Biology subjects

Hosseini, V.

Publications and source records attributed to Hosseini, V..

3 recordsLinked to original sources

bioRxiv2023

Epstein-Barr virus-encoded BART9 and BART15 miRNAs are elevated in exosomes of cerebrospinal fluid from relapsing-remitting multiple sclerosis patients

Epstein-Barr virus (EBV) infection is approved as the main environmental trigger of multiple sclerosis (MS). In this path, we quantified EBV-encoded BART9-3p and BART15 miRNAs in exosomes of cerebrospinal fluid (CSF) of untreated relapsing-remitting MS (RRMS) patients in comparison with the control group. Interestingly, patients displayed significant upregulation of BART9-3p (18.4-fold) and BART15 (3.1-fold) expression in CSF exosomes. Moreover, the expression levels of miR-21-5p and miR-146a-5p were found to be significantly elevated in the CSF samples obtained from the patient group in comparison to those obtained from the HC group. The levels of Interferon gamma (IFN-{gamma}), interleukin-1{beta} (IL-1{beta}), interleukin- 6 (IL-6), interleukin-17 (IL-17), interleukin-23 (IL-23), transforming growth factor beta (TGF- {beta}), and tumor necrosis factor alpha (TNF-) were observed to be significantly elevated in the serum and CSF exosomes of the patients. The highest increase was observed in TGF-{beta} (8.5- fold), followed by IL-23 (3.9-fold) in CSF exosomes. These findings are in agreement with the association between EBV infection and inflammatory cytokines induction. Furthermore, the ratios of TGF-{beta}:TNF- and TGF-{beta}:IFN-{gamma} attained values of 4 to 16.4 and 1.3 to 3.6, respectively, in the CSF exosomes of the patients, in comparison to those of the control group. Remarkable stimulation of EBV BART9-3p, BART15 miRNAs, and inflammatory cytokines expression in CSF exosomes confers a substantial link between EBV in MS onset and also the infection-to-MS transition.

molecular biology↗

bioRxiv2020

Human induced pluripotent stem cell-derived arteries as personalized models of atherosclerosis on-a-chip

Atherosclerosis is an arterial disease characterized by intravascular plaques. Disease hallmarks are vessel stenosis and hyperplasia, eventually escalating into plaque rupture and acute clinical presentations. Innate immune cells and local variations in hemodynamics are core players in the pathology, but their mutual relationship has never been investigated before due to the lack of modeling systems with adequate degree of complexity. Here, we combined computational fluid dynamics and tissue-engineering to achieve, for the first time in vitro, full atherosclerotic plaque development. Our model incorporates induced pluripotent stem cell-derived populations into small-caliber arteries that are cultured in atheroprone conditions. Using machine-learning-aided immunophenotyping, molecular and nanoprobe-based tensile analyses, we found that immune cells, extracellular matrix components and tensional state were comparable between in vitro and ex vivo human lesions. Our results provide further insights into the relation between hemodynamics and inflammation, introducing a versatile, scalable modeling tool to study atherosclerosis onset and progression.

bioengineering↗

bioRxiv2018

miR-216b-5p is Down-Regulated in Human Breast Cancer and Inhibits Proliferation and Progression by Targeting HDAC8 Oncogene

BackgroundPrevious studies showed the role of histone deacetylases (HDACs) on the progression of some malignancies. Recently, there is more attention to therapeutic applications of epigenetic factors such as microRNAs (miRs). To the best of our knowledge, there are no other results regarding the contribution of miR-216b-5p and its potential target, HDAC8, in progression of cancer.\n\nAimIn the present study, we investigated the role of miR-216b-5p on HDAC8 and there following impacts on breast cancer (BC) progression.\n\nMethodsHuman BC specimens and noncancerous tissues were acquired from Iran Tumor Bank (I.T.B). The MDA-MB-231, MCF-7 and MCF-10A BC cell lines were also prepared. The tissue and cell line expression levels of miR-216b-5p and HDAC8 were determined by quantitative real-time PCR (qPCR). Protein levels of HDAC8 were also measured by Western blotting assay. The cell cycle, cell proliferation and colony formation assay were determined and the role of HDAC8 was investigated using a knockout vector. Targeting the 3' untranslated region (3'UTR) of HDAC8 by miR-216b-5p were confirmed using a luciferase reporter assay.\n\nResultsOur results show the significant decline in miR-216b-5p and highly increase in HDAC8 levels in human breast cancer tissues and cell lines. Overexpression of miR-216b-5p in BC cell lines inhibited cellular proliferation and progression and inhibition of miR-216b-5p reverse these effects. We also confirmed that HDAC8 is directly down-regulated by miR-216b-5p. Knockout of HDAC8 had also the effects as miR-216b-5p overexpression. Furthermore, we found that lower levels of miR-216b-5p are negatively correlated with lymph node metastasis and advanced tumor size.\n\nConclusionTaken together, our data shown that targeted overexpression of miR-216b-5p can suppress the growth of BC cells down-regulation of HDAC8. Therefore, inhibition of HDAC8 by miR-216b-5p will be helpful developing newer therapies for the effective treatment of BC.

cancer biology↗