ORCID Profile
0000-0002-7492-413X
Current Organisation
National Institute of Genetic Engineering and Biotechnology (NIGEB)
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Publisher: Springer Science and Business Media LLC
Date: 09-12-2011
Publisher: Wiley
Date: 25-10-2018
DOI: 10.1002/JCB.27868
Abstract: Previous studies have identified the heart as a source and a target tissue for oxytocin and relaxin hormones. These hormones play important roles in the regulation of cardiovascular function and repair of ischemic heart injury. In the current study, we examined the impact of oxytocin and relaxin on the development of cardiomyocytes from mesenchymal stem cells. For this purpose, mouse adipose tissue–derived stem cells (ADSCs) were treated with different concentrations of oxytocin or relaxin for 4 days. Three weeks after initiation of cardiac induction, differentiated ADSCs expressed cardiac‐specific genes, Gata4 , Mef2c , Nkx2.5, Tbx5 , α‐ and β‐Mhc , Mlc2v , Mlc2a and Anp , and cardiac proteins including connexin 43, desmin and α‐actinin. 10 −7 M oxytocin and 50 ng/mL relaxin induced the maximum upregulation in the expression of cardiac markers. A combination of oxytocin and relaxin induced cardiomyocyte differentiation more potently than the in idual factors. In our experiment, oxytocin‐relaxin combination increased the population of cardiac troponin I‐expressing cells to 6.84% as compared with 2.36% for the untreated ADSCs, 3.7% for oxytocin treatment and 3.41% for relaxin treatment groups. In summary, the results of this study indicated that oxytocin and relaxin hormones in idually and in combination can improve cardiac differentiation of ADSCs, and treatment of the ADSCs and possibly other mesenchymal stem cells with these hormones may enhance their cardiogenic differentiation and survival after transplantation into the ischemic heart tissue.
Publisher: Wiley
Date: 14-02-2020
DOI: 10.1002/IUB.2249
Publisher: Elsevier BV
Date: 12-2021
Publisher: Wiley
Date: 10-05-2022
DOI: 10.1002/JCB.30264
Abstract: Recent studies have provided evidence for tumor suppressive function of the embryonic stem cell‐specific miR‐302/367 cluster through induction of a reprogramming process. Aspirin has been found to induce reprogramming factors of mesenchymal‐to‐epithelial transition in breast cancer cells. Therefore, we aimed to investigate whether overexpression of miR‐302/367 cluster and aspirin treatment cooperate in the induction of reprogramming and tumor suppression in breast cancer cells. MDA‐MB‐231 and SK‐BR‐3 human breast cancer cell lines were transfected with a miR‐302/367 expressing vector and treated with aspirin. The cells were evaluated for indices of apoptosis, proliferation, migration, and invasion. In both cell lines, treatment of miR‐302/367‐transfected cells with aspirin upregulated expression of some main pluripotency factors such as OCT4, SOX2, NANOG , and KLF4 , and downregulated expression of some invasion and angiogenesis markers at gene and protein levels. Aspirin increased the apoptotic rate in both cell lines transfected with miR‐302/367. Both miR‐302/367 and aspirin upregulated the expression of FOXD3 protein which is a known inducer of OCT4 and NANOG. Our results demonstrate that aspirin can enhance miR‐302/367‐induced reprogramming of breast cancer cells possibly through upregulation of FOXD3 expression. This can further augment the reversal of epithelial–mesenchymal transition and inhibits migration, invasion, and angiogenic signaling in breast cancer cells reprogrammed by miR‐302/367. Therefore, aspirin may serve as a useful adjuvant for reprogramming of cancer cells.
Publisher: Springer Science and Business Media LLC
Date: 06-01-2013
DOI: 10.1007/S12032-012-0413-7
Abstract: MicroRNA-34 family has anti-proliferative and apoptotic roles. Recent studies have shown that p53 upregulates miR-34 family leading to direct repression of several key oncogenes. Inactivation of miR-34a has been reported in multiple types of malignancies including breast cancer. The critical role of miR-34a in p53-mediated cell cycle arrest and apoptosis invokes studies focusing on the specific role of miR-34a dysregulation in carcinogenesis. While presence of p53 mutations has frequently been described in breast cancer, still most of the breast tumors do not show any variation in the p53 coding sequence or protein expression. Therefore, it is important to clarify possible involvement of other mediators of p53 pathway in breast cancer. In this study, expression of mature miR-34a in breast tumors with wild-type p53 was investigated in order to find any correlation between dysregulation of miR-34a expression and breast cancer. In about 40 % of the wild-type p53 s les, miR-34a was significantly downregulated. Neither hypermethylation of the miR-34a promoter nor genetic variations of the p53-binding site were detected in tumor s les with downregulated miR-34a. This study has provided evidence that miR-34a expression can be affected in a significant proportion of breast tumors independent of p53. Furthermore, downregulation of miR-34a was significantly associated with metastasis, while there was a significant correlation between upregulation of miR-34a and non-metastatic condition indicating a protective role for miR-34a against more invasive disease. Knowledge of miR-34a status may provide additional useful information regarding the nature of breast tumors, especially when p53 testing does not show any aberration.
