Gene expression analysis of human adipose-derived stem cells.
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE51030 | GEO | 2013/09/21
SECONDARY ACCESSION(S): PRJNA219718
REPOSITORIES: GEO
Similar Datasets
Project description:Transcriptional activity was identified in all categories of genes expressed by ADSC, including collagens, ECM and basement membrane constituents, adhesion molecules involved in cell-cell and cell-matrix interactions, and proteases involved in degradation of the ECM and their inhibitors. Importantly, it was observed that ADSC synthesize and secrete all three collagen VI chains, suggesting suitability of ADSC for collagen VI congenital muscular dytrophy treatment. We developed a procedure for isolation of human stem cells from adipose layer of neonatal foreskin skin. The adipose-derived stem cells (ADSC) were examined for expression of extracellular matrix (ECM) and related genes using gene expression array analysis.
2013-09-21 | E-GEOD-51030 | biostudies-arrayexpress
Project description:Collagen VI-related disorders (COL6-RDs) are a group of rare muscular dystrophies caused by pathogenic variants in collagen VI genes. ¬¬Collagen type VI is a heterotrimeric, microfibrillar component of the muscle extracellular matrix (ECM), predominantly secreted by resident fibroadipogenic precursor cells in skeletal muscle. Collagen VI absence or mislocalization in the skeletal muscle ECM underlies the non-cell autonomous dystrophic changes and dysfunction in skeletal muscle in COL6-RDs with an as of yet elusive direct mechanistic link between the ECM and myofiber dysfunction. Here, we derive a novel mouse model of COL6-RD, Col6a2-/- mice, and conduct a comprehensive natural history study in male and female animals aged to 60 weeks of age. Col6a2-/- mice have a normal lifespan but develop muscle weakness based on standardized behavioral tests (grip and hanging wire test), muscle atrophy with histologic hallmarks of muscular dystrophy, and reduced muscle force prodcution on physiologic parameters. We also report a robust dysregulation of TGFβ pathway early in the disease process and thus propose a new mechanism for pathogenesis of the disease that links the ECM regulation of TGFβ with downstream skeletal muscle abnormalities, paving the way for developing therapeutics that target this pathway.
2023-12-04 | GSE228223 | GEO
Project description:Although it is postulated that dysfunctional extracellular matrices (ECM) drive aging and disease, how ECM integrity assures longevity is unknown. Here, using proteomics and in-vivo monitoring of fluorescently tagged ECM proteins, we systematically examined the ECM composition during Caenorhabditis elegans aging revealing three distinct collagen dynamics. We show that age-dependent stiffening of inert collagen was slowed by longevity interventions through prolonged replenishing of collagens. In genetic and automated lifespan screens for the regulators that drive this remodeling, we identify hemidesmosome-containing structures that span from the exoskeletal ECM through the hypodermis, basement membrane ECM, to the muscles, coupling mechanical forces to adjust ECM gene expression across tissues. The hemidesmosome tension-induced adaptation is mediated via transcriptional co-activator YAP. Our data reveal a novel mechanism of mechano-coupling and synchronizing of two functionally distinct and spatially distant ECMs that is indispensable for longevity. Thus, besides signaling molecules, mechanotransduction-coordinated ECM remodeling systemically promotes healthy aging.
2023-11-16 | PXD046470 | Pride
Project description:The aim of this study is to characterize how the extracellular matrix secreted by adipose-derived stem cells (ADSC) during osteogenesis affects the differentiation process. Specifically, ADSC undergo osteogenesis by following similar maturational phases as bone marrow-derived stem cells. However, it is unclear how the differentiation process is the same and how it differs. We first focused on ADSC behavior by analyzing whole transcriptome changes in response to osteogenic media supplements added into the tissue culture medium. We then developed osteogenic differentiation expression profiles for the ADSC and identify key genes and pathways that serve as an osteogenesis signature. This expression signature acted as a template for comparison of how extracellular matrix (ECM) affected ADSC differentiation. We studied ADSC induced to differentiate on ECM isolated from day 16 in the differentiation process (the midpoint in osteogenesis) as well as ECM from day 11 in the differentiation process. Ultimately, we aim to dissect the relationship between cells grown on ECM as an in vitro growth substrate and cells grown on tissue culture plastic; both in the presence of osteogenic supplements. This study, will allow us to determine the extent to which ECM affects the differentiation process.
2012-01-01 | E-MEXP-3340 | biostudies-arrayexpress
Project description:Col1a1 is located on mouse distal chromosome 11 (Celera 94607393-94622990bp; 15kb) and encodes type I procollagen that associates stoichiometrically with col1a2 in forming secreted type I mature collagen that self-assembles into a supramolecular fibrillar structure consisting of a protein family. Type I collagens are predominantly enriched in bone, cartilage, skin, tendons, and eye (i.e. in major fibrous tissues) making up the main extracellular matrix (ECM) component for support and scaffolding purposes. Col1a1 is known to be expressed in the embryo (E9.5; Northern dot blot), perioptic mesenchyme (E11), cornea (E11), skeleton (E14.5), brain meninges (E14.5), and cartilage (E14.5) at relatively early stages. Most evidence of type I collagen function is coupled to the latter stages of skeletal development, thus bypassing the major events of axis formation, tissue differentiation, and mesenchlymal-epithial interactions, for example, that are more symbolic of morphogens and growth factors. Members of the integrin cell surface receptor family of molecules mediate cell adhesion to ECM proteins such as collagen (mainly to type IV basement membrane collagen that forms into a polygonal meshwork), fibronectin, and laminin implicated in wound healing and inflammatory responses (e.g. Crohn disease, ulcerative colitis) in connective tissues. There is some evidence for protein-protein interactions between leukocyte-associated integrins and the interstitial matrix in promoting the migration and/or activation of extravasated leukocytes (e.g., T cells and monocytes) within the perivascular compartment, an ECM-rich environment. This region is surmised to be an important location where certain human leukocytes undergo differentiation (e.g. monocytes) and activation (neutrophils, monocytes, lymphocytes) upon extravascular migration. The von Willebrand factor (vWF), type C motif is found in various plasma proteins like complement factors, the integrins, collagen types, and other extracellular proteins. Thus, the majority of vWF-containing proteins are extracellular and a common feature appears to be involvement in multi protein complexes participating in numerous biological events (e.g. cell adhesion, migration, homing, pattern formation, and signal transduction). Three organs (lung, heart and bone) of 5 AGA002 mutant mice (age 2x 10 days and 3x 11 days) were analysed by cDNA microarray technology. As reference five mice, 11 days old were used 50% of the chip hybridisations are dye swap experiments.
