIT) cells were induced to form embryonic bodies (EBs) for 7 days. EBs were treated with 10 µM retinoic acid (RA) in the presence or absence of 10 µM venlafaxine (VEN) for 7 days. Cells on differentiation day 1 and 7 were collected for two-dimensional gel electrophoresis (2DE) assay. B: Measurement of the differentiation potential of EBs. After exposing EBs to 10 µM RA in the presence or absence of 10 µM VEN for 7 days, immunocytochemistry was used to measure the Nestin (neural stem cell marker), TU20 (neuron marker), GFAP (astrocyte marker), and O4 (oli-godendrocyte marker). Cells exposed to RA in the absence of VEN served as controls (CON).
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Figure 1: Induction of differentiation of embryonic bodies derived from NCCIT cells. A: Experimental scheme. Human embryonic carcinoma (NCCIT) cells were induced to form embryonic bodies (EBs) for 7 days. EBs were treated with 10 µM retinoic acid (RA) in the presence or absence of 10 µM venlafaxine (VEN) for 7 days. Cells on differentiation day 1 and 7 were collected for two-dimensional gel electrophoresis (2DE) assay. B: Measurement of the differentiation potential of EBs. After exposing EBs to 10 µM RA in the presence or absence of 10 µM VEN for 7 days, immunocytochemistry was used to measure the Nestin (neural stem cell marker), TU20 (neuron marker), GFAP (astrocyte marker), and O4 (oli-godendrocyte marker). Cells exposed to RA in the absence of VEN served as controls (CON).

Mentions: To evaluate the effects of venlafaxine during neural differentiation, EBs derived from NCCIT cells were seeded in 100-mm tissue culture dishes and incubated with differentiation medium containing 10 µM RA in the absence or presence of 10 µM venlafaxine (Wyeth Korea, Seoul, Korea) (Figure 1A). The 10 µM concentration of venlafaxine was decided as was done in previous studies that the concentration did not induce apoptosis.27,28 Cultures were fed with fresh differentiation medium every 2 to 3 days up to 7 days.


Profiling of Proteins Regulated by Venlafaxine during Neural Differentiation of Human Cells.

Doh MS, Han DM, Oh DH, Kim SH, Choi MR, Chai YG - Psychiatry Investig (2015)

Induction of differentiation of embryonic bodies derived from NCCIT cells. A: Experimental scheme. Human embryonic carcinoma (NCCIT) cells were induced to form embryonic bodies (EBs) for 7 days. EBs were treated with 10 µM retinoic acid (RA) in the presence or absence of 10 µM venlafaxine (VEN) for 7 days. Cells on differentiation day 1 and 7 were collected for two-dimensional gel electrophoresis (2DE) assay. B: Measurement of the differentiation potential of EBs. After exposing EBs to 10 µM RA in the presence or absence of 10 µM VEN for 7 days, immunocytochemistry was used to measure the Nestin (neural stem cell marker), TU20 (neuron marker), GFAP (astrocyte marker), and O4 (oli-godendrocyte marker). Cells exposed to RA in the absence of VEN served as controls (CON).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4310925&req=5

Figure 1: Induction of differentiation of embryonic bodies derived from NCCIT cells. A: Experimental scheme. Human embryonic carcinoma (NCCIT) cells were induced to form embryonic bodies (EBs) for 7 days. EBs were treated with 10 µM retinoic acid (RA) in the presence or absence of 10 µM venlafaxine (VEN) for 7 days. Cells on differentiation day 1 and 7 were collected for two-dimensional gel electrophoresis (2DE) assay. B: Measurement of the differentiation potential of EBs. After exposing EBs to 10 µM RA in the presence or absence of 10 µM VEN for 7 days, immunocytochemistry was used to measure the Nestin (neural stem cell marker), TU20 (neuron marker), GFAP (astrocyte marker), and O4 (oli-godendrocyte marker). Cells exposed to RA in the absence of VEN served as controls (CON).
Mentions: To evaluate the effects of venlafaxine during neural differentiation, EBs derived from NCCIT cells were seeded in 100-mm tissue culture dishes and incubated with differentiation medium containing 10 µM RA in the absence or presence of 10 µM venlafaxine (Wyeth Korea, Seoul, Korea) (Figure 1A). The 10 µM concentration of venlafaxine was decided as was done in previous studies that the concentration did not induce apoptosis.27,28 Cultures were fed with fresh differentiation medium every 2 to 3 days up to 7 days.

Bottom Line: To study the effects of venlafaxine during neural differentiation at the cellular level, we looked at its effect on protein expression and regulation mechanisms during neural differentiation.Treatment with venlafaxine decreased expression of prolyl 4-hydroxylase (P4HB), ubiquitin-conjugating enzyme E2K (HIP2) and plastin 3 (T-plastin), and up-regulated expression of growth factor beta-3 (TGF-β3), dihydropyrimidinase-like 3 (DPYSL3), and pyruvate kinase (PKM) after differentiation for 1 and 7 days.Our findings may contribute to improve understanding of molecular mechanism of venlafaxine.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular and Life Sciences, Hanyang University, Ansan, Republic of Korea.

ABSTRACT

Objective: Antidepressants are known to positively influence several factors in patients with depressive disorders, resulting in increased neurogenesis and subsequent relief of depressive disorders. To study the effects of venlafaxine during neural differentiation at the cellular level, we looked at its effect on protein expression and regulation mechanisms during neural differentiation.

Methods: After exposing NCCIT cell-derived EBs to venlafaxine during differentiation (1 day and 7 days), changes in protein expression were analyzed by 2-DE and MALDI-TOF MS analysis. Gene levels of proteins regulated by venlafaxine were analyzed by real-time RT-PCR.

Results: Treatment with venlafaxine decreased expression of prolyl 4-hydroxylase (P4HB), ubiquitin-conjugating enzyme E2K (HIP2) and plastin 3 (T-plastin), and up-regulated expression of growth factor beta-3 (TGF-β3), dihydropyrimidinase-like 3 (DPYSL3), and pyruvate kinase (PKM) after differentiation for 1 and 7 days. In cells exposed to venlafaxine, the mRNA expression patterns of HIP2 and PKM, which function as negative and positive regulators of differentiation and neuronal survival, respectively, were consistent with the observed changes in protein expression.

Conclusion: Our findings may contribute to improve understanding of molecular mechanism of venlafaxine.

No MeSH data available.


Related in: MedlinePlus