CTHRC1 is a new therapeutic target and serum diagnostic biomarker for aortic dissection [Cthrc1_wt_ko_RNAseq]
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ABSTRACT:
PROVIDER: PRJNA1265128 | ENA |
REPOSITORIES: ENA
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Project description:Aortic dissection (AD) is a cardiovascular disease with rapid onset and extremely high short-term mortality, currently lacking specific peripheral blood-based biomarkers and effective treatments. Here, our analyses of AD samples from animal models and human patients revealed elevated blood levels of CTHRC1, a protein secreted by vascular fibroblasts. Furthermore, CTHRC1 regulates the phenotypic switch of vascular smooth muscle cells (VSMCs) during arterial remodeling by binding to ADAM9 on the VSMC membrane, activating the ERK1/2 signaling pathway, and promoting a contractile-to-synthetic transition. In Ang-II/BAPN induced AD mouse models, genetic ablation or antibody-mediated blockade of CTHRC1 effectively prevented AD formation and development. These findings unveil activated vascular fibroblast derived CTHRC1 as a critical regulator of VSMC phenotype and aortic structural integrity via the ERK1/2 signaling pathway, suggesting its potential as a novel serum diagnostic biomarker for AD diagnostic and a promising therapeutic target. Collectively, our data propose a new and effective strategy for diagnosis and clinical management of patients with AD.
2025-08-19 | GSE297520 | GEO
Project description:Aortic dissection (AD) is a cardiovascular disease with rapid onset and extremely high short-term mortality, currently lacking specific peripheral blood-based biomarkers and effective treatments. Here, our analyses of AD samples from animal models and human patients revealed elevated blood levels of CTHRC1, a protein secreted by vascular fibroblasts. Furthermore, CTHRC1 regulates the phenotypic switch of vascular smooth muscle cells (VSMCs) during arterial remodeling by binding to ADAM9 on the VSMC membrane, activating the ERK1/2 signaling pathway, and promoting a contractile-to-synthetic transition. In Ang-II/BAPN induced AD mouse models, genetic ablation or antibody-mediated blockade of CTHRC1 effectively prevented AD formation and development. These findings unveil activated vascular fibroblast derived CTHRC1 as a critical regulator of VSMC phenotype and aortic structural integrity via the ERK1/2 signaling pathway, suggesting its potential as a novel serum diagnostic biomarker for AD diagnostic and a promising therapeutic target. Collectively, our data propose a new and effective strategy for diagnosis and clinical management of patients with AD.
2025-08-19 | GSE297519 | GEO
Project description:Aortic dissection (AD) is a cardiovascular disease with rapid onset and extremely high short-term mortality, currently lacking specific peripheral blood-based biomarkers and effective treatments. Here, our analyses of AD samples from animal models and human patients revealed elevated blood levels of CTHRC1, a protein secreted by vascular fibroblasts. Furthermore, CTHRC1 regulates the phenotypic switch of vascular smooth muscle cells (VSMCs) during arterial remodeling by binding to ADAM9 on the VSMC membrane, activating the ERK1/2 signaling pathway, and promoting a contractile-to-synthetic transition. In Ang-II/BAPN induced AD mouse models, genetic ablation or antibody-mediated blockade of CTHRC1 effectively prevented AD formation and development. These findings unveil activated vascular fibroblast derived CTHRC1 as a critical regulator of VSMC phenotype and aortic structural integrity via the ERK1/2 signaling pathway, suggesting its potential as a novel serum diagnostic biomarker for AD diagnostic and a promising therapeutic target. Collectively, our data propose a new and effective strategy for diagnosis and clinical management of patients with AD.
2025-08-19 | GSE297518 | GEO
Project description:CTHRC1 is a new therapeutic target and serum diagnostic biomarker for aortic dissection
| PRJNA1268468 | ENA
Project description:CTHRC1 is a new therapeutic target and serum diagnostic biomarker for aortic dissection [MOVAS_rhCTHRC1_RNAseq]
| PRJNA1265124 | ENA
Project description:CTHRC1 is a new therapeutic target and serum diagnostic biomarker for aortic dissection [Ab_mouse_RNAseq]
| PRJNA1265127 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2025-08-19 | GSE298176 | GEO
Project description:Microarrays with 1,205 human microRNAs and 142 viral microRNAs were used for screening candidate diagnostic markers in the 3 categories of subjects from 24 plasma samples including acute aortic dissection, healthy and aortic aneurysm subjects. There were two microRNAs overlapping in the 3 group comparisons. Finally, 16 candidate microRNAs discovered via microarrays were selected for the further validation.
2017-11-15 | GSE92427 | GEO
Project description:Collagen triple helix repeat containing 1 (CTHRC1) has been found to be up-regulated in many human solid tumors. In this study, we investigated the changes of gene expression by comparing CTHRC1-siRNA and Scramble-siRNA control in hepatocellular carcinoma cell line HCCLM3, which has high expression levels of CTHRC1. Differential gene expression was assessed by Affymetrix microarray experiments for 2 samples: CTHRC1-siRNA-treated HCCLM3 cells and Scramble-siRNA-treated HCCLM3 cells.
2012-04-22 | E-GEOD-37208 | biostudies-arrayexpress
Project description:Bone remodeling is characterized by the sequential, local tethering of osteoclasts and osteoblasts, and is key to the maintenance of bone integrity. While bone matrix-mobilized growth factors, such as TGF-β, are proposed to regulate remodeling, no in vivo evidence exists that an osteoclast-produced molecule is the enigmatic coupling factor. We have identified Cthrc1, a protein secreted by mature bone-resorbing osteoclasts, that targets stromal cells so as to stimulate osteogenesis. The expression of Cthrc1 is robustly induced when mature osteoclasts are placed on dentin or hydroxyapatite, and also by increasing extracellular calcium. Cthrc1 expression in bone increases in a high turnover state, such as that which is induced by RANKL injections in vivo, whereas it decreases with aging or following alendronate treatment, conditions associated with suppressed bone turnover. The targeted deletion of the Cthrc1 gene eliminates Cthrc1 expression in bone, whereas its deficiency in osteoblasts does not exert any significant effect. Osteoclast-specific deletion of the Cthrc1 gene results in osteopenia due to reduced bone formation: it also impairs the coupling process following resorption induced by RANKL injections, with a resultant impairment of bone mass recovery. Thus, Cthrc1 is an osteoclast-secreted “coupling factor” that regulates bone remodeling and hence, skeletal integrity. Total bone marrow cells were prepared from the femurs and tibias of 8-10-week-old C57BL/6 mice and cultured in the presence of M-CSF (100ng/ml) for 3 days as described previously (Takeshita et al., 2000 JBMR 15:1477-1488). Cells were harvested with 0.02% EDTA/PBS and used as bone marrow macrophages (BMMs). These BMMs were cultured in the presence of M-CSF (100 ng/ml) and RANKL (100ng/ml) for 2 days. TRAP positive mononuclear cells were harvested and used as pre-osteoclasts (pOC). These pOC cells were further cultured in the presence of M-CSF and RANKL for 2 days in normal plastic plate or on dentin slices. After 2 days, multinucleated TRAP positive mature osteoclasts were generated as mature osteoclasts on plate (mOCp) and mature resorbing osteoclasts on dentin (mOCd), respectively. RNAs were extracted from four different stages of osteoclast lineage cells; BMMs, pOC, mOCp and mOCd, and used for microarray analysis.
2015-04-01 | E-GEOD-45656 | biostudies-arrayexpress