scholarly journals Gene Expression Profiling of Extracellular Matrix as an Effector of Human Hepatocyte Phenotype in Primary Cell Culture

2007 ◽  
Vol 97 (2) ◽  
pp. 384-397 ◽  
Author(s):  
J. L. Page ◽  
M. C. Johnson ◽  
K. M. Olsavsky ◽  
S. C. Strom ◽  
H. Zarbl ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Culture ◽  
Extracellular Matrix ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Primary Cell Culture ◽  
Human Hepatocyte ◽  
Primary Cell

DNA methylation and gene expression profiling reveal MFAP5 as a regulatory driver of extracellular matrix remodeling in varicose vein disease

Epigenomics ◽  
2018 ◽  
Vol 10 (8) ◽  
pp. 1103-1119 ◽  
Author(s):  
Mariya A Smetanina ◽  
Alexander E Kel ◽  
Ksenia S Sevost'ianova ◽  
Igor V Maiborodin ◽  
Andrey I Shevela ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Extracellular Matrix ◽  
Gene Expression Profiling ◽  
Varicose Vein ◽  
Expression Profiling ◽  
Extracellular Matrix Remodeling ◽  
Matrix Remodeling ◽  
Vein Disease

Gene Expression Profiling of Human Mesenchymal Stem Cells for Identification of Novel Markers in Early- and Late-Stage Cell Culture

2008 ◽  
Vol 144 (3) ◽  
pp. 399-408 ◽  
Author(s):  
Shihori Tanabe ◽  
Yoji Sato ◽  
Takayoshi Suzuki ◽  
Kazuhiro Suzuki ◽  
Taku Nagao ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stem Cells ◽  
Cell Culture ◽  
Mesenchymal Stem Cells ◽  
Gene Expression Profiling ◽  
Late Stage ◽  
Expression Profiling ◽  
Human Mesenchymal Stem Cells

scholarly journals Extracellular Matrix-Related Genes Are Deregulated in Peripheral Blood from Patients with Myelofibrosis and Related Neoplasms

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 5491-5491
Author(s):  
Vibe Skov ◽  
Mads Thomassen ◽  
Lasse Kjær ◽  
Caroline Riley ◽  
Thomas Stauffer Larsen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Bone Marrow ◽  
Extracellular Matrix ◽  
Gene Expression Profiling ◽  
Whole Blood ◽  
Expression Profiling ◽  
Serum Levels ◽  
Gene Signature ◽  
Type I ◽  
Endothelial Proliferation

Abstract Introduction: The Philadelphia-negative chronic myeloproliferative neoplasms (MPNs) which include essential thrombocythemia (ET), polycythemia vera (PV) and primary myelofibrosis (PMF) are characterized by varying degrees of bone marrow fibrosis and endothelial proliferation. We and others have previously reported that these stromal alterations are reflected by increased serum levels of matrix derived metabolites, striated collagens type I/III and basement membrane components. The existence of a prefibrotic seromarker profile in MPNs is further evidenced by reports on increased serum levels of matrix metalloproteinase-3 (MMP-3) and decreased tissue inhibitor of metalloproteinase- I (TIMP-I). Using whole blood gene expression profiling, we aimed to provide a comprehensive gene signature of extracellular matrix-related proteins in MPNs with particular focus on genes associated with the regulation of major stromal proteins and MMPs. Methods: Gene expression profiling was performed on whole blood from 21 control subjects, 19 patients with ET, 41 patients with PV, and 9 patients with PMF. RNA was converted to biotin labeled amplified RNA (aRNA) using the MessageAmpTM III RNA amplification kit, and fragmented aRNA was hybridized to Affymetrix HG-U133 Plus 2.0 microarray chips recognizing 54,675 probe sets (38,500 genes). The R statistical software was applied to perform data preprocessing and statistical analysis of microarray data. Results: We identified 20,439, 25,307, and 17,417 probe sets that were differentially expressed between controls and patients with ET, PV, and PMF, respectively (FDR£0.05). These genes included 116 genes encoding extracellular matrix and adhesion molecules (ECM) important for cell-cell and cell-matrix interactions. These genes are represented on the Qiagen Human ECM panel, and in addition, all remaining collagen genes have been included. In patients with ET, COL1A1, COL1A2, COL3A1, COL4A2, COL4A5, LAMA2, LAMB1, MMP1, MMP7, MMP11, MMP12, MMP14, AND TIMP3 were among the 42 upregulated ECM genes (FDR<0.05). In patients with PV, 53 ECM genes were upregulated including COL1A1, COL1A2, COL3A1, COL4A2, LAMA2, LAMB1, MMP1, MMP7, MMP8, MMP9, MMP11, MMP12, MMP14, and TIMP3 (FDR<0.05). In PMF, COL1A2, COL3A1, COL4A2, COL4A5, LAMA2, MMP1, MMP8, MMP9, MMP14, and TIMP3 were among the 26 upregulated genes (FDR<0.05) (Table 1). 17, 14, and 13 ECM genes were significantly downregulated in ET, PV, and PMF, respectively (FDR<0.05) (data not shown). ITGA7, ITGB3, and MMP1 were significantly upregulated from ET over PV to PMF, whereas ITGAL, SPG7, and TGFBI were significantly downregulated from ET over PV to PMF. ADAMTS8, ADAMTS13, COL10A1, COL14A1, COL1A2, COL29A1, COL3A1, COL4A2, COL6A1, ITGA7, ITGB3, ITGB5, LAMA2, MMP1, MMP14, NCAM1, THBS2, and TIMP3 were significantly upregulated in both ET, PV, and PMF (FDR<0.05). COL4A3BP, COL6A2, ITGA4, ITGA5, ITGAL, ITGB1, PECAM1, SPG7, and TGFBI were significantly downregulated in both ET, PV, and PMF (FDR<0.05). In table 2a-b are shown the 10 most significantly up- and downregulated genes. Discussion and conclusions: Bone marrow fibrosis and endothelial proliferation in MPNs are elicited due to the release of fibrogenic and angiogenic growth factors primarily from hyperproliferating megakaryocytes. The connective tissue components of the bone marrow in MPNs include type III collagen, which is deposited in the early disease stages (ET/PV) as "reticulin fibrosis" being accompanied and substituted by mature Van Giesson positive collagen (type I collagen) in the advanced myelofibrosis stage. Increased endothelial cell proliferation is followed by the development of continuous sheets of basement membrane material beneath endothelial cells as assessed by increased deposition of type IV collagen and laminin. Using whole blood gene expression profiling, we provide evidence that abnormal extracellular matrix metabolism is reflected in the gene signature of peripheral blood cells from patients with MPNs. Further studies are needed to determine whether these changes represent local bone marrow fibrogenesis and/or systemic disease manifestations. Disclosures Hasselbalch: Novartis: Research Funding.

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