Cell Journal (Yakhteh)
Volume:25 Issue: 12, Dec 2023

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 celltherapy, 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 dentalpulp stem cells (hDPSCs) into neural cells for use in stem cell therapy of neurological disorders. We searched internationaldatabases for articles about the effect of biomaterials on neuronal differentiation of hDPSCs. The relevant articles werescreened by title, abstract, and full text, followed by selection and data extraction. Totally, we identified 731 articles and chose18 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 appliedthe floating sphere technique. hDPSCs could heal nerve damage in regenerative medicine. In the third iteration of nerveconduits, scaffolds, stem cells, regulated growth factor release, and ECM proteins restore major nerve damage. hDPSCsmust differentiate into neural cells or neuron-like cells to regenerate nerves. Plastic-adherent cultures, floating dentospherecultures, CS, polymeric scaffolds, hydrogels, and ECM mimics have been used to differentiate hDPSCs. According toour findings, the floating dentosphere technique and 3D-PLAS are currently the two best techniques since they result inneuroprogenitor cells, which are the starting point of differentiation and they can turn into any desired neural cell.

Stem cells (SCs) can improve the functional defects of brain injury. Rodents use their whiskers to get tactileinformation from their surroundings. The aim of this study was to investigate whether the transplantation of SCs into thelesioned barrel cortex can help neuronal function in the contralateral cortex. Sixteen male Wistar rats (200-230 g) were used in this experimental study. We induceda mechanical lesion in the right barrel cortex area of rats by removing this area by a 3 mm skin punch. Four groupscontaining one intact group of rats: group 1: control, and three lesion groups, group 2: lesion+un-differentiated dentalpulp SCs (U-DPSCs), group 3: lesion+differentiated dental pulp SCs (D-DPSCs), and group 4: cell medium (vehicle)that were injected in the lesion area. Three weeks after transplantation of SCs or cell medium, the rats’ responses ofleft barrel cortical neurons to controlled deflections of right whiskers were recorded by using the extracellular single-unitrecordings technique. The results showed that the neural spontaneous activity and response magnitude of intact barrel cortexneurons in the lesion group decreased significantly (P<0.05) compared to the control group while ON and OFF responseswere improved in the D-DPSCs (P<0.001) group compared to the vehicle group three weeks after transplantation. Transplantation of dental pulp mesenchymal SCs significantly improved the neural responses of the leftbarrel cortex that was depressed in the vehicle group.

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-mesenchymaltransition (EMT) and in vivo tumor growth. In this experimental study, liver cancer tissues and cell lines were analyzed for lncRNA 91Hexpression using quantitative reverse transcription polymerase chain reaction (qRT-PCR). By employing si-RNA tosilence 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 quantifiedusing Annexin V-FITC staining and flow cytometry, respectively. Migration and invasion capabilities of liver cancer cellswere assessed through transwell assay. EMT was assessed by analyzing protein expression levels of EMT-associatedmarkers through western blotting. In vivo effect of 91H was assessed through xenograft experiments. Significantly higher levels of lncRNA 91H were observed in the liver cancer tissues and cell lines, than thenormal cells. Silencing 91H in liver cancer cells led to a notable reduction of cell proliferation by inducing apoptosisand arresting the cell cycle. Liver cancer cells with decreased 91H expression exhibited diminished migration andinvasion abilities, suggesting a role for 91H in promoting these processes. Furthermore, 91H knockdown weakenedEMT in liver cancer cells, indicating its involvement in modulating this critical cellular transition. Furthermore, growth ofsubcutaneous xenograft tumors and weight was effectively suppressed by sh-lncRNA 91H. 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.

Non-small cell lung cancer (NSCLC) stands as a prominent contributor to cancer-related fatalities on aglobal scale, necessitating the search for novel therapeutic agents. SP-8356, a derivative of (1S)-(–)-verbenone, hasshown promise as an anticancer agent in preclinical studies. However, specific mechanisms underlying its effects inNSCLC remain to be elucidated. The aim of this research was to explore the in vitro anti-NSCLC effects of SP-8356,elucidate its mechanisms of action, and assess its efficacy in inhibiting tumor formation in a murine model. In this experimental study, NSCLC cell lines were treated with various concentrations of SP-8356. Cell viability and proliferation were assessed using MTT and colony formation assays, respectively. Cell cycledistribution was analyzed by flow cytometry, and apoptosis was evaluated by determining apoptotic protein expression.Western blot analysis was conducted to assess protein expression levels of the both p53 and MDM2. Additionally, weevaluated efficacy of the SP-8356 in inhibiting tumor formation of the nude mouse model. SP-8356 demonstrated a concentration-dependent inhibition of cell proliferation in the NSCLC cell lines. Flowcytometric analysis showed that SP-8356 led to cell cycle arrest at the G2/M phase, indicating its potential influenceon regulating the cell cycle. SP-8356 treatment was associated with the downregulation of CDK1 and Cyclin B1.Additionally, SP-8356 significantly enhanced apoptosis in NSCLC cells. SP-8356 treatment was associated with thedownregulation of Bcl-2, while Bax expression was upregulated. Mechanistically, SP-8356 led to accumulation of thep53 protein levels within the NSCLC cells. This accumulation was mediated through inhibition of its negative regulator,MDM2. Using a nude mouse model demonstrated that SP-8356 effectively inhibited tumor formation in vivo. Our findings shed light on the molecular mechanisms underlying anticancer activity of SP-8356 andhighlight its potential as a promising therapeutic candidate for NSCLC treatment.

