Purity of CTGF is greater than 90% as determined by SDS-PAGE.
Connective Tissue Growth Factor (CTGF) is part of the CCN protein family, which includes Cyr61, CTGF, Nov, WISP-1, WISP-2, and WISP-3. These proteins are secreted and interact with the extracellular matrix (ECM) and cell membranes. CCN proteins are matricellular, meaning they regulate cell functions like growth, specialization, survival, adhesion, and movement. They are present in tissues derived from all three embryonic layers and play a role in the development of various organs, including the kidneys, nervous system, muscles, bone marrow, cartilage, and bones. In adults, they are involved in wound healing, bone fracture repair, and diseases such as fibrosis, vascular issues, and tumor development. Full-length CCN proteins can inhibit cell growth, while shorter versions might promote growth and act as oncogenes. Structurally, CCN proteins have four modules: Module I resembles IGFBPs, Module II contains a VWC repeat, Module III includes a TSP1 repeat for binding glycoconjugates and cell adhesion, and Module IV (CT domain) is crucial for CCN protein functions and resembles domains in proteins like Von Willebrand factor. Proteolysis of secreted CCN2 and CCN3 can create peptides with different binding affinities. While truncated CCN2 isoforms are biologically active, the function of truncated CCN3 is unclear. Increased CCN2 expression is linked to various cancers, including invasive mammary ductal carcinomas, dermatofibromas, and pancreatic tumors. In chondrosarcomas, CCN2 expression correlates with tumor grade. CCN2 is involved in brain tumor angiogenesis, as shown by its presence in glioblastoma tumor cells and proliferating endothelial cells. In astrocytomas, high CCN2 levels are linked to higher tumor grades and increased cell proliferation. In acute lymphoblastic leukemia, CCN2 is found in a larger proportion of mononuclear cells.
The CTGF protein was lyophilized from a sterile filtered solution containing 0.1% Trifluoroacetic Acid (TFA) in water.
To reconstitute the lyophilized CTGF, it is recommended to dissolve it in sterile 18 megaohm-cm water to a concentration of at least 100 micrograms per milliliter. This solution can then be further diluted as needed with other aqueous solutions.
Lyophilized CTGF is stable at room temperature for up to 3 weeks. However, for long-term storage, it should be stored in a dry environment below -18 degrees Celsius. Once reconstituted, CTGF can be stored at 4 degrees Celsius for 2-7 days. For longer storage periods, it is advisable to freeze the solution at -18 degrees Celsius. To ensure optimal stability during long-term storage, it is recommended to add a carrier protein such as 0.1% HSA or BSA. Avoid repeated freezing and thawing of the CTGF solution.
The purity of CTGF is determined to be greater than 90% based on SDS-PAGE analysis.
CTGF is structurally characterized by four conserved, cysteine-rich domains :
These domains enable CTGF to bind to various cell surface receptors, including integrin receptors, cell surface heparan sulfate proteoglycans (HSPGs), LRPs, and TrkA . Additionally, CTGF interacts with growth factors and extracellular matrix proteins, such as aggrecan, VEGF, members of the TGF-β superfamily, fibronectin, perlecan, fibulin-1, slit, and mucins .
CTGF is essential for embryonic development and normal physiological functions. Knockout mice with disrupted Ctgf genes exhibit severe chondrodysplasia and die at birth due to respiratory stress . These mice also show defects in angiogenesis, impaired interaction between endothelial cells and pericytes, and collagen IV deficiency in the endothelial basement membrane . CTGF is also important for pancreatic beta cell development and normal ovarian follicle development and ovulation .
CTGF is associated with wound healing and virtually all fibrotic pathologies . It is believed that CTGF can cooperate with TGF-β to induce sustained fibrosis and exacerbate extracellular matrix production in association with other fibrosis-inducing conditions . Overexpression of CTGF in fibroblasts promotes fibrosis in the dermis, kidney, and lung, while deletion of Ctgf in fibroblasts and smooth muscle cells greatly reduces bleomycin-induced skin fibrosis .