Sandwich ELISA, Biotin-labelled antibody
Serum, Plasma-EDTA, Plasma-Heparin, Plasma-Citrate, Urine
At ambient temperature. Upon receipt, store the product at the temperature recommended below.
Store the complete kit at 2–8°C. Under these conditions, the kit is stable until the expiration date (see label on the box).
0.63 – 20 ng/ml
Limit of Detection
n = 8, CV = 2.9 %
n = 8, CV = 4.3 %
- It is intended for research use only
- The total assay time is less than 3.5 hours-
- The kit measures total CTGF in plasma (EDTA, citrate, heparin), serum, and urine
- Assay format is 96 wells
- Standard is recombinant protein based
- Components of the kit are provided ready to use, concentrated or lyophilized
Apoptosis, Cardiovascular disease, Coronary artery disease, Oncology, Others, Pulmonary diseases, Animal studies
Connective Tissue Growth Factor (CTGF, CCN2, HCS24, IGFBP8, NOV2) is a heparin-binding glycoprotein with molecular weight of 36–38 KDa, composed of 343–349 amino acid residues and belonging to the CCN family. The CCN family of proteins is a complex family of multifunctional proteins containing six members designated CCN1 to CCN6. CTGF/CCN2 is a secreted protein with major roles in angiogenesis, chondrogenesis (cartilage regeneration), osteogenesis, tissue repair, cancer and fibrosis (cell adhesion, migration and proliferation). The primary function of CTGF is to modulate and coordinate signaling responses involving cell surface proteoglycans and growth factors. Abnormal amplification of CTGF dependent signals results in failure to terminate tissue repair, leading to pathological scarring in conditions such as fibrosis and cancer. The role of CTGF in fibrogenesis suggests this protein as a potential fibrogenic marker, because CTGF expression is induced by transforming growth factor β (TGF-β), which is the most important fibrogenic cytokine, and also, CTGF is expressed increasingly in major profibrogenic cell types (hepatocytes, biliary epithelial cells and hepatic stellate cells) during their transdifferentiation in extracellular matrix-producing myofibroblasts. The expression of CTGF is strongly upregulated in fibrotic liver tissue and CTGF is secreted into extracellular space, thus, it can reach the systemic circulation directly. The mean concentration of CTGF was the highest in serum of patients with fibrosis and chronic viral hepatitis, but lower in patients with fully developed cirrhosis. The data confirm hypothesis that CTGF increases in the circulation of patients with active, fibrogenic liver diseases. No statistical relations between CTGF levels and parameters of liver injury (AST, ALT) were noticed, but CTGF levels in serum are correlated negatively with serum albumin levels and platelet counts. CTGF was reported to be associated with and released by platelets during the coagulation process. In hepatocellular carcinoma (HCC) patients, CTGF concentrations decreased with tumor progression and size. Increase in CTGF concetration in plasma, serum and urine have been suggested as a surrogate marker of fibrotic disease activity in scleroderma, pulmonary fibrosis, diabetic nephropathy (DN) and glomerulosclerosis. CTGF appears to be an important growth factor implicated in the development of diabetes complications. Plasma CTGF-N (NH2-terminal fragment) concentrations are elevated in type 1 diabetic patients with nephropathy and correlate with proteinuria and creatinine clearance. In the previous study it was found that the presence of CTGF in urine and the relationship to diabetes and renal disease in an experimental animal model (rats). Low levels of urinary CTGF were found in healthy rats, but higher levels were found in diabetic animals. In DN patients, urinary CTGF (uCTGF) was independently associated with markers of proximal and distal tubular dysfunction and damage. Urinary CTGF levels in nephropathy may indicate the patients who are destined for progressive glomerulosclerosis and end-stage renal disease (ESRD). In conclusion, uCTGF in DN patients is elevated as a result of both increased local production and reduced reabsorption due to tubular dysfunction. It was observed that serum CTGF levels were significantly higher in non-renal systemic lupus erythematosus and correlated with chronic renal interstitial injury and doubling of serum creatinine in patients with lupus nephritis. CTGF was the most abundantly expressed growth factor present in chondrocytes of patients with osteoarthritis (OA). CTGF was detected in plasma and synovial fluid of patients with primary knee osteoarthritis and positively correlated with radiographic grading of knee OA. Results of several studies suggest that myocardial CTGF/CCN2 is upregulated in heart failure of both ischemic and non-ischemic etiologies in experimental models as well as humans. Plasma CTGF levels have also been reported to be elevated in heart failure patients and correlated with NYHA-class (the New York Heart Association Functional Classification). This study indicates that CTGF concentration in plasma is a novel diagnostic marker for cardiac dysfunction and myocardial fibrosis in chronic heart failure patients. Increased myocardial CTGF activities after myocardial infarction are associated with attenuation of left ventricular (LV) remodeling and improved LV function mediated by attenuation of inflammatory responses and inhibition of apoptosis. Plasma CTGF levels were elevated in patients with stable asthma and were correlated with parameters of pulmonary function tests and asthma control.