Affect of antidepressants on the in vitro differentiation of rat bone marrow mesenchymal stem cells into neuronal cells

Borkowska, Paulina; Kowalska, J.; Fila-Daniłow, Anna; Bielecka, Anna; Paul-Samojedny, Monika; Kowalczyk, Małgorzata; Kowalski, Jan

doi:10.1016/j.ejps.2015.03.016

Cited by 11 publications

(8 citation statements)

References 25 publications

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“…In studies related to the differentiation of heart muscle cells and monocytes, SSRIs decreased the cell differentiation, and their results were in agreement with our results according to the reduction of differentiation. But in studies related to the differentiation of ectodermic and neurogenic cells, these drugs increased the cell differentiation that these results were not in consistent with our results .…”

Section: Discussioncontrasting

confidence: 99%

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The effects of fluoxetine on the human adipose‐derived stem cell proliferation and differentiation

Khademi

Ghavamabadi

Taghavi

et al. 2018

Fundamemntal Clinical Pharma

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Fluoxetine is one of the most commonly used antidepressants. Fluoxetine could prevent the mesenchymal stem cell differentiation in lung fetus of rat. Moreover, the mesenchymal stem cells are also present in adult tissues. Therefore, in the current study, we aimed to investigate the effects of fluoxetine (FLX) on both proliferation and adipogenic/osteogenic differentiation of human adipose‐derived stem cells (ADSCs). After culturing of human ADSCs, these cells were treated with two concentrations of FLX (10 and 20 μm). Then, cells were differentiated by adding osteogenic and adipogenic media. The effect of FLX on human ADSCs proliferation was evaluated by MTT assay. Fluoxetine role on adipogenic and osteogenic differentiation of human ADSCs was analyzed by oil red and alizarin red staining and RT‐PCR reaction. According to MTT assay, FLX showed a time‐ and concentration‐dependent proliferation response and eventually decreased human ADSCs proliferation. RT‐PCR analysis indicated that FLX significantly diminished the expression of osteogenesis‐related genes such as RUNX2 and alkaline phosphatase (ALP). Data also revealed a significant reduction in the expression of peroxisome proliferator‐activated receptor γ (PPARγ) and fatty acid‐binding protein (FABP) (specific genes of adipogenic lineage). In addition, FLX decreased mineralized matrix and the amount of lipid droplets in human ADSCs by staining methods. Our observation demonstrated that the effects of FLX may be time‐dependent. This drug possesses an increasing phase in proliferation and survival of human ADSCs (first 24 h) following a decreasing phase (after 48 h). Moreover, FLX could attenuate both osteogenic and adipogenic differentiation of human ADSCs.

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Section: Discussioncontrasting

confidence: 99%

“…Some studies reported that FLX may exert a role as apoptosis inducer however antiapoptotic properties of FLX also were discussed [10][11][12]. Some studies expressed that FLX could prevent cell differentiation, on the other hand, there are some documents on differentiation process improvement by FLX [9,[13][14][15].…”

Section: Introductionmentioning

confidence: 99%

The effects of fluoxetine on the human adipose‐derived stem cell proliferation and differentiation

Khademi

Ghavamabadi

Taghavi

et al. 2018

Fundamemntal Clinical Pharma

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“…For example, fluoxetine increased the proliferation of embryo-derived NPCs through up-regulating GSK-3β/β-catenin signaling and this is linked with serotonin receptor activation [ 19 ]. In addition, fluoxetine induced the neuronal differentiation of BMSCs and increased the number of dendrites [ 18 ]. However, in the present study, fluoxetine decreased the survival of ASCs and suppressed the adipogenic differentiation of ASCs.…”

Section: Resultsmentioning

confidence: 99%

“…Fluoxetine was originally developed as an antidepressant and it acts as a selective serotonin reuptake inhibitor [ 16 , 17 ]. Of interest, it has been reported that fluoxetine induced the neuronal differentiation of adult stem or progenitor cells in vivo [ 18 , 19 ]. Clinical studies demonstrated that serotonergic drugs specifically reduced appetite prior to and following the consumption of fixed caloric loads, and reduced pre-meal appetite and caloric intake [ 20 , 21 , 22 ].…”

Section: Introductionmentioning

confidence: 99%

Fluoxetine Decreases the Proliferation and Adipogenic Differentiation of Human Adipose-Derived Stem Cells

Sun

Kim

Choi

et al. 2015

IJMS

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Fluoxetine was originally developed as an antidepressant, but it has also been used to treat obesity. Although the anti-appetite effect of fluoxetine is well-documented, its potential effects on human adipose-derived stem cells (ASCs) or mature adipocytes have not been investigated. Therefore, we investigated the mechanisms underlying the inhibitory effects of fluoxetine on the proliferation of ASCs. We also investigated its inhibitory effect on adipogenic differentiation. Fluoxetine significantly decreased ASC proliferation, and signal transduction PCR array analysis showed that it increased expression of autophagy-related genes. In addition, fluoxetine up-regulated SQSTM1 and LC3B protein expression as detected by western blotting and immunofluorescence. The autophagy inhibitor, 3-methyladenine (3-MA), significantly attenuated fluoxetine-mediated effects on ASC proliferation and SQSTM1/LC3B expression. In addition, 3-MA decreased the mRNA expression of two autophagy-related genes, beclin-1 and Atg7, in ASCs. Fluoxetine also significantly inhibited lipid accumulation and down-regulated the levels of PPAR-γ and C/EBP-α in ASCs. Collectively, these results indicate that fluoxetine decreases ASC proliferation and adipogenic differentiation. This is the first in vitro evidence that fluoxetine can reduce fat accumulation by inhibiting ASC proliferation and differentiation.

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“…The antidepressant fluoxetine, which is frequently used for treating post-stroke depressive syndromes, has been found to promote neurogenesis in vitro (Borkowska et al, 2015 ) and to extend the therapeutic window for brain rewiring after focal cerebral ischemia in mice (Ng et al, 2015 ). In a small randomized placebo-controlled study in human stroke patients, fluoxetine (20 mg per day) promoted motor recovery evaluated by the Fugl-Meyer motor scale over up to 3 months (Chollet et al, 2011 ).…”

Section: Translation Of Treatments To Human Stroke Patientsmentioning

confidence: 99%

Correlates of Post-Stroke Brain Plasticity, Relationship to Pathophysiological Settings and Implications for Human Proof-of-Concept Studies

Sánchez-Mendoza

Hermann

2016

Front. Cell. Neurosci.

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The promotion of neurological recovery by enhancing neuroplasticity has recently obtained strong attention in the stroke field. Experimental studies support the hypothesis that stroke recovery can be improved by therapeutic interventions that augment neuronal sprouting. However plasticity responses of neurons are highly complex, involving the growth and differentiation of axons, dendrites, dendritic spines and synapses, which depend on the pathophysiological setting and are tightly controlled by extracellular and intracellular signals. Thorough mechanistic insights are needed into how neuronal plasticity is influenced by plasticity-promoting therapies in order not to risk the success of future clinical proof-of-concept studies.

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Affect of antidepressants on the in vitro differentiation of rat bone marrow mesenchymal stem cells into neuronal cells

Cited by 11 publications

References 25 publications

The effects of fluoxetine on the human adipose‐derived stem cell proliferation and differentiation

The effects of fluoxetine on the human adipose‐derived stem cell proliferation and differentiation

Fluoxetine Decreases the Proliferation and Adipogenic Differentiation of Human Adipose-Derived Stem Cells

Correlates of Post-Stroke Brain Plasticity, Relationship to Pathophysiological Settings and Implications for Human Proof-of-Concept Studies

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