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. 2016 Oct-Dec;8(4):152-158.

Paroxetine Can Enhance Neurogenesis during Neurogenic Differentiation of Human Adipose-derived Stem Cells

Maliheh Jahromi  1 , Shahnaz Razavi  1 , Nushin Amirpour  1 , Zahra Khosravizadeh  2
Affiliations

Paroxetine Can Enhance Neurogenesis during Neurogenic Differentiation of Human Adipose-derived Stem Cells

Maliheh Jahromi et al. Avicenna J Med Biotechnol. 2016 Oct-Dec.

Abstract

Background: Some antidepressant drugs can promote neuronal cell proliferation in vitro as well as hippocampal neurogenesis in human and animal models. Furthermore, adipose tissue is an available source of adult stem cells with the ability to differentiate in to multiple lineages. Therefore, human Adipose-Derived Stem Cells (hAD-SCs) may be a suitable source for regenerative medical applications. Since there is no evidence for the effect of Paroxetine as the most commonly prescribed antidepressant drug for neurogenic potential of hADSCs, an attempt was made to determine the effect of Paroxetine on proliferation and neural differentiation of hADSCs.

Methods: ADSCs were isolated from human abdominal fat. These cells differentiated to neuron-like cells and were treated with Paroxetine. 3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyl tetrazolium bromide (MTT) assay and immunofluorescence technique were used for assessment of cell proliferation and neurogenic differentiation potential of induced cells, respectively.

Results: MTT assay analysis showed that Paroxetine significantly increased the proliferation rate of induced hADSCs (p<0.05), while immunofluorescent staining indicated that Paroxetine treatment during neurogenic differentiation could enhance the mean percentage of Nestin and MAP2 (Microtubule-associated protein-2) positive cells but the mean percentage of GFAP (Glial acidic fibrillary protein) positive cells significantly decreased relative to control group (p<0.05).

Conclusion: Our results provide evidence that Paroxetine can promote proliferation and differentiation rate during neurogenic differentiation of hADSCs. Moreover, Paroxetine can reduce gliogenesis of induced hADSCs during neurogenic differentiation.

Keywords: Antidepressant drugs; Neurogenic differentiation; Paroxetine; Proliferation; Stem cells.

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Figures

Figure 1.
Figure 1.
Phase contrast microscopic morphological changes of hADSCs following differentiation with 1 μM Paroxetine in vitro. A) Undifferentiated ADSC. B) After 6–7 days of culture in pre induction medium, the cells exhibited sphere shape; C) In control group, the induced cells with 1 μM Paroxetine formed contracted cell bodies with long cytoplasmic processes 10 days post induction, (D) In the treated group, the cell bodies became bipolar and multipolar 10 days post induction. Scale bar=20 μm
Figure 2.
Figure 2.
Determination of the mean of Optical Density (OD) for treatment with 1 μM Paroxetine in assessing the proliferation rate at 2, 4 and 6 days after induction. Compared with control group, exposure to 1 μM Paroxetine resulted in a significant increase of cell proliferation after 4 and 6 days (**p≤0.01,***p≤0.001).
Figure 3.
Figure 3.
Immunocytochemical staining for specific neural markers in neurogenic differentiated cells (Nestin and MAP2), and GFAP as a marker of astrocyte treated with 1 μM Paroxetine, A) and control group B). In each experiment, the nuclei were counterstained with DAPI. Scale bar=100 μm.
Figure 4.
Figure 4.
The mean percentage of immunoreaction of positive cells for Nestin, MAP2 and GFAP in treatment with 1 μM Paroxetine compared with control group. The mean percentage of MAP2-positive cells increased in the Paroxetine treated group as compared to control group, while the mean percentage of Nestin-positive cells significantly increased in the Paroxetine treated group as compared to control group (**p≤0.01), but the mean percentage of GFAP positive cells in the treated group significantly decreased relative to control group (**p≤0.01).
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