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Leukocyte cell derived chemotaxin 1

chondromodulin-I, ChM-I, chondromodulin-1, chondromodulin, CHM-1
This gene encodes a glycosylated transmembrane protein that is cleaved to form a mature, secreted protein. The N-terminus of the precursor protein shares characteristics with other surfactant proteins and is sometimes called chondrosurfactant protein although no biological activity has yet been defined for it. The C-terminus of the precursor protein contains a 25 kDa mature protein called leukocyte cell-derived chemotaxin-1 or chondromodulin-1. The mature protein promotes chondrocyte growth and inhibits angiogenesis. This gene is expressed in the avascular zone of prehypertrophic cartilage and its expression decreases during chondrocyte hypertrophy and vascular invasion. The mature protein likely plays a role in endochondral bone development by permitting cartilaginous anlagen to be vascularized and replaced by bone. It may be involved also in the broad control of tissue vascularization during development. Alternative splicing results in multiple transcript variants encoding different isoforms. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CD45, TUBE, vascular endothelial growth factor, SBS, ACID
Papers on chondromodulin-I
IL-1β-regulating angiogenic factors expression in perforated temporomandibular disk cells via NF-κB pathway.
Long et al., Wuhan, China. In J Oral Pathol Med, Feb 2016
METHODS: Expressions of vascular endothelial growth factor (VEGF), angiogenin-1 (Ang-1), chondromodulin-1 (ChM-1), and thrombospondins-1 (TSP-1) were compared between healthy and perforated TMJ disk cells with or without interleukin-1β (IL-1β) incubation.
CHM-1 Suppresses Formation of Cell Surface-associated GRP78-p85α Complexes, Inhibiting PI3K-AKT Signaling and Inducing Apoptosis of Human Nasopharyngeal Carcinoma Cells.
Ng et al., Taiwan. In Anticancer Res, Oct 2015
Hereιin we report that 2'-fluoro-6,7-methylenedioxy-2-phenyl-4-quinolone (CHM-1) induces apoptosis of human nasopharyngeal carcinoma (NPC) cells, as characterized by morphological changes, DNA fragmentation, caspase-3 activation, and cleavage of poly (ADP-ribose) polymerase.
Expression of DMP1 in the developing mouse tongue embryo.
Sato et al., Tokyo, Japan. In Ann Anat, Jul 2015
We also detected the mRNA abundance of tongue morphogenesis markers such as FGF6, TGF-β1, Collagen I, osteocalcin, chondromodulin 1, tenomodulin, Vascular endothelial growth factor (VEGF), caspase-3, and Aifm from embryonic stages by real-time RT-PCR.
Inhibition of the insulin-like growth factor 1 receptor by CHM-1 blocks proliferation of glioblastoma multiforme cells.
Way et al., Taiwan. In Chem Biol Interact, May 2015
In this study, we examined the anti-tumor effects of CHM-1, a synthetic 6,7-methylenedioxy substituted 2-phenyl-4-quinolone derivative, on GBM cells in vitro and in vivo.
Reciprocal interactions between mitral valve endothelial and interstitial cells reduce endothelial-to-mesenchymal transition and myofibroblastic activation.
Bischoff et al., Boston, United States. In J Mol Cell Cardiol, Mar 2015
VECs or conditioned media from VECs reversed the spontaneous cell culture-induced change in VICs to an activated phenotype, as indicated by reduced expression of α-SMA and type I collagen, increased expression chondromodulin-1 (Chm1), and reduced contractile activity.
Chondrogenic differentiation of ChM-I gene transfected rat bone marrow-derived mesenchymal stem cells on 3-dimensional poly (L-lactic acid) scaffold for cartilage engineering.
Wang et al., Dalian, China. In Cell Biol Int, Mar 2015
We have explored the role of Chondromodulin-I (ChM-I) in chondrogenesis of bone marrow-derived mesenchymal stem cells (BMSCs) in 3-dimensional (3D) scaffold for cartilage tissue engineering.
The influence of Chm-I knockout on ectopic cartilage regeneration and homeostasis maintenance.
Zhou et al., Shanghai, China. In Tissue Eng Part A, Feb 2015
Different from MSCs, chondrocytes can maintain stable chondrogenic phenotype in ectopic microenvironment, which was speculated to be related with the existence of antiangiogenic factors such as Chondromodulin-I (Chm-I).
Coagulation and angiogenic gene expression profiles are defined by molecular subgroups of medulloblastoma: evidence for growth factor-thrombin cross-talk.
Rak et al., Montréal, Canada. In J Thromb Haemost, 2014
These factors cooperate with thrombin, impacting the profile of vascular regulators, including interleukin 1β (IL1B) and chondromodulin 1 (LECT1).
Bevacizumab, an anti-vascular endothelial growth factor antibody, inhibits osteoarthritis.
Mochida et al., In Arthritis Res Ther, 2013
In articular cartilage, expression levels of aggrecan, collagen type 2, and chondromodulin-1 were higher in the OAB IV group than in the OA group.
Defects in tendon, ligament, and enthesis in response to genetic alterations in key proteoglycans and glycoproteins: a review.
Veillette et al., Toronto, Canada. In Arthritis, 2012
The genes reviewed are for small leucine-rich proteoglycans (lumican, fibromodulin, biglycan, decorin, and asporin); dermatan sulfate epimerase (Dse) that alters structure of glycosaminoglycan and hence the function of small leucine-rich proteoglycans by converting glucuronic to iduronic acid; matricellular proteins (thrombospondin 2, secreted phosphoprotein 1 (Spp1), secreted protein acidic and rich in cysteine (Sparc), periostin, and tenascin X) including human tenascin C variants; and others, such as tenomodulin, leukocyte cell derived chemotaxin 1 (chondromodulin-I, ChM-I), CD44 antigen (Cd44), lubricin (Prg4), and aggrecan degrading gene, a disintegrin-like and metallopeptidase (reprolysin type) with thrombospondin type 1 motif, 5 (Adamts5).
Antiangiogenic and anticancer molecules in cartilage.
Sandell et al., Saint Louis, United States. In Expert Rev Mol Med, 2011
Of these components, a few such as thrombospondin-1, chondromodulin-1, the type XVIII-derived endostatin, SPARC (secreted protein acidic and rich in cysteine) and the type II collagen-derived N-terminal propeptide (PIIBNP) have demonstrated antiangiogenic or antitumour properties in vitro and in vivo preclinical trials that involve several complicated mechanisms that are not completely understood.
Role of angiogenetic factors in cardiac valve homeostasis and disease.
Fukuda et al., Tokorozawa, Japan. In J Cardiovasc Transl Res, 2011
Recently, we found that chondromodulin-I, tenomodulin, and periostin play essential roles in degeneration and/or rupture of the cardiac valve complex by controlling angiogenesis and matrix metalloproteinase production.
BRICHOS domain associated with lung fibrosis, dementia and cancer--a chaperone that prevents amyloid fibril formation?
Presto et al., Uppsala, Sweden. In Febs J, 2011
The BRICHOS domain was initially defined from sequence alignments of the Bri protein associated with familial dementia, chondromodulin associated with chondrosarcoma and surfactant protein C precursor (proSP-C) associated with respiratory distress syndrome and interstitial lung disease (ILD).
Chondromodulin 1 stabilizes the chondrocyte phenotype and inhibits endochondral ossification of porcine cartilage repair tissue.
Gelse et al., Erlangen, Germany. In Arthritis Rheum, 2011
chondromodulin 1 stabilizes the chondrocyte phenotype by supporting chondrogenesis but inhibiting chondrocyte hypertrophy and endochondral ossification.
Localization of chondromodulin-I at the feto-maternal interface and its inhibitory actions on trophoblast invasion in vitro.
Hiraki et al., Kyoto, Japan. In Bmc Cell Biol, 2010
the inhibitory action of ChM-I on trophoblast migration and invasion, implying the potential role of the ChM-I expression in decidual cells for the regulated tissue remodeling and angiogenesis at feto-maternal interface.
Histone modifiers, YY1 and p300, regulate the expression of cartilage-specific gene, chondromodulin-I, in mesenchymal stem cells.
Toguchida et al., Kyoto, Japan. In J Biol Chem, 2010
Inhibition of YY1 in combination with forced expression of p300 and Sp3 restored the expression of ChM-I in cells with a hypomethylated promoter region, but not in cells with hypermethylation.
Impairment of VEGF-A-stimulated lamellipodial extensions and motility of vascular endothelial cells by chondromodulin-I, a cartilage-derived angiogenesis inhibitor.
Hiraki et al., Kyoto, Japan. In Exp Cell Res, 2010
Data suggest that chondromodulin-I impairs the VEGF-A-stimulated motility of endothelial cells by destabilizing lamellipodial extensions.
Molecular mechanisms underlying the onset of degenerative aortic valve disease.
Fukuda et al., Tokyo, Japan. In J Mol Med (berl), 2009
Having noted avascularity of normal cardiac valves, we recently identified chondromodulin-I (chm-I) as a crucial anti-angiogenic factor.
Altered fracture callus formation in chondromodulin-I deficient mice.
Yasui et al., Tokushima, Japan. In Bone, 2008
results suggest that Chm-I is involved in hypertrophic maturation of periosteal chondrocytes. Although a direct effect of Chm-I on bones is still unclear, bony callus formation was increased while external cartilaginous callus decreased in Chm1(-/-) mice
Chondromodulin-I maintains cardiac valvular function by preventing angiogenesis.
Fukuda et al., Tokyo, Japan. In Nat Med, 2006
chondromodulin-I has a pivotal role in maintaining valvular normal function by preventing angiogenesis that may lead to valvular heart diseases
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