Specialized regulatory T cells control venous blood clot resolution through SPARC
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA649772 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12354563_1.fastq.gz | Fastqsanger.gz | |||
| SRR12354563_2.fastq.gz | Fastqsanger.gz |
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Project description:The cells and mechanisms involved in blood clot resorption are only partially known. Regulatory T cells (Treg) accumulate in venous blood clots and regulate thrombolysis by controlling the recruitment, differentiation and matrix metalloproteinase (MMP) activity of monocytes. The clot Treg population is heterogeneous and contains a population of Treg that forms the matricellular acid- and cysteine-rich protein (SPARC). SPARC induces MMP activity in monocytes and SPARC+ Treg are required for clot resorption.
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Project description:Antiphospholipid syndrome (APS) is associated with arterial and venous thrombosis. The unfavorable fibrin clot phenotype, including formation of dense and poorly lysable clots, has been reported both in thrombotic APS and venous thromboembolism (VTE). The presence and amount of different proteins within a plasma clot, not only associated with the coagulation system, may influence clot properties. To our knowledge, there is a lack of data on plasma fibrin-clot bound proteins in patients with thrombotic APS or VTE. The aim of our study was to perform a quantitative proteomic analysis of fibrin clots prepared from citrated plasma from subjects with thrombotic APS and prior VTE, along with fibrin clot permeability (Ks) and clot lysis time (CLT) assessed ex vivo. We investigated 23 consecutive patients with APS, 18 with a history of first-ever VTE, and 20 age and sex matched healthy subjects. A multiple enzyme digestion filter aided sample preparation and a multienzyme digestion (MED) FASP method combined with LC-MS/MS analysis performed on a Proxeon Easy-nLC System coupled to the Q Exactive HF mass spectrometer were used. The proteomic analysis revealed that clot composition regarding 117 proteins in APS patients and 48 proteins in VTE patients was changed as compared to healthy controls, while 72 clot-bounded proteins differed between APS and VTE subjects. In healthy controls, Ks was associated with fibrinogen alpha and gamma chains (r=0.46 and r=0.46, both p<0.05, respectively) or apolipoprotein B-100 (r=-0.53, p<0.05), while CLT correlated with annexin A2 (r=-0.58, p<0.05), apolipoportein(a) (r=0.47, p<0.05), or platelet glycoprotein 4 (r=0.59, p<0.05). In VTE patients correlations of Ks with complement C1q and histone H2B, as factors closely linked with thrombosis, were observed (r=-0.52 and r=-0.47, both p<0.05, respectively). In patients with thrombotic APS all above-mentioned associations were not found. This study is the first to show that different proteins are able to influence the clot formation, structure, and properties. Since, prothrombotic conditions abolished associations observed in healthy subjects fibrin clots, differences in protein clot components might explain the links between prothrombotic fibrin clot phenotype and thromboembolic events.
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Project description:The aim of this study was evaluate the transcriptome changes in the comparison between triple negative tumors with increased SPARC expression and triple negative tumors with decreased SPARC expression according to Nagai et al., 2011 (Breast Cancer Res Treat (2011) 126:1–14) The results generated could be of particular interest to better define the prognostic impact of SPARC expression in triple negative breast tumors
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Project description:SPARC is a matricellular glycoprotein involved in regulation of the extracellular matrix, growth factors, adhesion, and migration. SPARC-null mice have altered basement membranes and develop posterior sub-capsular cataracts with cell swelling and equatorial vacuoles. Exchange of fluid, nutrients, and waste products in the avascular lens is driven by a unique circulating ion current. Here we demonstrate that SPARC-null mouse lenses exhibit abnormal circulation of fluid, ion, and small molecules which leads to altered fluorescein distribution in vivo, loss of resting membrane polarization, and altered distribution of small molecules. Microarray analysis of SPARC-null lenses showed changes in gene expression of ion channels and receptors, matrix and adhesion genes, cytoskeleton, immune response genes, and cell signaling molecules. Our results demonstrate that the regulation of SPARC on cell-capsular matrix interactions can influence the circulation of fluid and ions in the lens, and the phenotype in the SPARC-null mouse lens is the result of multiple intersecting pathways.
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Project description:SPARC is a matricellular glycoprotein involved in regulation of the extracellular matrix, growth factors, adhesion, and migration. SPARC-null mice have altered basement membranes and develop posterior sub-capsular cataracts with cell swelling and equatorial vacuoles. Exchange of fluid, nutrients, and waste products in the avascular lens is driven by a unique circulating ion current. Here we demonstrate that SPARC-null mouse lenses exhibit abnormal circulation of fluid, ion, and small molecules which leads to altered fluorescein distribution in vivo, loss of resting membrane polarization, and altered distribution of small molecules. Microarray analysis of SPARC-null lenses showed changes in gene expression of ion channels and receptors, matrix and adhesion genes, cytoskeleton, immune response genes, and cell signaling molecules. Our results demonstrate that the regulation of SPARC on cell-capsular matrix interactions can influence the circulation of fluid and ions in the lens, and the phenotype in the SPARC-null mouse lens is the result of multiple intersecting pathways. Experiment Overall Design: Lens epithelial cells from 7 lenses of littermate mice were isolated by laser capture microdissection. 3 wild-type lenses from 3 different mice and 4 knock-out lenses from 3 different mice were used as biological replicates.
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Project description:Alport syndrome (AS) is a hereditary kidney disease with no curative treatment, which characterized by hematuria, proteinuria, and progressive kidney failure. Podocyte injury has been observed in AS, whereases, the mechanism is still unclear. Reported studies showed the expression level of secreted protein acidic and rich in cysteine (SPARC) correlated with podocyte injury in chronic kidney diseases, yet its mechanism still unknown. Especially, its role in AS-related podocyte injury is unclear. Therefore, the kidney of Col4a3-/- AS mice was used to detect SPARC expression, location, and podocyte injury, and mouse podocyte cell line (MPC5) was used to explore the mechanism of SPARC-induced podocyte injury. Besides, SPARC expression in both urine and kidney samples from AS patients were analyzed. The results showed, SPARC upregulated and located in podocytes were detected in Col4a3-/- AS mice, and increased inflammatory cytokines, impaired podocyte structure and function were identified in SPARC-overexpression MPC5, importantly, knockdown adhesion G protein-coupled receptor B1 (ADGRB1) exerted a protective effect. In AS patients, urinary increased level of SPARC was detected, SPARC deposition in glomeruli of kidney sections was identified. Our findings identified SPARC as a key mediator of podocyte injury in AS, with ADGRB1 acting as its downstream effector.
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