Similar Datasets
Project description:RNA sequencing analysis was performed on leukemia cells sorted from sex and age matched SLC6A6 WT and KO leukemic mice
2025-04-04 | GSE227082 | GEO
Project description:The effect of Slc6a6 loss on MSC function.
| PRJNA1262422 | ENA
Project description:Therapeutic use of mesangial stem cells (MSCs) for tissue repair, including heart, has great potential. MSCs from multiple sources, including those derived from human umbilical matrix, namely Wharton's jelly, may serve as a resourceful candidate. Even after more than a decade, low engraftment efficacy of MSCs, in vivo, remains a limitation which requires in-depth understanding of the mechanisms and factors involved to facilitate a better and clinically relevant outcome. We recently hypothesized and demonstrated that the sex hormone – 17-beta estradiol (E2) – facilitates protective processes within the cardiovascular system by modulating MSC function, in vitro. Here, using a proteomic approach, we investigated the angiogenic potential of MSCs in vivo and the modulatory actions of E2 on mechanisms involved in tissue repair (potentially post-ischemic injury). Employing an in vivo approach with an ovariectomized (OVX) mice model, we evaluated the effects of E2 on MSC-induced angiogenesis using Matrigel plug assay.
2022-02-17 | PXD026380 | Pride
Project description:Transcriptional profiling of PNPase KO liver hepatocytes (HepKO) generated from Albumin-Cre/wt (liver-specific) Pnpt1 fl/fl C57BL/6J mice. Samples comparing liver hepatocyte PNPase KO (HepKO) cells to litter-, age-, and sex-matched wildtype hepatocyte control cells. The goal of this experiment was to determine effects of PNPase loss on the total RNA transcriptome under physiologic in vivo conditions.
2018-05-03 | GSE109210 | GEO
Project description:Carcinoma-associated mesenchymal stem cells (CA-MSCs) are critical stromal progenitor cells within the tumor microenvironment. We previously demonstrated that CA-MSCs differentially express BMP genes, promote tumor cell growth, increase cancer ‘stemness’ and chemotherapy resistance. Here we use RNA sequencing of normal omental MSCs and ovarian CA-MSCs to demonstrate CA-MSCs have global changes in gene expression. Using these expression profiles we create a unique predictive algorithm to classify CA-MSCs. Our classifier, accurately distinguishes normal omental, ovary and bone marrow MSCs from ovarian cancer CA-MSCs. Suggesting broad applicability, the model correctly classifies pancreatic and endometrial cancer CA-MSCs and distinguishes cancer associated fibroblasts (CAFs) from CA-MSCs. Using this classifier, we definitively demonstrate ovarian CA-MSCs arise from tumor mediated reprograming of local tissue MSCs. While cancer cells alone cannot induce a CA-MSC phenotype, the in vivo ovarian tumor micoenvironment (TME) can reprogram omental or ovary MSCs to protumorigenic CA-MSC (classifier score of >0.96). In vitro studies suggest that both tumor secreted factors and hypoxia are critical to induce the CA-MSC phenotype. Interestingly, while the breast cancer TME can reprogram BM MSCs into CA-MSCs, the ovarian TME cannot, demonstrating for the first time that tumor mediated CA-MSC conversion is tissue and cancer type dependent. Together these findings (1) provide a critical tool to define CA-MSCs and (2) highlight cancer cell influence on distinct normal tissues providing powerful insights into the mechanisms underlying cancer specific metastatic niche formation. Carcinoma-associated mesenchymal stem cells (CA-MSCs) are critical stromal progenitor cells within the tumor microenvironment. We previously demonstrated that CA-MSCs differentially express BMP genes, promote tumor cell growth, increase cancer ‘stemness’ and chemotherapy resistance. Here we use RNA sequencing of normal omental MSCs and ovarian CA-MSCs to demonstrate CA-MSCs have global changes in gene expression. Using these expression profiles we create a unique predictive algorithm to classify CA-MSCs. Our classifier, accurately distinguishes normal omental, ovary and bone marrow MSCs from ovarian cancer CA-MSCs. Suggesting broad applicability, the model correctly classifies pancreatic and endometrial cancer CA-MSCs and distinguishes cancer associated fibroblasts (CAFs) from CA-MSCs. Using this classifier, we definitively demonstrate ovarian CA-MSCs arise from tumor mediated reprograming of local tissue MSCs. While cancer cells alone cannot induce a CA-MSC phenotype, the in vivo ovarian tumor micoenvironment (TME) can reprogram omental or ovary MSCs to protumorigenic CA-MSC (classifier score of >0.96). In vitro studies suggest that both tumor secreted factors and hypoxia are critical to induce the CA-MSC phenotype. Interestingly, while the breast cancer TME can reprogram BM MSCs into CA-MSCs, the ovarian TME cannot, demonstrating for the first time that tumor mediated CA-MSC conversion is tissue and cancer type dependent. Together these findings (1) provide a critical tool to define CA-MSCs and (2) highlight cancer cell influence on distinct normal tissues providing powerful insights into the mechanisms underlying cancer specific metastatic niche formation.
