Bulk RNA-seq detects cMPCs HO signature in B/T mouse blood samples - dataset #2
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1109845 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Bulk RNA-seq detects cMPCs HO signature in B/T mouse blood samples - dataset #1
| PRJNA1109846 | ENA
Project description:Heterotopic ossification (HO), the aberrant bone in soft tissues, is one of the most debilitating complications associated with severe burn and traumatic injuries as well as joint replacement surgeries due to its insidious development. Currently, no technologies exist to either support early HO detection or to guide early prophylactic strategies. Furthermore, no technologies exist to assess treatment efficacy. In this study, we used microfluidic iChip, designed to isolate circulating rare non-hematopoietic cells from whole blood, to isolate and analyze circulating mesenchymal progenitor cells (cMPCs) released in a clinically relevant mouse model of traumatic HO. RNA sequencing of cMPCs revealed the unique expression of HO-associated MPC genes observed as soon as 6 hours post HO-inducing injury, 41 days earlier than gold standard radiographic diagnostic strategies. Using multiple lineage tracing systems, we determined that the cMPCs derived from the periosteum rather than the bone marrow. We then formulated a cMPC HO score and evaluated the diagnostic ability of the liquid biopsy approach for the early detection of HO. By using Youden’s J Statistic for optimizing sensitivity and specificity, our score yielded a sensitivity of 82% and specificity of 100% for detecting HO in mice.
2026-01-18 | GSE267143 | GEO
Project description:Heterotopic ossification (HO), the aberrant bone in soft tissues, is one of the most debilitating complications associated with severe burn and traumatic injuries as well as joint replacement surgeries due to its insidious development. Currently, no technologies exist to either support early HO detection or to guide early prophylactic strategies. Furthermore, no technologies exist to assess treatment efficacy. In this study, we used microfluidic iChip, designed to isolate circulating rare non-hematopoietic cells from whole blood, to isolate and analyze circulating mesenchymal progenitor cells (cMPCs) released in a clinically relevant mouse model of traumatic HO. RNA sequencing of cMPCs revealed the unique expression of HO-associated MPC genes observed as soon as 6 hours post HO-inducing injury, 41 days earlier than gold standard radiographic diagnostic strategies. Using multiple lineage tracing systems, we determined that the cMPCs derived from the periosteum rather than the bone marrow. We then formulated a cMPC HO score and evaluated the diagnostic ability of the liquid biopsy approach for the early detection of HO. By using Youden’s J Statistic for optimizing sensitivity and specificity, our score yielded a sensitivity of 82% and specificity of 100% for detecting HO in mice.
2026-01-18 | GSE267142 | GEO
Project description:Heterotopic ossification (HO), the aberrant bone in soft tissues, is one of the most debilitating complications associated with severe burn and traumatic injuries as well as joint replacement surgeries due to its insidious development. Currently, no technologies exist to either support early HO detection or to guide early prophylactic strategies. Furthermore, no technologies exist to assess treatment efficacy. In this study, we used microfluidic iChip, designed to isolate circulating rare non-hematopoietic cells from whole blood, to isolate and analyze circulating mesenchymal progenitor cells (cMPCs) released in patients that underwent hip artroplasty. RNA sequencing of cMPCs revealed the unique expression of HO-associated MPC genes observed post operation day 1, weeks earlier than gold standard radiographic diagnostic strategies.
2026-01-18 | GSE316836 | GEO
Project description:Heterotopic ossification (HO), the aberrant bone in soft tissues, is one of the most debilitating complications associated with severe burn and traumatic injuries as well as joint replacement surgeries due to its insidious development. Currently, no technologies exist to either support early HO detection or to guide early prophylactic strategies. Furthermore, no technologies exist to assess treatment efficacy. In this study, we used microfluidic iChip, designed to isolate circulating rare non-hematopoietic cells from whole blood, to isolate and analyze circulating mesenchymal progenitor cells (cMPCs) released in a clinically relevant mouse model of traumatic HO. RNA sequencing of cMPCs revealed the unique expression of HO-associated MPC genes observed as soon as 6 hours post HO-inducing injury, 41 days earlier than gold standard radiographic diagnostic strategies. Using multiple lineage tracing systems, we determined that the cMPCs derived from the periosteum rather than the bone marrow. We then formulated a cMPC HO score and evaluated the diagnostic ability of the liquid biopsy approach for the early detection of HO. By using Youden’s J Statistic for optimizing sensitivity and specificity, our score yielded a sensitivity of 82% and specificity of 100% for detecting HO in mice.