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

The collagen-induced arthritis (CIA) model is the most commonly studied autoimmune model of rheumatoidarthritis (RA). In this study, we investigated the usefulness of collagen type II emulsified in Freund's incompleteadjuvant (CII/IFA) as a suitable method for establishing RA in Lewis rats. The aim of the present study was to presenta straightforward and effective method for inducing CIA in rats. In this experimental study, animals were divided into two equal groups (n=5); control andCIA. Five rats were injected intradermally at the base of the tail with a 0.2 ml CII/IFA emulsion. On the seventh day,a 0.1 ml CII/IFA emulsion booster was injected. Arthritis symptoms that arose were evaluated at clinical, histological,radiological, and at protein expression levels to find out if the disease had been induced successfully. Our finding showed a decreasing trend in the body weight during the RA induction period, while the arthritisscore and paw thickness were increased during this period. The results of the enzyme-linked immunosorbent assay(ELISA) for serum samples revealed that the levels of proinflammatory cytokines, interleukin (IL)-1β, IL-6, IL-17, andtumor necrosis factor (TNF)-α and anti-CII IgG were significantly increased in CIA rats compared to the control group.After CIA induction, the level of anti-inflammatory protein IL-10 was decreased significantly. Radiographic examinationof the hind paws showed soft tissue swelling, bone erosion, and osteophyte formation in CIA rats. Additionally, basedon histological evaluations, the hind paws of the CIA group showed pannus formation, synovial hyperplasia, and boneand cartilage destruction. It seems that CII/IFA treatment can be an appropriate and effective method to induce RA disease in Lewisrats. This well-established and well-characterized CIA model in female Lewis rats could be considered to study aspectsof RA and develop novel anti-arthritic agents.

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 rs1894720polymorphism decreases IS risk by reducing lncRNA MIAT expression.

In this case-control study, we studied 232 Iranian patients and 232 controls. The blood sampleswere collected from patients admitted at different times after stroke symptoms. We enrolled 80, 78, and 74 patientswho 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-timepolymerase chain reaction (PCR).

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 MIATlevels 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 factorsand types of stroke in IS patients. Receiver operating characteristic (ROC) curve analysis showed that the level oflncRNA MIAT after IS could be diagnostic with an area under the curve (AUC) of 0.82. The sensitivity and specificitywere 80.17 and 67.24%, respectively (P<0.001).

Our study demonstrated that the MIAT rs1894720 polymorphism (GT) might increase the risk of IS in theIranian population. MIAT expression was up-regulated in our IS patients. Hence, it could be a diagnostic biomarker for IS.

Wound healing is a complex process involving the coordinated interaction of various genes and molecularpathways. The study aimed to uncover novel therapeutic targets, biomarkers and candidate genes for drug developmentto improve successful wound repair interventions. This study is a network-meta analysis study. Nine wound healing microarray datasets obtainedfrom the Gene Expression Omnibus (GEO) database were used for this study. Differentially expressed genes (DEGs)were described using the Limma package and shared genes were used as input for weighted gene co-expressionnetwork analysis. The Gene Ontology analysis was performed using the EnrichR web server, and construction of aprotein-protein interaction (PPI) network was achieved by the STRING and Cytoscape. A total of 424 DEGs were determined. A co-expression network was constructed using 7692 shared genesbetween nine data sets, resulting in the identification of seven modules. Among these modules, those with the top 20genes of up and down-regulation were selected. The top down-regulated genes, including TJP1, SEC61A1, PLEK,ATP5B, PDIA6, PIK3R1, SRGN, SDC2, and RBBP7, and the top up-regulated genes including RPS27A, EEF1A1,HNRNPA1, CTNNB1, POLR2A, CFL1, CSNk1E, HSPD1, FN1, and AURKB, which can potentially serve as therapeutictargets were identified. The KEGG pathway analysis found that the majority of the genes are enriched in the "Wntsignaling pathway". In our study of nine wound healing microarray datasets, we identified DEGs and co-expressed modulesusing WGCNA. These genes are involved in important cellular processes such as transcription, translation, and posttranslationalmodifications. We found nine down-regulated genes and ten up-regulated genes, which could serve aspotential therapeutic targets for further experimental validation. Targeting pathways related to protein synthesis and celladhesion and migration may enhance wound healing, but additional experimental validation is needed to confirm theeffectiveness and safety of targeted interventions.