Cell Journal (Yakhteh)
Volume:25 Issue: 8, Aug 2023

The objective of this systematic review and meta-analysis is to examine the effects of resistance exercise training on muscle stem cells in older adults. A database search was performed (PubMed, Scopus, Web of Science and Google Scholar) to identify controlled clinical trials in English language. The mean difference (MD) with 95% confidence intervals (CIs) and overall effect size were calculated for all comparisons. The PEDro scale was used to assess the methodological quality. Nineteen studies were included in the review. The meta-analysis found a significant effect of resistance training (RT) on muscle stem cells in the elderly (difference in means=-0.008, Z=-3.415, P=0.001). Also, muscle stem cells changes were similar in men and women (difference in means=-0.004, Z=-1.558, P=0.119) and significant changes occur in type II muscle fibers (difference in means=-0.017, Z=-7.048, P=0.000). Resistance-type exercise training significantly increased muscle stem cells content in intervention group that this result is similar in men and womenthis increase occurred more in type II muscle fibers.

Macrophages are multifunctional immune cells widely used in immunological research. While autologous macrophages have been widely used in several biomedical applications, allogeneic macrophages have also demonstrated similar or even superior therapeutic potential. The umbilical cord blood (UCB) is a well-described source of abundant allogenic monocytes and macrophages that is easy to collect and can be processed without invasive methods. Current monocyte isolation procedures frequently result in heterogenous cell products, with limited yields, activated cells, and high cost. This study outlines a simple isolation method that results in high yields and pure monocytes with the potential to differentiate into functional macrophages.

In the experimental study, we describe a simple and efficient protocol to isolate highpurity monocytes. After collection of human UCB samples, we used a gradient-based procedure composed of three consecutive gradient steps: i. Hydroxyethyl starch-based erythrocytes sedimentation, followed by ii. Mononuclear cells (MNCs) isolation by Ficoll-Hypaque gradient, and iii. Separation of monocytes from lymphocytes by a slight hyperosmolar Percoll gradient (0.573 g/ml). Then the differentiation potential of isolated monocytes to pro- and antiinflammatory macrophages were evaluated in the presence of granulocyte colony-stimulating factor (GM-CSF) and macrophage CSF (M-CSF), respectively. The macrophages were functionally characterized as well.

A high yield of monocytes after isolation (25 to 50 million) with a high purity (>95%) could be obtained from every 100-150 ml UCB. Isolated monocytes were defined based on their phenotype and surface markers expression pattern. Moreover, they possess the ability to differentiate into pro- or anti-inflammatory macrophages with specific phenotypes, gene/surface protein markers, cytokine secretion patterns, T-cell interactions, and phagocytosis activity.

Here we describe a simple and reproducible procedure for isolation of pure monocytes from UCB, which could be utilized to provide functional macrophages as a reliable and feasible source of allogenic macrophages for biomedical research.

Metabolic syndrome (MetS) is a complex multifactorial disorder that considerably burdens healthcare systems. We aim to classify MetS using regularized machine learning models in the presence of the risk variants of GCKR, BUD13 and APOA5, and environmental risk factors.

A cohort study was conducted on 2,346 cases and 2,203 controls from eligible Tehran Cardiometabolic Genetic Study (TCGS) participants whose data were collected from 1999 to 2017. We used different regularization approaches [least absolute shrinkage and selection operator (LASSO), ridge regression (RR), elasticnet (ENET), adaptive LASSO (aLASSO), and adaptive ENET (aENET)] and a classical logistic regression (LR) model to classify MetS and select influential variables that predict MetS. Demographics, clinical features, and common polymorphisms in the GCKR, BUD13, and APOA5 genes of eligible participants were assessed to classify TCGS participant status in MetS development. The models’ performance was evaluated by 10-repeated 10-fold crossvalidation. Various assessment measures of sensitivity, specificity, classification accuracy, and area under the receiver operating characteristic curve (AUC-ROC) and AUC-precision-recall (AUC-PR) curves were used to compare the models.

