Therapeutic potential of mesenchymal stem cells on cholesterol homeostasis-associated genes in AD-like rats.

Cholesterol is vital for nerve processes. Changes in cholesterol homeostasis lead to neurodegeneration and Alzheimer's disease (AD). In recent years, extensive research has confirmed the influential role of adipose tissue mesenchymal stem cells (MSCs) in managing AD.

Adipose Tissue-Derived Mesenchymal Stem Cells Alter Metabolites of Brain Cholesterol Homeostasis in An Alzheimer's Model.

Objective: Disruption of cholesterol homeostasis in Alzheimer's disease (AD) plays a crucial role in disease pathogenesis, making it a potential therapeutic target. Mesenchymal stem cells (MSCs) show promise in treating cognitive impairment and provide a novel therapeutic approach. This study aims to investigate the effects of MSCs on specific metabolites associated with brain cholesterol homeostasis in an AD rat model.

Amyloid Beta Alters the Expression of microRNAs Regulating HMGCR and ABCA1 Genes in Astrocytes of C57BL/6J Mice.

Dysregulation of brain cholesterol homeostasis causes the accumulation of extracellular protein deposits called amyloid plaques in the hippocampus which eventually leads to neuronal death, memory and learning deficits. The aim of the present study was to investigate the effect of beta amyloid on miRNAs regulating HMGCR and ABCA1 as cholesterol synthesis and homeostasis genes. Primary astrocytes were isolated from C57BL/6J mice, and were treated with 0.

The Effect of Platelet-Rich Plasma on the Osteoblastic Differentiation of Human Adipose Tissue-Derived Mesenchymal Stromal Cells.

Background: Mesenchymal stem cells (MSCs) are cell populations that have the potential to proliferate and differentiate. The process of stem cell differentiation from pluripotent cells to bone cells requires general changes in their pattern of gene expression, the most well-known of which are changes in miRNA-dependent settings. Platelet-enriched plasma (PRP) releases growth factors that are mitogenic to mesenchymal cells and can accelerate the process of osteogenic differentiation.

Organochlorine pesticides, oxidative stress biomarkers, and leukemia: a case-control study.

Exposure to pesticides has been linked to an elevated risk of leukemia. The present research aimed to evaluate the relationship between organochlorine (OC) pesticides and biomarkers of oxidative stress in leukemia patients. This work was conducted on 109 patients with leukemia and 109 healthy controls.

Mesenchymal Stem Cells Therapy Led to the Improvement of Spatial Memory in Rats with Alzheimer's disease Through Changing the Expression of LncRNA TUSC7/ miR-449a/ PPARγ and CD36 Genes in the Brain Tissue.

Mesenchymal stem cells (MSCs) have the ability to phagocytize amyloid beta (Aβ) plaques and lower inflammation through the activity of microglia. Peroxisome proliferator-activated receptor gamma (PPARγ) is a protein involved in reducing inflammation through the activity of microglia and the phagocytosis of Aβ plaques by scavenger receptor CD36, in this study, the effect of MSCs therapy on memory function and plaques was investigated. A total of 24 adult male Wistar rats were randomly divided into three groups:1) the control group, 2) the Aβ-treated group (Alzheimer's disease (AD)), and 3) the MSC-treated group (AD + MSC).

Organochlorine pesticides may induce leukemia by methylation of CDKN2B and MGMT promoters and histone modifications.

Epigenetics is the science of altering gene expression without changing nucleotide sequences and may be induced by various environmental factors, including pesticides. The aim of this study was to investigate certain epigenetic changes including the methylation of CDKN2B, CDKN2A, and MGMT gene promoters and histone modifications of H3K9ac, H4K16ac, H4K20me3, and H3K4me3, as well as their association with the levels of organochlorine pesticides (OCPs) in children with acute lymphoblastic leukemia (ALL). The evaluation of OCP levels, promoter methylation, gene expression, and expression of histone modifications was performed by gas chromatography (GC), methylation-specific polymerase chain reaction (MS-PCR), reverse transcription PCR (RT-PCR), and western blotting, respectively.

High Levels of Organochlorines Are Associated with Induction of Promoter Methylation in Children with Acute Lymphoblastic Leukemia.

Exposure to organochlorines is associated with epigenetic changes, including methylation change in the promoter of tumor suppressor genes, thereby leading to cancer induction. The aim of this study was to investigate the relationship between organochlorine pesticides (OCPs) and promoter methylation in child patients with acute lymphoblastic leukemia (ALL) and the control group. The methylation rate of the promoter was evaluated using the methylation-specific polymerase chain reaction method, and the level of OCPs in patients with ALL and healthy children was measured using gas chromatography.

Organochlorine pesticides, oxidative stress biomarkers, and leukemia: a case-control study.

Exposure to pesticides has been linked to an elevated risk of leukemia. The present research aimed to evaluate the relationship between organochlorine (OC) pesticides and biomarkers of oxidative stress in patients with leukemia. This work was conducted on 109 patients with leukemia and 109 healthy controls.