Cell Journal (Yakhteh)

813-821

Authors: Maedeh Khatami; Yousef Moradi; Ramyar Rahimi Darehbagh; Donya Azizi; Arash Pooladi; Rojin Ramezani; Seyedeh Asrin Seyedoshohadaei

Neural cells are the most important components of the nervous system and have the duty of electrical signal transmission. Damage to these cells can lead to neurological disorders. Scientists have discovered different methods, such as stem cell therapy, to heal or regenerate damaged neural cells. Dental stem cells are among the different cells used in this method. This review attempts to evaluate the effect of biomaterials mentioned in the cited papers on differentiation of human dentalBiomaterials Human Dental Pulp Stem Cell Neural Differentiation pulp stem cells (hDPSCs) into neural cells for use in stem cell therapy of neurological disorders. We searched international databases for articles about the effect of biomaterials on neuronal differentiation of hDPSCs. The relevant articles were screened by title, abstract, and full text, followed by selection and data extraction. Totally, we identified 731 articles and chose 18 for inclusion in the study. A total of four studies employed polymeric scaffolds, four assessed chitosan scaffolds (CS), two utilised hydrogel scaffolds, one investigation utilised decellularised extracellular matrix (ECM), and six studies applied the floating sphere technique. hDPSCs could heal nerve damage in regenerative medicine. In the third iteration of nerve conduits, scaffolds, stem cells, regulated growth factor release, and ECM proteins restore major nerve damage. hDPSCs must differentiate into neural cells or neuron-like cells to regenerate nerves. Plastic-adherent cultures, floating dentosphere cultures, CS, polymeric scaffolds, hydrogels, and ECM mimics have been used to differentiate hDPSCs. According to our findings, the floating dentosphere technique and 3D-PLAS are currently the two best techniques since they result in neuroprogenitor cells, which are the starting point of differentiation and they can turn into any desired neural cell.

829-838

Authors: Zhiyuan Mo; Zhuangqiang Wang

Objective: This study aimed to investigate functional role of long ncRNA (lncRNA) 91H in liver cancer tumorigenesis, focusing on its effect on cell proliferation, apoptosis, cell cycle progression, migration, invasion, epithelial-mesenchymal transition (EMT) and in vivo tumor growth. Materials and Methods: In this experimental study, liver cancer tissues and cell lines were analyzed for lncRNA 91H expression using quantitative reverse transcription polymerase chain reaction (qRT-PCR). By employing si-RNA to silence 91H, we aimed to gain a more in-depth understanding of its specific contributions and effects within these cells. Cell proliferation was assessed through the CCK-8 assay, while apoptosis and cell cycle progression were quantified using Annexin V-FITC staining and flow cytometry, respectively. Migration and invasion capabilities of liver cancer cells were assessed through transwell assay. EMT was assessed by analyzing protein expression levels of EMT-associated markers through western blotting. In vivo effect of 91H was assessed through xenograft experiments. Results: Significantly higher levels of lncRNA 91H were observed in the liver cancer tissues and cell lines, than the normal cells. Silencing 91H in liver cancer cells led to a notable reduction of cell proliferation by inducing apoptosis and arresting the cell cycle. Liver cancer cells with decreased 91H expression exhibited diminished migration and invasion abilities, suggesting a role for 91H in promoting these processes. Furthermore, 91H knockdown weakened EMT in liver cancer cells, indicating its involvement in modulating this critical cellular transition. Furthermore, growth of subcutaneous xenograft tumors and weight was effectively suppressed by sh-lncRNA 91H. Conclusion: Our study strongly supports lncRNA 91H's role in liver cancer progression by enhancing proliferation, migration, invasion, and EMT. Targeting 91H reduced in vivo tumor growth, highlighting its potential as a therapeutic liver cancer target. These findings suggest 91H's pivotal role in liver cancer aggressiveness, opening doors for future therapeutic approaches.

