Similar Datasets
Project description:Collagenase digestion (d) and cellular outgrowth (og) are the current modalities of meniscus fibrochondrocytes (MFC) isolation for bioengineering and mechanobiology related studies. However, how these modalities may impact study outcomes are unknown. Here, we show og- and d-isolated MFC have distinct proliferative capacity, transcriptomic profiles via RNA sequencing (RNAseq), extracellular matrix (ECM)-forming and migratory capacities. Our data show that microtissue models developed from og-isolated MFC display a contractile phenotype with higher expressions of α-smooth muscle actin (ACTA2) and transgelin (TAGLN) and are mechanically stiffer than their counterparts from d-MFC. Moreover, we introduce a novel method of MFC designated digestion-after-outgrowth (dog). The transcriptomic prolife of dog-MFC are distinct from d-and og-MFC including a higher expression of mechanosensing caveolae-associated caveolin-1 (CAV1). Additionally, dog-MFC were superior chondrogenically and generated larger-size microtissue models containing a higher frequency of smaller collagen fiber diameters. Thus, we demonstrate that the modalities of MFC isolation influences the downstream outcomes of bioengineering and mechanobiology-related studies.
2024-09-30 | GSE259265 | GEO
Project description:The aim of this study is to demonstrate that mechanical unloading via SMG will induce a higher osteoarthritic-like gene profile in bioengineered meniscal cartilage from healthy female MFC versus healthy male MFC. This would serve as the molecular basis for early onset of knee osteoarthritis in females
2022-05-20 | GSE192983 | GEO
Project description:We analyzed 14 patients with Myelofibrosis (MF) to determine the miRNA profile of patients not responding to current MF treatment. We used Affymetrix miRNA-3 array to profile the differentially expressed miRNA in bone-marrow between patients with MF that respond to current MF treatment and the patients with MF that do not respond to current MF treatment.
2019-12-18 | GSE142239 | GEO
Project description:MFC 10A for bru-seq comparison For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
2022-12-04 | GSE219794 | GEO
Project description:Epigenetic changes deregulate gene expression to drive oncogenesis. The reversible nature of these changes enables therapeutic targeting, as in cutaneous T-cell lymphoma (MF/SS), Histone deacetylase inhibitors (HDACi), which alter epigenetic modifications, are effective in ~30% of MF/SS patients. However, there are no markers that predict MF/SS progression or therapy resistance. We hypothesized that epigenetic alterations drive MF/SS progression and promote HDACi drug resistance. Therefore, we profiled the epigenomes and transcriptomes of malignant T cell purified from skin biopsies and peripheral blood from MF/SS patients (N=21) before and after treatment with HDACi, as well as in vitro HDACi-treated CD4+ T cells from healthy donors. Here we report for the first time the epigenome-wide map of acetylation changes in MF/SS patients treated with HDACi, and define the significant differences in regulatory element activity and corresponding transcriptional changes in HDACi-sensitive versus resistant tumors. Our studies identified genes not previously associated with MF/SS, nor with disease progression or HDACi resistance, and were enriched in pathways that regulate apoptosis (BIRC5), cell cycle (RRM2), and chromosome cohesion (CENPH). We also identified a striking number of genes whose products are involved in cell adhesion and migration, including CCR6, LAIR2, VCAM1, and EPCAM. The mRNA of LAIR2, which encodes a receptor protein secreted by activated T cells that binds collagen and prevents binding of the inhibitory receptor LAIR1, was significantly upregulated in MF/SS tumors that were resistant to HDACi therapy and manifested in both skin and peripheral blood. We also detected elevated levels of LAIR2 protein in the plasma of MF/SS patients with progressive disease. Taken together, these studies defined the first epigenome-wide acetylation landscape of HDACi responsive and resistant MF/SS tumors, identified significantly altered patterns of epigenetic regulation and corresponding gene expression in HDACi resistant MF/SS tumors, and connected them to novel pathways of disease progression, particularly in cell adhesion and migration. These findings may represent novel predictive markers for MF/SS progression that are also targets for future therapeutic development.
2019-08-09 | GSE132053 | GEO
Project description:To address whether ELF-MF influences the epigenetic landscape in the T cell lymphoma cell line Jurkat , we exposed Jurkat cells in the exponential growth phase to ELF MF or a sham control for 72 h, applying intermittently (5’ on/10’ off) a 50 Hz sine ELF-MF at a flux density of 1 mT. Additionally, cells were treated with the histone deacetylation inhibitor trichostatin A (TSA) at a subtoxic dose of 10 nM. Genome-wide profiling of active and repressive histone modifications did not reveal significant alterations. However, ELF-MF exposure has an influence on the robustness of the epigenetic landscape in leukaemic cells. Our data suggests that ELF-MF has a stochastic effect on the epigenetic landscape of individual cells.
2017-03-01 | GSE85601 | GEO