During the follow-up period, 50.38% of participants developed MetS. The groups were not similar in terms of baseline characteristics and risk variants. MetS was significantly associated with age, gender, schooling years, body mass index (BMI), and alternate alleles in all the risk variants, as indicated by LR. A comparison of accuracy, AUCROC, and AUC-PR metrics indicated that the regularization models outperformed LR. Regularized machine learning models provided comparable classification performances, whereas the aLASSO model was more parsimonious and selected fewer predictors.

Regularized machine learning models provided more accurate and parsimonious MetS classifying models. These high-performing diagnostic models can lay the foundation for clinical decision support tools that use genetic and demographical variables to locate individuals at high risk for MetS.

Owing to the lethality of liver cancer, it is considered as one of the devastating types of cancers across the globe. Consistently, the study was designed to elucidate the role and to explore the therapeutic implications of miR-145 in human liver cancer. Materials &

In the current experimental study, gene expression was determined by RT-PCR analysis. Transfection of cancer cells was carried out using Lipofectamine 2000. The cell proliferation of liver cancer cells was estimated by MTT assay. Clonogenic assay was performed for analysis of colony forming potential of cancer cells. Flow cytometry was done to analyze the cell cycle phase distribution of cancer cells. Transwell chamber assay was performed to assess the motility of cancer cells. Western blotting was done to estimate the expression levels of proteins. Dual luciferase assay was performed for interaction analysis of miR-145 with CDCA3.

The miR-145 expression was found to be downregulated in liver cancer cells. The transfection mediated overexpression of miR-145 inhibited the cancer cell proliferation and when miR-145 inhibitor was transfected, cancer cells showed higher proliferation rates. Enrichment of miR-145 levels led to cell cycle arrest at G2/M phase by inhibiting cyclin B1. miR-145 also restricted the migration and invasion of cancer cells. CDCA3 was shown to be the intracellular target of miR-145 and it was found that the inhibitory effects of miR-145 were modulated through CDCA3, intracellularly.

The current study clearly revealed that there is a need to investigate the regulatory role of different molecular entities like microRNAs in cancer development to better understand mechanics behind this pathogenesis and design more effective combating strategies against cancer.

To investigate the effect of β-sitosterol on endometrial cells to understand the underlying mechanism.

This is a laboratory-based experimental study conducted on animals and cells. Histological assays were performed to determine the effect of β-sitosterol on endometrial cells. The CCK-8 assay was used to assess the inhibitory effect of β-sitosterol on the proliferation of ectopic endometrial stromal cells (hEM15A). Flow cytometry was performed to evaluate the induction of apoptosis by β-sitosterol in hEM15A cells. The transwell invasion assay was conducted to measure the suppression of hEM15A cell migration by β-sitosterol. Western blot analyses were performed to analyze the effect of β-sitosterol on the expression of Smad family member 7 (Smad7) and the activity of transforming growth factor-β (TGF-β1), as well as the phosphorylation of Smad2 and Smad3.

Histological assays showed that β-sitosterol regulates histopathology and induces apoptosis of endometrial cells in vivo. The CCK-8 assay revealed that β-sitosterol could inhibit the proliferation of hEM15A in human endometriosis patients. Flow cytometry showed that apoptosis was triggered by β-sitosterol in hEM15A. The transwell invasion assay indicated that the hEM15A migration under the β-sitosterol treatment group was suppressed. Western blot analyses suggested that β-sitosterol increased the expression of Smad7, decreased the activity of TGF-β1, and reduced the phosphorylation of Smad2 and Smad3. The effect of β-sitosterol was weakened by the silence of Smad7.

The results suggest that β-sitosterol can inhibit the proliferation of endometrial cells and relieve endometriosis by inhibiting TGF-β-induced phosphorylation of Smads through regulation of Smad7.

Diabetes in pregnancy is a prevalent disease that can affect the central nervous system of the fetus by hyperglycemia. This study aimed to investigate the impact of maternal diabetes on neuronal apoptosis in the superior colliculus (SC) and the lateral geniculate nucleus (LGN) in male neonates born to diabetic mothers.

