Advanced searches left 3/3

Mice marrow cells - Europe PMC

Summarized by Plex Scholar
Last Updated: 17 April 2022

* If you want to update the article please login/register

The regulatory effect of miR-181c-5p on the differentiation function of bone marrow mesenchymal stem cells in postmenopausal osteoporotic mice

Osteoporosis is a metabolic bone disease disorder for which there is no such cure. miR-181c-5p in BMMSCs were overexpressed or blocked by cell transfection, cell transfection was inhibited by cell transfection, and the clinical effects of miR-181c-5p on BMMSC proliferation and osteogenic-adipogenic differentiation were investigated using MTT, multi-directional differentiation induction, alizarin red staining, qRT-PCR, and Western blot. MiR-181c-5p target gene prediction tools and bioinformatics websites were tested by target gene prediction software and bioinformatics websites, and target gene validation was performed, and target gene prediction was conducted. MiR-181c-5p regulation may reduce the osteogenic capability and improve BMMSCs' adipogenic ability, as well as improve the adipogenic capability and BMMSC's adipogenic ability, while miR-181c-5p downregulation could raise the osteogenic ability and reduce the adipogenic ability of BMMSCs and reduce the adipogenic ability, as well as the adipogenic ability and reduce the adipogenic ability and decrease BMMSCs. Foxo1 was confirmed as a direct target gene for miR-181c-5p, and miR-181c-5p negatively restricted Foxo1 expression.

Source link: https://europepmc.org/article/PPR/PPR481785


The AR in bone marrow progenitor cells protects against short-term high caloric diet induced weight gain in male mice.

In male mice, we previously found a new route of testosterone administration by the androgen receptor in bone marrow mesenchymal precursor cells that can both reduce fat storage and improve metabolic function. paraphrasedoutput tissue and retroperitoneal visceral tissue mass had significantly elevated subcutaneous white adipose tissue and retroperitoneal visceral tissue mass in comparison to chow-fed controls following eight weeks of HCD, WT, and Global-ARKOs. Following prolonged HCD feeding for 18 weeks, the PC-AR Gene Replacements were no longer resistant to elevated WAT and VAT adiposity; however, they maintained their improved whole-body insulin sensitivity with an increased incidence of glucose removal and increased glucose uptake into subcutaneous WAT. In conclusion, testosterone in BM-PCs has been shown to negatively regulate fat mass and improve metabolism, as well as partial protection from long-term diet-induced obesity in male mice.

Source link: https://europepmc.org/article/MED/35388795


Modulating endothelial cells with EGFL7 to diminish aGVHD after allogeneic bone marrow transplantation in mice.

We hypothesized that rising EGFL7 levels following allo-HSCT may reduce the severity of aGVHD due to previous studies that endothelial cell dysfunction is present in aGVHD and that epidermal cell activation and T-cell migration. In two separate murine models of aGVHD, treatment with recombinant EGFL7 reduces aGVHD risk and enhances survival in recipient mice after allogeneic transplantation without impacting graft-versus-leukemia.

Source link: https://europepmc.org/article/MED/34654057


Intravenous injection of SDF-1α-overexpressing bone marrow mesenchymal stem cells has a potential protective effect on myocardial ischemia in mice.

Following myocardial infarction, Chemokine SDF-1 and its related receptor CXCR4 are upregulated, and this can play a significant role in stem cell homing. Objectives This research was designed to investigate the potential therapeutic benefit of SDF-1-modified bone marrow mesenchymal stem cells on myocardial ischemia/reperfusion injury. Methods We investigated the role of SDF-1-derived bone marrow mesenchymal stem cells in vivo and vitro. SDF-1 was mostly controlled and hidden by cardiomyocytes, and cardiomyocytes, and cardiomyocytes largely manufactured SDF-1, and cardiomyocytes recruited stem cells into cardiomyocytes under H/R to reduce the damage caused by polymorphic mononuclear neutrophils to cardiomyocytes. SDF-1 upregulation increased the migration capability of BMSC Stem Cells to H/R-induced cardiomyocytes by a fibrosis mutation. In vitro, intravenous injection of SDF-1 gene-modified BMSC Stem Cells reduced inflammatory infiltration in the injured area, as well as the presence of systemic inflammatory markers.

Source link: https://europepmc.org/article/MED/35306996

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

Search Recommendations

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions