Compstatin treatment decreases sepsis-induced expression of extracellular matrix genes, including eight collagen genes.
Osteoprogenitor cells express runx2, which modulates the expression of bone matrix genes including col1a1 and is necessary and sufficient for bone formation [ 23, 25].
miR-29 targeted several extracellular matrix genes including COL1A2, COL3A1 and COL5A2, and has been validated in nasopharyngeal carcinomas and HTM (human trabecular meshwork) cells [ 63, 64].
The three proteins, together, have been shown to activate numerous cartilage-specific extracellular matrix genes, including Col2a1, Col11a2, Matrilin-1, Col27a1, and Agc1 that maintain the differentiated chondrocyte environment.
The importance of the fine protein network and ECM structural integrity in postnatal cartilage health is well documented in studies of deficiencies or mutations in cartilage matrix genes, including Col2a1, Col9a1, Col11a1, aggrecan, matrilin-3, or fibromodulin alone or together with biglycan, which lead to age-dependent cartilage degeneration similar to that in OA patients [ 140, 148, 149].
The target genes included extracellular matrix genes including collagen genes, MMPs, and the ADAM family of metalloprotease-disintegrins all of which are reported to be involved in cell migration and invasion (Supplementary Table S2 and S3) (Newby, 2006; Daley et al, 2008).
The number of gene expression data matrix genes, included into clusters of significantly up-regulated (or down-regulated) genes and showing higher (or lower) expression level in corresponding precursor versus CD34+ cells, results to be significantly higher than expected by chance (p < = 0.01), accordingly with hypergeometric distribution (Table 3).
Hybridization peaks were detected in a series of cartilage extracellular matrix (ECM) genes including Col2a1, Col11a2, Aggrecan and Cdrap as well as in genes for specific transcription factors and signaling molecules.
Engineered cartilage in co-culture 5 5 group showed the densest elastic fibers and the highest Young's modulus, which were consistent with the expression profile of cartilage matrix-related genes including DCN and LOXL2 genes.
Matrix metalloproteinase pathway (MMP) genes, including matrix metallopeptidases 7, 14 and 16 and the tissue inhibitor of metallopeptidase (TIMP) 1-4 (Additional file 3), were also significantly down-regulated.
In OA chondrocytes, the hypertrophy or matrix degradation-related genes including COL10A1 (collagen, type X, α1), 1 2 matrix(metallo-peptidase-13dase-13), 3 ADAMTS-5 (a disintegrin and metalloproteinase with thrombospondin motifs 5) 4 5 and Runx2 (runt-related transcription factor-2) 6 are upregulated.
