Role of SPARC in autoimmunity
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA603581 | ENA |
REPOSITORIES: ENA
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Project description:We performed gene expression profiling to evaluate whether macrophages from pristane-treated WT and Sparc-/- mice display a different inflammatory phenotype
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Project description:SPARC is a member of matricellular protein, and emerging evidence suggests that it plays a critical role in integrated metabolic and inflammatory responses. However, the mechanism how SPARC activates inflammation is still unanswered. Here we showed that excess SPARC induced sterile inflammation, and converted anti-inflammatory macrophage to pro-inflammatory macrophage. RNA-sequencing analysis revealed that SPARC elicits interferon-stimulated genes (ISGs) by transcription factor IRF7. SPARC also dampened mitochondrial respiration that induced pro-glycolytic inflammatory macrophage. Altogether, we discovered a mechanism how SPARC triggers sterile inflammatory response in anti-inflammatory macrophage, and this implicates the potential role of SPARC as a modulator of anti-inflammatory macrophages to maintain tissue homeostasis.
2022-08-12 | GSE167950 | GEO
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
2018-07-01 | GSE98931 | GEO
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.
2025-10-04 | GSE309489 | GEO
Project description:Mesenchymal stem cells (MSCs) have garnered significant attention over the past three decades due to their robust regenerative potential, primarily mediated by their paracrine activity by releasing soluble bioactive factors and extracellular vesicles (EVs). The MSC secretome plays a pivotal role in wound healing by influencing cellular migration, inflammation, angiogenesis, extracellular matrix (ECM) remodeling, and re-epithelialization. SPARC (Secreted Protein Acidic and Rich in Cysteine), a multifunctional ECM glycoprotein involved in tissue repair and remodeling, regulates key processes such as cell migration, proliferation, angiogenesis, and survival. Despite its known role in ECM dynamics, the impact of SPARC expression on the regenerative properties of MSCs remains underexplored. In this study, we hypothesized that SPARC overexpression in MSCs enhances their secretome's regenerative capacity. Using lentiviral systems, we generated SPARCoverexpressing (+SPARC) and SPARC-knockdown (KD-SPARC) MSCs to investigate SPARC's role in wound healing. Conditioned media (CM) derived from these MSCs were analyzed in vitro for their effects on human skin keratinocytes and fibroblasts. Our results revealed that SPARC expression significantly influences cell-specific migration and cell cycle. Furthermore, in an in vivo wound healing model, CM from +SPARC MSCs accelerated regeneration, while SPARC absence in MSCs CM delayed the healing process. These findings underscore the critical role of SPARC in modulating MSC secretome composition and enhancing its regenerative efficacy. This study highlights SPARC as a promising therapeutic target for the development of advanced regenerative therapies aimed at improving cutaneous wound healing outcomes
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Project description:Hepatocellular carcinoma (HCC), the most common type of primary liver cancer, is characterized as a highly aggressive tumor entity and has become a health challenge worldwide. Intracellular secreted protein acidic and rich in cysteine (SPARC) has been described as secreted protein that serves as paracrine mediator between cells extracellular matrix (ECM), however, its intracellular role remains unclear. Genetically modified HCC cell lines, cancer patient-derived organoids, and mouse models were used to analyze SPARC on metabolic processes, as well as the invasive behavior and sorafenib resistance of HCC cells. Transcriptome, interactome, and biochemical analyses were performed to study how SPARC regulate cholesterol homeostasis. High expression of intracellular SPARC was significantly associated with elevated cholesterol levels and an enhanced invasive phenotype in HCC. Our findings unveil a previously unrecognized interplay between SPARC and cholesterol homeostasis. Targeting SPARC-triggered cholesterol-dependent oncogenic signaling serves as a promising strategy for treating advanced HCC.
2024-03-01 | GSE240747 | GEO
Project description:SPARC is a matricellular glycoprotein that plays critical roles in the pathologies associated with obesity and diabetes, as well as tumorigenesis. The objective of this study was to investigate the role of SPARC in the process of trophoblast invasion which shares many similarities with tumor cells invasion. Our results reveals that hormones, cell adhesion molecules, ECM molecules, growth factors and cytokines all are mediated by SPARC in EVT invasion. HTR-8/SVneo cells were transfected with SPARC siRNA or a 25-nucleotide universal negative control siRNA using Lipofectamine 2000 according to the manufacturer’s protocol. Seventy-two hours after transfection, cells were harvested and RNA was isolated using standard procedures.
2012-04-27 | E-GEOD-37639 | biostudies-arrayexpress
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.
2009-05-01 | GSE13402 | GEO
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.
2009-05-11 | E-GEOD-13402 | biostudies-arrayexpress