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Showing 4 results for Shakeri

Fatemeh Pourkeramati, Malek Hossein Asadi, Shahryar Shakeri, Alireza Farsinejad,
Volume 23, Issue 1 (1-2019)
Abstract

Background: ZFX is a transcriptional regulator in embryonic stem cells and plays an important role in pluripotency and self-renewal. ZFX is widely expressed in pluripotent stem cells and is down-regulated during differentiation of embryonic stem cells. ZFX has five different variants that encode three different protein isoforms. While several reports have determined the overexpression of ZFX in a variety of somatic cancers, the expression of ZFX-spliced variants in cancer cells is not well-understood. Methods: We investigated the expression of ZFX variants in a series of breast cancer tissues and cell lines using quantitative PCR. Results: The expression of ZFX variant 1/3 was higher in tumor tissue compared to marginal tissue. In contrast, the ZFX variant 5 was down-regulated in tumor tissues. While the ZFX variant 1/3 and ZFX variant 5 expression significantly increased in low-grade tumors, ZFX variant 4 was strongly expressed in high-grade tumors, demonstrating lymphatic invasion. In addition, our result revealed a significant association between the HER2 status and the expression of ZFX-spliced variants. Conclusion: Our data suggest that the expression of ZFX-spliced transcripts varies between different types of breast cancer and may contribute to their tumorigenesis process. Hence, ZFX-spliced transcripts could be considered as novel tumor markers with a probable value in diagnosis, prognosis, and therapy of breast cancer.
Mr Ahmad Taherpoor, Mr Arastoo Vojdani, Dr Seyed Mohamad Ali Hashemi, Mr Arian Amali, Mr Mohammad Reza Mardani, Dr Majid Ghayour Mobarhan, Dr Habibollah Esmaily, Dr Mohammadtaghi Shakeri, Mrs Mansoureh Bakhshi, Dr Mojtaba Meshkat, Mr Amin Hooshyar Chechaklou, Dr Samaneh Abolbashari, Dr Aida Gholoubi, Dr Zahra Meshkat,
Volume 27, Issue 2 (3-2023)
Abstract

Background: Considering the high prevalence and clinical importance of herpes simplex virus (HSV) infection worldwide, we aimed to evaluate the seroprevalence of HSV-1 and HSV-2 in a population aged between 15 and 35 years in Mashhad, Iran.
Methods: This cross-sectional study was conducted on 916 cases composed of 288 (31.4%) men and 628 (68.6%) women. Using ELISA method, the presence of IgM and IgG antibodies against HSV-1 and HSV-2 was assessed.
Results: Among the population studied, 681 (74.3%) cases were positive for anti-HSV antibodies, while 235 (25.7%) cases were negative. Moreover, no IgMs were found and all positive subjects had IgG antibodies. Age (p < 0.001), occupation (p < 0.001), education (p = 0.006), smoking (p = 0.029), and BMI (p = 0.004) demonstrated a significant association with HSV-1 and HSV-2 infection.

Conclusion: Our study indicates a high seroprevalence of HSV infection; however, there was no cases positive for IgM antibodies, suggesting the high prevalence of latent infection.
 

Mojtaba Rashidi, Emad Matour, Hasti Beheshtinasab, Maryam Cheraghzadeh, Elham Shakerian,
Volume 27, Issue 4 (7-2023)
Abstract

Background: Currently, liver fibrosis is growing worldwide; unfortunately, there is no definite cure for this disease.  Hence, understanding the molecular pathways involved in the development of liver fibrosis can help to find a proper treatment. In this study, we aimed to evaluate the effects of isorhamnetin as an antifibrotic agent on platelet-derived growth factor (PDGF)-BB-activated hepatic stellate cells (HSC)-T6 cells in a concentration-dependent manner. We have also attempted to assess signaling pathways that may affect liver fibrosis.
Methods: PDGF-BB was used to activate the HSC-T6 rat hepatic stellate cell line. The activated cells were treated with Isorhamnetin for 24 h. Finally, we compared the mRNA expression level of COLA1 α-SMA and also the level of phosphorylated AKT protein with the control group.
Results: The obtained data revealed a significant increase in the expression level of the COLA1 and α-SMA genes (p > 0.05), as well as phosphorylated AKT protein, in the cells treated with PDGF-BB. In addition, 75 and 100 µM concentrations of Isorhamnetin markedly declined the COLA1 and α-SMA expression and also the phosphorylated AKT protein level in the HSC-T6 cells.
Conclusions: Our findings suggest that Isorhamnetin decreases HSC-T6 activation, the expression of COLA1 and α-SMA, in vitro, which could act as an antifibrotic element to reduce and treat liver fibrosis disease.

Shahla Asadizadeh, Mahdi Hatami, Samaneh Salehipour Bavarsad, Benyamin Kabizade, Elham Shakerian, Mojtaba Rashidi,
Volume 28, Issue 1 (1-2024)
Abstract

Background: Liver fibrosis, associated with hepatic stellate cells (HSCs), occurs when a healthy liver sustains damage, thereby impairing its function. NADPH oxidases (NOXs), specifically isoforms 1, 2, and 4, play a role in reactive oxygen species (ROS) production during hepatic injuries, resulting in fibrosis. Curcumin has shown strong potential in mitigating liver fibrosis. Our research aimed to investigate the effects of curcumin on lowering NOX and ROS levels. This compound was also studied for its effects on NOXs, ROS concentrations through the inhibition of Smad3 phosphorylation in transforming growth factor beta (TGF-β)-activated human HSCs.
Methods: MTT assay investigated the cytotoxic effects of curcumin on HSCs. The cells were activated by exposure to TGF-β (2 ng/mL) for 24 hours. After activating, the cells were treated with curcumin at 25-150 μM concentrations. After administering curcumin to the cells, we employed RT-PCR and Western blot techniques to evaluate the related gene and protein expression levels. This evaluation was primarily focused on the mRNA expression levels of NOX1, NOX2, NOX4 and phosphorylated Smad3C.
Results: The mRNA expression level of aforesaid NOXs as well as α-smooth muscle actin (α-SMA), collagen1-α, and ROS levels were significantly reduced following 100 μM curcumin treatment. Furthermore, curcumin significantly decreased the p-Smad3C protein level in TGF-β-activated cells, with fold changes of 3 and 2 observed at 75 and 100 μM, respectively.
Conclusions: Curcumin decreased the levels of ROS and NOX, as well as the expression of α-SMA and collagen1-α. The primary mechanism for this reduction could be linked to the level of p-Smad3C. Hence, curcumin could serve as an effective therapeutic agent for liver fibrosis.


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