2026-01-18 | GSE267144 | GEO
Project description:Single cell RNA-seq detects cMPCs expressing HO gene expression signature in B/T mouse blood samples
| PRJNA1109847 | ENA
Project description:This dataset contains RNA sequencing profiles of colonic epithelial organoids isolated from mice with intestinal epithelial-specific deletion of Hmox1 and littermate controls. Organoids were exposed to hemin for 24 hours to assess the influence of epithelial HO-1 on transcriptional responses to heme-induced stress.
2025-12-12 | GSE312912 | GEO
Project description:Hydrogenobaculum sp. HO genome sequencing project
| PRJNA41741 | ENA
Project description:Heme Oxygenase-1 (HO-1) is expressed in many cancers and influences the growth, survivall and metastasis of tumors, however, the molecular mechanisms remains largely unknown. To identify a common mechanism of action of HO-1 in cancer, we studied the global effect of HO-1 on the transcriptome of multiple tumors. Genome-wide expression profiling of HO-1 expressing versus HO-1 silenced cancer cells and a further data mining analysis of the preexisting expression database of 190 human tumors of 14 cancer types led us to identify 14 genes, the expression of which correlated firmly and universally with that of HO-1 (P < 0.001). These genes included regulators of cell plasticity and extracellular matrix remodeling (MMP2, ADAM8, TGFβ1, BGN, COL21A1, PXDN), signaling (CRIP2, MICB), amino acid transport and glycosylation (SLC7A1 and ST3GAL2), estrogen and phospholipid biosynthesis (AGPAT2 and HSD17B1), protein stabilization (IFI30) and phosphorylation (ALPPL2). PXDN, one of the genes being co-expressed with HO-1, was selected for further analysis. Immunofluorescence and western blotting confirmed positive correlation of PXDN with HO-1 levels in BeWo cancer cells as well as co-localization in invasive extravillous trophoblast cells of first trimester placenta. Loss of HO-1 in BeWo cells correlated with reduced cell adhesion to Collagen type I, Fibronectin and Laminin. The adhesion-promoting effects of HO-1 were dependent on PXDN expression, as loss of PXDN in HO-1 expressing BeWo cells led to reduced cell attachment to Laminin and Fibronectin coated wells. We used gene expression profiling to determine the genome-wide effect of HO-1 on the transcriptome of BeWo trophoblast cells. We specifically selected BeWo cells for our studies because these cells express HO-1 naturally. We knocked down endogenous HO-1 in BeWo cells using retroviral transduction with a micro-RNA adapted retroviral vector targeting human HO-1 sequence. RNA isolated from control (LMP) or miHO1 infected (miHO-1) cells was labeled and hybridized to human genome-wide gene level 1.0 ST arrays
2011-02-15 | E-GEOD-20404 | biostudies-arrayexpress
Project description:Heme Oxygenase-1 (HO-1) is expressed in many cancers and influences the growth, survivall and metastasis of tumors, however, the molecular mechanisms remains largely unknown. To identify a common mechanism of action of HO-1 in cancer, we studied the global effect of HO-1 on the transcriptome of multiple tumors. Genome-wide expression profiling of HO-1 expressing versus HO-1 silenced cancer cells and a further data mining analysis of the preexisting expression database of 190 human tumors of 14 cancer types led us to identify 14 genes, the expression of which correlated firmly and universally with that of HO-1 (P < 0.001). These genes included regulators of cell plasticity and extracellular matrix remodeling (MMP2, ADAM8, TGFβ1, BGN, COL21A1, PXDN), signaling (CRIP2, MICB), amino acid transport and glycosylation (SLC7A1 and ST3GAL2), estrogen and phospholipid biosynthesis (AGPAT2 and HSD17B1), protein stabilization (IFI30) and phosphorylation (ALPPL2). PXDN, one of the genes being co-expressed with HO-1, was selected for further analysis. Immunofluorescence and western blotting confirmed positive correlation of PXDN with HO-1 levels in BeWo cancer cells as well as co-localization in invasive extravillous trophoblast cells of first trimester placenta. Loss of HO-1 in BeWo cells correlated with reduced cell adhesion to Collagen type I, Fibronectin and Laminin. The adhesion-promoting effects of HO-1 were dependent on PXDN expression, as loss of PXDN in HO-1 expressing BeWo cells led to reduced cell attachment to Laminin and Fibronectin coated wells.
2011-02-15 | GSE20404 | GEO