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Comprehensive analysis of mesenchymal cells reveals a deregulated TGF-B/Wnt/HOXB7 axis in patients with myelofibrosis

ABSTRACT: Comprehensive analysis of mesenchymal cells reveals a deregulated TGF-B/Wnt/HOXB7 axis in patients with myelofibrosis

PROVIDER: PRJNA981171 | ENA |

REPOSITORIES: ENA

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Comprehensive analysis of mesenchymal cells reveals a deregulated TGF-B/Wnt/HOXB7 axis in patients with myelofibrosis [RNA-seq]

Project description:In this study, through a patient-sample driven transcriptomic and epigenetic description of the MF microenvironment landscape and cell-based analyses, we identify HOXB7 overexpression and more precisely a novel TGF-B-Wnt-HOXB7 pathway as associated to a pro-fibrotic and pro-osteoblastic biased differentiation of mesenchymal stromal cells (MSCs).

2024-12-18 | GSE234388 | GEO

Comprehensive analysis of mesenchymal cells reveals a deregulated TGF-B/Wnt/HOXB7 axis in patients with myelofibrosis [ATAC-seq]

2024-12-18 | GSE234389 | GEO

Comprehensive analysis of mesenchymal cells reveals a deregulated TGF-B/Wnt/HOXB7 axis in patients with myelofibrosis [ATAC-seq]

Project description:Comprehensive analysis of mesenchymal cells reveals a deregulated TGF-B/Wnt/HOXB7 axis in patients with myelofibrosis [ATAC-seq]

| PRJNA981175 | ENA

Comprehensive analysis of mesenchymal cells reveals a deregulated TGF-B/Wnt/HOXB7 axis in patients with myelofibrosis [RNA-seq]

Project description:Comprehensive analysis of mesenchymal cells reveals a deregulated TGF-B/Wnt/HOXB7 axis in patients with myelofibrosis [RNA-seq]

| PRJNA981172 | ENA

Comprehensive analysis of mesenchymal cells reveals a deregulated TGF-B/Wnt/HOXB7 axis in patients with myelofibrosis

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-12-18 | GSE234390 | GEO

Comprehensive analysis of mesenchymal cells reveals a dysregulated TGF-β/WNT/HOXB7 axis in patients with myelofibrosis.

Project description: Not available

| S-EPMC11623938 | biostudies-literature

Comprehensive spatial profiling of the spleen in human myelofibrosis [ST_Visium]

2026-06-29 | GSE332563 | GEO

Comprehensive spatial profiling of the spleen in human myelofibrosis [snRNAseq]

2026-06-29 | GSE332562 | GEO

Therapeutic activity of GARP:TGF-b1 blockade in murine primary myelofibrosis

Project description:Primary myelofibrosis (PMF) is a myeloproliferative neoplasm characterized by clonal expansion of myeloid cells, notably megakaryocytes (MKs), and aberrant cytokine production leading to bone marrow (BM) fibrosis and insufficiency. Current treatment options are limited. TGF-b1, a profibrotic and immunosuppressive cytokine, is involved in PMF pathogenesis. While all cell types secrete inactive, latent TGF-b1, only a few activate the cytokine via cell type-specific mechanisms. The cellular source of the active TGF-b1 implicated in PMF is not known. Transmembrane protein GARP binds and activates latent TGF-b1 on the surface of regulatory T lymphocytes (Tregs) and MKs or platelets. Here, we found increased expression of GARP in BM and spleen of mice undergoing PMF and tested the therapeutic potential of a monoclonal antibody that blocks TGF-b1 activation by GARP-expressing cells. GARP:TGF-b1 blockade reduced not only fibrosis, but also clonal expansion of transformed cells. Using mice carrying a genetic deletion of Garp in either Tregs or MKs, we found that the therapeutic effects of GARP:TGF-b1 blockade in PMF imply targeting GARP on Tregs. These therapeutic effects, accompanied by increased IFN-g signals in the spleen, were lost upon CD8 T cell depletion. Our results suggest that selective blockade of TGF-b1 activation by GARP-expressing Tregs increase a CD8 T cell-mediated immune reaction that limits transformed cell expansion, providing a novel approach that could be tested to treat patients with myeloproliferative neoplasms.

2022-10-27 | GSE216221 | GEO

Comprehensive spatial profiling of the spleen in murine myelofibrosis identifies targetable immune-stromal interactions

Project description:Splenomegaly is a defining feature of myelofibrosis, yet the contribution of splenic mesenchymal stroma to disease progression remains unclear. We perferomed spatial transcriptomics of murine spleens to map extramedullary hematopoiesis niches. Activated red pulp reticular cells localize near hematopoietic stem and progenitor cells, and early disease shows marginal zone disruption with lymphoid depletion preceding stromal remodeling. Trajectory analyses reveal a shift of reticular cells from hematopoiesis-supportive to inflammatory and pro-fibrotic states driven by macrophage- and megakaryocyte-derived signals that activate complement and induce TNFα, TGF-β, extracellular matrix, and Thbs1 programs. Stromal deletion or pharmacological inhibition of complement component C3 suppresses these pathways, restores splenic architecture, and reduces splenomegaly and bone marrow fibrosis. These findings identify complement-dependent stromal reprogramming as a mechanism governing hematopoietic niches and a targetable axis in myelofibrosis.

2026-07-03 | GSE337447 | GEO

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