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miR-18a was decreased during lung fibrosis in vitro and in vivo, as well as in patients with IPF. Moreover, knockdown of miR-18a led to fibrogenesis in lung fibroblasts, whereas enhanced expression of miR-18a attenuated TGF-beta1-induced lung fibrosis by directly targeting the regulation of connecting tissue growth factor.
we also found that CTGF/CCN2 is expressed in astrocytes and neurons, predominantly in dorsal areas of spinal cord from symptomatic hSOD1G93A mice. Together, these results reveal that CTGF/CCN2 might be a novel therapeutic target to ameliorate symptoms and improve the quality of life of ALS patients.
Inhibition of CTGF ameliorates peritoneal fibrosis through suppression of fibroblast and myofibroblast accumulation and angiogenesis.
These results reveal a novel mechanism of macrophage migration into glomeruli with nephritis mediated by connective tissue growth factor derived from mesangial cells.
miR-26b-5p interacted with 3'UTRs of Col1a2 and CTGF, and circ_000203 could block the interactions of miR-26b-5p and 3'UTRs of Col1a2 and CTGF.
early myocardial CTGF mRNA expression (six hours) after Ang-II exposure is likely dependent on latent TGF-beta activation via the canonical Smad-dependent pathway in resident cardiac cells.
These results indicate that the hepatocytic expression of TGF-beta and CTGF is mediated by Wnt signalling in Schistosoma japonicum infection.
Data (including data from studies using transgenic mice) suggest that Ctgf secreted from vascular endothelium in pancreas plays critical role in up-regulation of insulin secretion in pancreatic beta-cells during pregnancy; here, pregnant mice with global Ctgf haplo-insufficiency (heterozygous for loss-of-function mutation) (a) exhibit impairment in maternal beta-cell proliferation and (b) develop gestational diabetes.
The data demonstrate that MMP13 and CTGF play a crucial role in modulation of fibrogenic mediators while promoting hepatic fibrogenesis.
p-SMAD2/3 and p-ERK1/2 might play a regulatory role in TGF-beta1 induced CTGF exp p-SMAD2/3 and p-ERK1/2 might play a regulatory role in TGF-beta1 induced CTGF expression during tooth development.
Ctgf is the direct target gene of SOX9 in chondrocytes and nucleus pulposus cells.
As shown in mouse model of kidney fibrosis CTGF is significantly involved in fibrosis-associated renal lymphangiogenesis through regulation of, and direct interaction with, VEGF-C.
CTGF and BMP2 are induced following myocardial ischemia in mice and humans.
this study suggested that CTGF antibody protected podocytes against injury in DN mice by reducing beta-catenin overexpression and preventing podocyte EMT, which might provide new insight into the mechanism of CTGF inhibition in the treatment of DN.
LPA-LPA1 signaling initiates profibrotic epithelial cell fibroblast communication mediated by epithelial cell derived connective tissue growth factor.
Down-regulation of CTGF is effective in inhibiting postoperative scarring in vivo. This suggests that RNAi with CTGF siRNA may potentially pave the road for a novel therapeutic strategy to improve glaucoma surgery results.
CTGF role in cardiac fibrosis. Long noncoding RNA H19 mediates CTGF expression.
Notch1 haploinsufficiency decreased the expression of Ctgf in the aorta and in vitro cell culture system. In vitro studies on SMCs using the Notch1 intracellular domain (NICD) plasmid, dominant negative mastermind-like (dnMAML), or specific siRNA suggest that Notch1, not Notch3, directly modulates the expression of CTGF
these findings show that cardiac ERK1/2 activity is modulated in part by TGF-b/Smad signaling, leading to altered activation of CTGF/CCN2 to mediate fibrosis and alter cardiac function. This identifies a novel mechanism in the development of LMNA cardiomyopathy.
the mechanistic target of rapamycin (mTOR) pathway in neurons regulates CTGF production and secretion, revealing a paracrine mechanism by which neuronal signaling regulates oligodendrocyte maturation and myelination in tuberous sclerosis complex (TSC).
CCN2 is synthesized and secreted as a preproprotein that is autoinhibited by its two N-terminal domains and requires proteolytic processing and homodimerization to become fully biologically active.
In regards to extracellular matrix remodelling, treprostinil significantly reduced PDGF-BB-TGF-beta1-CTGF induced synthesis and deposition of collagen type I and fibronectin, in a cAMP sensitive manner
Curcumin can suppress TGF-beta1-induced CTGF expression in human gingival fibroblasts through the interruption of Smad2 signaling.
a significant negative correlation between hsamiR1455p and CTGF in ovarian cancer development, is reported.
These results suggest that Angiotensin II induces CTGF expression and extracellular matrix accumulation through a special TGF-beta-independent interaction between the NF-kappaB and Smad2/3 signals elicited by the AT1/PKCalpha/p38 MAPK pathway.
Connective tissue growth factor (CTGF), a matricellular protein, combines with TGF-beta in the pathomechanism of many fibrotic disorders. This interaction takes place in asthma as well, as fibroblast to myofibroblast transition contributes to bronchial wall remodelling in persistent asthma.
Study describes the molecular and biological characteristics of CTGF, its regulation and various functions in the spectrum of development and regeneration to fibrosis. [review]
This work indicates that NELL-1, HMGB1, and CCN2 might enhance bone defect healing via the recruitment of endogenous cells and induction of vascularization and act via different processes than BMP2.
TRAF1, CTGF, and CX3CL1 genes are hypomethylated in osteoarthritis
Down-regulation of CTGF could markly decrease proliferation.