Publisher: Wiley
Date: 07-09-2018
DOI: 10.1002/JCP.27081
Abstract: Epigenetic reprogramming by embryonic stem cell‐specific miR‐302/367 cluster has shown some tumor suppressive effects in cancer cells of different tissues such as skin, colon, and cervix. Vitamin C has been known as a reprogramming enhancer of human and mouse somatic cells. In this study, first we aimed to investigate whether exogenous induction of miR‐302/367 in breast cancer cells shows the same tumor suppressive effects previously observed in other cancer cells lines, and whether vitamin C can enhance reprogramming of breast cancer cells and also improve the tumor suppressive function of miR‐302/367 cluster. Overexpression of miR‐302/367 cluster in MDA‐MB‐231 and SK‐BR‐3 breast cancer cells upregulated expression of miR‐302/367 members and also some core pluripotency factors including OCT4A , SOX2 and NANOG , induced mesenchymal to epithelial transition, suppressed invasion, proliferation, and induced apoptosis in the both cell lines. However, treatment of the miR‐302/367 transfected cells with vitamin C suppressed the expression of pluripotency factors and augmented the tumorigenicity of the breast cancer cells by restoring their proliferative and invasive capacity and compromising the apoptotic effect of miR‐302/367. Supplementing the culture medium with vitamin C downregulated expression of TET1 gene which seems to be the reason behind the negative impact of vitamin C on the reprogramming efficiency of miR‐302/367 cluster and its anti‐tumor effects. Therefore application of vitamin C may not always serve as a reprogramming enhancer depending on its switching function on TET1 . This phenomenon should be carefully considered when considering a reprogramming strategy for tumor suppression.
Publisher: Elsevier BV
Date: 02-2014
DOI: 10.1016/J.JBIOTEC.2013.11.028
Abstract: Neural differentiation of embryonic and adult stem cells has been reported previously. Several studies have used different proportions of serum or a cocktail of growth and differentiation factors for this purpose. In the present study, we examined neural differentiation of mouse embryonic stem (ES) cells in KoSR-containing media. We also investigated neural differentiation of mouse adipose tissue-derived stem cells (ADSCs) in a medium containing KoSR, a synthetic serum replacement, and compared it with neural differentiation in low-serum condition. Meanwhile, effect of β-ME on neural differentiation was investigated in both conditions. As revealed by RT-PCR and immunocytochemistry analyses, KoSR-containing medium induced neural differentiation of mouse ES cells. Moreover, under the culture conditions we tested, ADSCs were differentiated to neuron-like cells and expressed some neuronal markers. Low concentration of β-ME improved neuron-like differentiation of the ADSCs in the 4% FBS-supplemented medium, while addition of β-ME in KoSR condition decreased neural differentiation. KoSR-containing medium without any additional factor improved generation of neuron-like cells, upregulated the expression of mature neuronal markers and led to the formation of cytoplasmic processes. In summary, our findings are indicating that mouse embryonic and mesenchymal stem cells are capable of neural development in KoSR-containing media.
Publisher: Elsevier BV
Date: 04-2014
DOI: 10.1016/J.NEULET.2014.02.012
Abstract: The neurohypophyseal hormone oxytocin plays a role in stimulation of neurogenesis in the adult brain. However, the exact role of oxytocin in neural development is still not well understood. In the present study, we evaluated the effect of oxytocin on neural differentiation of mouse adipose tissue-derived stem cells (ADSCs). For this purpose, ADSCs were cultured in a medium containing Knockout™ Serum Replacement (KoSR) and treated with different concentrations of oxytocin at the first or eighth day of differentiation. Two weeks after neural induction, ADSCs expressed several early and late neuron-specific genes and proteins. MTT assay and cell cycle analysis revealed a stimulatory effect of oxytocin on viability and proliferation of differentiating ADSCs. As detected by quantitative real-time PCR, treatment of the ADSCs with low concentrations of oxytocin induced neurogenesis. Oxytocin treatment also upregulated the expression of oxytocin receptor mRNA. These results demonstrated for the first time that oxytocin treatment can promote neural differentiation of the ADSCs in a dose-dependent and time-dependent manner. Oxytocin has a significant role in neurogenesis, and this may have implications in regeneration of adult neurons.
Publisher: Elsevier BV
Date: 08-2019
DOI: 10.1016/J.NEULET.2019.134353
Abstract: Directing the fate of mesenchymal stem cells (MSCs) to dopaminergic neurons has great importance in both biomedical studies and cell therapy of Parkinson's disease. We recently generated dopamine-secreting cells from human adipose tissue-derived stem cells (hADSCs) by exposing the cells to a growth factor cocktail composed of SHH, bFGF, FGF8 and BDNF in low-serum condition. In the current study, we induced the cells by the same dopaminergic inducing cocktail in serum-free B27-supplemented Neurobasal medium. ADSCs differentiated in both conditions expressed several neuronal and dopaminergic markers. However, there were higher gene expression levels under the serum-free condition. Higher levels of TUJ1 and TH proteins were also detected in the cells exposed to the dopaminergic-inducing cocktail under serum-free Neurobasal condition. TH protein was expressed in about 28% and 60% of the cells differentiated in the low-serum and serum-free Neurobasal media, respectively. Moreover, the cells exposed to the dopaminergic-inducing cocktail in the serum-free Neurobasal condition released a more significant amount of dopamine in response to KCl-induced depolarization. Altogether, these findings show a greater efficiency of the serum-free Neurobasal condition for growth factor-directed differentiation of hADSCs to functional dopamine-secreting cells which may be valuable for transplantation therapy of Parkinson's disease in future.
Location: Iran (Islamic Republic of)
Location: Iran (Islamic Republic of)
Location: Japan
No related grants have been discovered for Masoumeh Fakhr Taha.