2010-06-01 | E-GEOD-12847 | biostudies-arrayexpress
Project description:It is well established that the expression profiles of multiple and possibly redundant matrix remodeling proteases (e.g. collagenases) strongly differ in health, disease and development. Although enzymatic redundancy might be inferred from their close similarity in structure, their in-vivo activity can lead to extremely diverse tissue-remodeling outcomes. We observed that proteolysis of collagen-rich natural extracellular matrix (ECM), generated uniquely by individual homologous proteases, leads to specific combinatorial events, which eventually affects overall ECM topography, visco-elastic properties and composition. We reveal striking differences in the movement and signaling patterns, morphology, and gene expression profiles of cells interacting with natural collagen-rich ECM degraded by different collagenases. Thus, unlike envisioned before matrix-remodeling systems are not redundant and give rise to precise ECM-cell crosstalk. As ECM proteolysis is an abundant biochemical process critical to tissue homoeostasis, these results improve our fundamental understanding of combinatorial factors dictating cell behavior.
2016-11-08 | GSE79749 | GEO
Project description:Type I, II, III and V collagens were commonly identified in human, pig, and mouse breast ECM. Mammary epithelial cells were able to form acini on certain types or combinations of the four collagens at normal breast tissue stiffness levels. Comparison of the collagen species in mouse normal breast and breast tumor ECM revealed common and distinct sets of collagens within the two types of tissues. Elevated collagen type I alpha 1 chain expression was found in human breast cancers. Collagen type XXV alpha 1 chain was identified in mouse breast tumors but not in normal breast tissues. Our data provide insights into modeling human breast pathophysiological structures and functions using native tissue-derived hydrogels and potential contributions of different collagen types or their monomers in breast cancer development.
2023-03-11 | PXD037900 | Pride
Project description:Type I, II, III and V collagens were commonly identified in human, pig, and mouse breast ECM. Mammary epithelial cells were able to form acini on certain types or combinations of the four collagens at normal breast tissue stiffness levels. Comparison of the collagen species in mouse normal breast and breast tumor ECM revealed common and distinct sets of collagens within the two types of tissues. Elevated collagen type I alpha 1 chain expression was found in human breast cancers. Collagen type XXV alpha 1 chain was identified in mouse breast tumors but not in normal breast tissues. Our data provide insights into modeling human breast pathophysiological structures and functions using native tissue-derived hydrogels and potential contributions of different collagen types or their monomers in breast cancer development.
2023-03-11 | PXD037920 | Pride
Project description:Collagens in the extracellular matrix (ECM) provide a physical barrier to tumor immune infiltration, while also acting as a ligand for immune inhibitory receptors. Transforming growth factor-β (TGF-β) is a key contributor to shaping the ECM by stimulating the production and remodeling of collagens. TGF-β-activation signatures and collagen-rich environments have both been associated with T-cell exclusion and lack of responses to immunotherapy. Here we describe the effect of targeting collagens that signal through the LAIR-1 inhibitory receptor in combination with blockade of TGF-β and programmed cell death ligand 1 (PD-L1). This approach remodeled the tumor collagenous matrix, enhanced tumor infiltration and activation of CD8+ T cells, and repolarized suppressive macrophage populations resulting in high cure rates and long-term tumor-specific protection across murine models of colon and mammary carcinoma. The results highlight the advantage of direct targeting of ECM components in combination with immune checkpoint blockade therapy.
2022-03-09 | GSE195685 | GEO
Project description:Collagens in the extracellular matrix (ECM) provide a physical barrier to tumor immune infiltration, while also acting as a ligand for immune inhibitory receptors. Transforming growth factor-β (TGF-β) is a key contributor to shaping the ECM by stimulating the production and remodeling of collagens. TGF-β-activation signatures and collagen-rich environments have both been associated with T-cell exclusion and lack of responses to immunotherapy. Here we describe the effect of targeting collagens that signal through the LAIR-1 inhibitory receptor in combination with blockade of TGF-β and programmed cell death ligand 1 (PD-L1). This approach remodeled the tumor collagenous matrix, enhanced tumor infiltration and activation of CD8+ T cells, and repolarized suppressive macrophage populations resulting in high cure rates and long-term tumor-specific protection across murine models of colon and mammary carcinoma. The results highlight the advantage of direct targeting of ECM components in combination with immune checkpoint blockade therapy.
2022-03-09 | GSE194421 | GEO