PVT1 was able to bind and degrade miR26b to promote connective tissue growth factor (CTGF) and angiopoietin 2 (ANGPT2) expression.
CTGF can reduce glycolysis and mitochondrial OXPHOS pathways by increasing mtTFA protein degradation and in turn reduces cancer migration and invasion in oral squamous cell carcinoma (OSCC).
Results show that mRNA and serum expression levels of Cyr61, CTGF, and VEGF in muscle tissues of patients with polymyositis (PM)/dermatomyositis (DM). These data suggest that these genes may be involved in the pathogenesis mainly by affecting the formation of blood vessels and promoting inflammatory response.
This study study discovered a positive feedback loop between CTGF and CCL18 in hepatocellular carcinoma metastasis.
Serum connective tissue growth factor (CTGF) is a promising diagnostic biomarker for rheumatoid arthritis (RA).
Connective tissue growth factor (CTGF) is an important mediator of renal allograft fibrosis, and urinary CTGF (CTGFu) levels correlate with the development of allograft interstitial fibrosis. We evaluated the predictive value of CTGF protein expression in 160 kidney transplant recipients with paired protocol biopsies at 3 months and 5 years after transplantation.
Lymphangiogenesis during tubulointerstitial fibrosis to be associated with increased expression of CTGF and VEGF-C in human obstructed nephropathy as well as in diabetic kidney disease. vitro, CTGF induced VEGF-C production in HK-2 cells, while CTGF siRNA suppressed transforming growth factor beta1-induced VEGF-C upregulation.
miR132 may target CTGF in regulating fibrosis in Ang IItreated cardiac fibroblasts.
CTGF-mediated temozolomide resistance in glioblastoma operates through TGF-beta1-dependent activation of Smad/ERK signaling pathways
CCN2 plays a promoting role in hepatocellular carcinoma (HCC)progression through activating LRP6 in a HSPGs-dependent manner. Heparin in combination with chemotherapy has a synergic effect and could be a treatment choice for HCCs with a high CCN2 expression.
Bovine CCN2 exhibits unique expression patterns during preimplantation development, and is required for the proper expression of key regulatory genes in bovine blastocysts.
Results confirm the prodevelopmental actions of activin A and indicate that CTGF may also function as an embryokine by regulating the number of ICM cells in the blastocyst and altering gene expression. Low concentrations of HGF were inhibitory to development.
The results indicate that CTGF suppresses the synthesis of biglycan but newly induced that of decorin in the cells when the cell density is low.
Actin cytoskeleton-dependent regulation of CTGF transcription and mRNA stability
During vascular regression, Yap/Taz is activated by blood circulation in the endothelial cells. This leads to induction of Ctgf and actin polymerization. Interference with Yap/Taz activation decreased Ctgf production, which decreased actin polymerization and vascular regression.
this study reveals that CTGF is necessary and sufficient to stimulate glial bridging and natural spinal cord regeneration.
CTGF/CCN2 plays an important role in notochord development and is required for general embryonic development
Recombinant CTGF added to embryonic mouse neural precursor cell culture increased the number of Sox-2-, GFAP-and GFAP/Nestin-positive cells, activated p44/42 signaling, and upregulated fibronectin. In human glioma cells, it induced GFAP and nestin.
Data show that connective-tissue growth factor regulates signalling through the Wnt pathway, in accord with its ability to bind to the Wnt co-receptor LDL receptor-related protein 6 (LRP6).
These data suggest that CTGF levels are increased in multiple organs after radiation exposure and that inflammatory cell infiltration may contribute to the elevated levels of CTGF in multiple organs.
A significant increase in TGF-beta1 and CTGF was found at 6 weeks in the subsynovial connective tissue in a rabbit model of carpal tunnel syndrome.
Stretch is an important primary trigger for CTGF-induction in the overloaded heart.
Connective tissue growth factor is expressed in the naive cornea, lens, iris, and retina, and is expressed immediately after epithelial injury. Loss of CTGF impairs efficient re-epithelialization of corneal wounds.
TGF-beta1 can inhibit the growth of urethra epithelium cells and induce the expression of CTGF.
Overexpression of CTGF in the blebs after trabeculectomy demonstrates that CTGF may play an important role in the process of wound healing.
CCN2 was transiently expressed at the leading keratinocyte edge in wound healing.
Atrial fibrillation patients and animals exhibited a significantly increased expression of connective tissue growth factor (CTGF). Angiotension II-induced CTGF expression might be involved in atrial substrate remodeling.
CTGF in trabecular meshwork is modulated by physiological agonists and by increased ocular pressure and mechanical stretch. Regulation of CTGF within outflow pathway may play role in homeostasis of intraocular pressure.
CTGF level was not altered in model of obliterative bronchiolitis.
The protein encoded by this gene is a mitogen that is secreted by vascular endothelial cells. The encoded protein plays a role in chondrocyte proliferation and differentiation, cell adhesion in many cell types, and is related to platelet-derived growth factor. Certain polymorphisms in this gene have been linked with a higher incidence of systemic sclerosis.
CCN family member 2
, Connective tissue growth factor precursor (CTGF) (FISP-12 protein) (Hypertrophic chondrocyte-specific protein 24)
, fibroblast inducible secreated protein
, fibroblast inducible secreted protein
, hypertrophic chondrocyte-specific gene product 24
, hypertrophic chondrocyte-specific protein 24
, IGF-binding protein 8
, insulin-like growth factor-binding protein 8
, connective tissue growth-related protein
, connective tissue growth factor
, connective tissue growth factor XCTGF
, Connective tissue growth factor
, connective tissue growth factor-like