847-853

Authors: Mahdi Mirahmadi; Malihe Aghasizadeh; Fatemeh Nazifkar; Mahla Ghafarian Choubdari; Reza Assaran-Darban; Shima Tavallaie; Hossein Hatamzadeh; Gordon Ferns; Mohammad Reza Mirinezhad; Hamed Baharara; Farzin Hadizadeh; Majid Ghayour-Mobarhan

Objective: The pathogenesis of metabolic syndrome (MetS) complications involves the excessive production of reactive oxygen species, inflammation, and endothelial dysfunction. Due to Lycopene, a highly unstable structure and its significant effects on modulating the metabolic system, there is a strong need for a formula that can increase its stability. The aim of this study was to develop an approach for encapsulating Lycopene and investigate its effects on inflammatory markers, oxidative stress, and liver enzymes in patients with MetS. Materials and Methods: This study is a simple randomized, double-blind, objective-based clinical trial that involved eighty subjects with MetS, who were equally and randomly assigned to two groups: one group received 20 mg of Lycopene per day for 8 weeks, and the Placebo group followed the same protocol as the Lycopene group but received a placebo instead of Lycopene. They were called Lycopene and placebo, respectively. During follow-up visits after 4 and 8 weeks, 20 ml of blood was collected for evaluation of liver enzymes and some inflammatory related markers. Results: Prior to the assignment of volunteers to their respective groups, there were no notable differences in C-reactive protein (CRP), serum liver enzymes, systolic and diastolic blood pressure, or pro-oxidant-antioxidant balance (PAB) between the Lycopene and placebo groups. However, our subsequent analysis revealed a significant reduction in the serum levels of CRP (P=0.001) and PAB (P=0.004) in the group that received Lycopene. Our encapsulated Lycopene treatment was not associated with a significant difference in serum levels of alanine aminotransferase (ALT), aspartate transferase (AST), or alkaline phosphatase (ALP) between our two groups. Conclusion: This study investigated the impact of Lycopene on individuals with MetS, revealing a noteworthy modulation effect on PAB and inflammation linked to MetS. However, no significant differences was demonstrated in serum levels of ALT, AST and ALP between the studied group (registration number: IRCT20130507013263N3).

863-873

Authors: Tahereh Asadabadi; Mohammad Javad Mokhtari; Mahnaz Bayat; Anahid Safari; Afshin Borhani-Haghighi

Objective: Genetic aspects can play an essential role in the occurrence and development of ischemic stroke (IS). Rs1894720 polymorphism is one of the eight single nucleotide polymorphisms (SNPs) in the long non-coding RNA (lncRNA) myocardial infarction-associated transcript (MIAT) locus. The aim of study is the lncRNA MIAT rs1894720 polymorphism decreases IS risk by reducing lncRNA MIAT expression. Materials and Methods: In this case-control study, we studied 232 Iranian patients and 232 controls. The blood samples were collected from patients admitted at different times after stroke symptoms. We enrolled 80, 78, and 74 patients who arrived at the hospital between 0-24, 24-48, and 48-72 hours after the first appearance of symptoms, respectively. DNA genotyping was done by the tetra-primer ARMS-PCR method. Circulating MIAT levels were evaluated by real-time polymerase chain reaction (PCR). Results: The GT genotype of MIAT rs1894720 showed a significant association with the risk of IS (OR=3.53, 95% CI=2.13-5.84, P<0.001). MIAT expression was higher relative to the control within the first hours after IS. The MIAT levels in IS patients with rs1894720 (GT) were significantly lower relative to patients who had the GG and TT genotypes. Linear regression model indicated a significant correlation between MIAT expression with atherosclerotic risk factors and types of stroke in IS patients. Receiver operating characteristic (ROC) curve analysis showed that the level of lncRNA MIAT after IS could be diagnostic with an area under the curve (AUC) of 0.82. The sensitivity and specificity were 80.17 and 67.24%, respectively (P<0.001). Conclusion: Our study demonstrated that the MIAT rs1894720 polymorphism (GT) might increase the risk of IS in the Iranian population. MIAT expression was up-regulated in our IS patients. Hence, it could be a diagnostic biomarker for IS.