In this experimental study, female adult rats were separated into three groups: control, diabetic (induced using an intraperitoneal injection of streptozotocin), and insulin-treated diabetic [diabetes controlled by subcutaneous neutral protamine hagedorn (NPH)-insulin injection]. Male neonates from each group were euthanized on 0, 7, and 14 postnatal days (P0, P7, and P14, respectively), and apoptotic cells were identified using TUNEL staining.

The numerical density per unit area (NA) of apoptotic cells was significantly higher in SC and the dorsal LGN (dLGN) in neonates born to the diabetic rats compared to the control group at P0, P7, and P14. However, insulin treatment normalized the number of apoptotic cells.

This study demonstrated that maternal diabetes increased apoptosis in dLGN and SC of male neonates at P0, P7, and P14.

Blood supply to the meniscus determines its recovery and is a reference for treatment planning. This study aimed to apply tissue clearing and three-dimensional (3D) imaging in exploring the quantitative distribution of blood vessels in the mouse meniscus.

In this experimental study, tissue clearing was performed to treat the bilateral knee joints of transgenic mice with fluorescent vascular endothelial cells. Images were acquired using a light sheet microscope and the vascular endothelial cells in the meniscus was analysed using 3D imaging. Quantitative methods were employed to further analyse the blood vessel distribution in the mouse meniscus.

The traditional three-equal-width division of the meniscus is as follows: the outer one-third is the red-red zone (RR), the inner one-third is the white-white zone (WW), and the transition area is the red-white zone (RW). The division revealed significant signal differences between the RW and WW (P<0.05) zones, but no significant differences between the RR and RW zones, which indicated that the division might not accurately reflect the blood supply of the meniscus. According to the modified division (4:2:1) in which significant differences were ensured between the adjacent zones, we observed that the width ratio of each zone was 38 ± 1% (RR), 24 ± 1% (RW), and 38 ± 2% (WW). Furthermore, the blood supply to each region was verified. The anterior region had the most abundant blood supply. The fluorescence count in the anterior region was significantly higher than in the central and posterior regions (P<0.05). The blood supply of the medial meniscus was superior to the lateral meniscus (P<0.05).

Analysis of the blood supply to the mouse meniscus under tissue clearing and 3D imaging reflect quantitative blood vessel distribution, which would facilitate future evaluations of the human meniscus and provide more anatomical references for clinicians.

This study evaluates the interaction of mouse blastocysts as a surrogate embryo on a recellularized endometrial scaffold by seeding human endometrial mesenchymal cells (hEMCs).

In this experimental study, prepared decellularized human endometrial tissues were characterized by morphological staining, DNA content analysis, and scanning electron microscopic (SEM) analysis. The scaffolds were subsequently recellularized by hEMCs. After seven days of cultivation, the mouse blastocysts were co-cultured on the recellularized scaffolds for 48 hours. Embryo attachment and implantation within these scaffolds were evaluated at the morphological, ultrastructural, molecular, and hormonal levels.

There was no morphological evidence of cells and nuclei in the decellularized scaffold. DNA content significantly decreased by 89.92% compared to the control group (P<0.05). Both decellularized and native tissues had similar patterns of collagen bundles and elastin fibers, and glycosaminoglycan (GAGs) distribution in the stroma. After recellularization, the hEMCs attached to the scaffold surface and penetrated different parts of these scaffolds. In the co-cultured group, the embryo attached to the surface of the scaffold after 24 hours and penetrated the recellularized endometrial tissue after 48 hours. We observed multi-layered organoid-like structures formed by hEMC proliferation. The relative expressions of epithelial-related genes, ZO-1 and COL4A1, and SSP1, MMP2, and PRL, as decidualizationrelated genes, were significantly higher in the recellularized group on day 9 in the presence of the embryo compared to the other groups (P<0.05). Beta human chorionic gonadotropin (β-hCG) and prolactin were statistically increased in the recellularized group on day 9 group (P<0.05).

hEMCs and mouse embryo co-cultured on a decellularized endometrial scaffold provides an alternative model to study embryo implantation and the earlier stage of embryo development