2018-08-17 | GSE118624 | GEO
Project description:Male and female knockout (KO) mice and age- and sex-matched C57BL/6J wild-type (WT) were compared. The KO mice had been backcrossed for more than 10 generations onto C57BL6/J background. The present study includes 4 strains of mice (WT, CCK1 receptor KO, CCK2 receptor KO, and CCK1+CCK2 receptor double KO). Animals that were subjected to gene expression profiling received no treatment and were killed under deep anesthesia.
2014-09-01 | E-MTAB-2824 | biostudies-arrayexpress
Project description:Lung resident MSCs were isolated from the Tbx4-rtTA/TetO-Cre/mT-mG reporter mice at 3 months of age, in which embryonic lung mesenchymal cells are genetically marked by doxycycline induction from embryonic day 6.5 to postnatal day 1. The cultured MSCs at passage 2 were sorted by FACS and total RNA was isolated. Samples were from different isolations.
2025-09-22 | GSE299841 | GEO
Project description:This study aimed to investigate the effects of electrical stimulation (ES) on the secretome of mesenchymal stem cells (MSCs). Using quantitative proteomics, we identified a total of 435 proteins secreted by MSCs and ES-treated MSCs (epMSCs), among which 418 were common between groups, with 14 and 8 unique to the epMSC and MSC groups, respectively. Differential expression analysis revealed that 42 proteins were upregulated and 49 were downregulated in the epMSC secretome. Functional enrichment analyses indicated that ES enhances the pro-angiogenic properties of MSCs by modulating pathways such as VEGFA-VEGFR2 signaling and the complement cascade. These findings provide insight into how ES alters MSC-derived secretomes to promote vascularization, which may have therapeutic relevance in regenerative medicine.
2025-09-22 | PXD066035 | Pride
Project description:The use of polypharmacy (5 or more concurrent medications) is common in older patients, particularly those with cardiovascular diseases. However, polypharmacy is associated with adverse geriatric outcomes, including increased risks in fall and frailty. Both ageing and sex influence pharmacological response and cardiac physiology. The mechanistic intersect between age, sex, and drug-drug interaction is poorly understood. Previously, we have developed a polypharmacy murine model whereby young (4 months) and old (23 months) healthy C57BL/6JArc mice of both sexes were randomised to either polypharmacy or control. The polypharmacy regimen has a High Drug Burden Index (HDBI) and contains 3 medications with anticholinergic/sedative medications (oxybutynin, oxycodone, citalopram) along with cardiovascular medications (simvastatin and metoprolol). Medications were given at oral therapeutic doses. HDBI has clinically been demonstrated to be particularly associated with adverse geriatric outcomes. Here, we profiled the left ventricular (LV) proteome following 10 weeks of HDBI polypharmacy treatment along with age- and sex-matched controls.
2025-06-02 | PXD057325 | Pride
Project description:Purpose: Prostate cancer most frequently metastasizes to bone and is incurable. Metastatic prostate cancer cells thrive in bone through molecular regulation of surrounding bone stroma, including upregulation of CXCL8 (CXCL1 in mice) in MSCs. This study characterizes the changes in the bone marrow mesenchymal stem cells (MSCs) upon targeted deletion of Cxcl1 in murine MSC. It also characterized the changes in the tumor/stromal cells of tumors with Cxcl1 KO MSCs or control MSCs. These studies seek to determine the importance of MSC-derived CXCL1 in bone-metastatic prostate cancer.
2025-08-13 | GSE268815 | GEO