CT-1 is a member of the IL-6 family of cytokines which also includes LIF, CNTF, OSM (Oncostatin M), IL-11, IL-6 and possibly NNT-1/BSF-3. CT-1 is a pleiotropic cytokine which is expressed in various tissues including the adult heart, skeletal muscle, ovary, colon, prostate and fetal lung, and signals through the LIF receptor and the gp130 receptor subunit. CT-1 has the ability to induce cardiac myocyte hypertrophy, and enhances the survival of cardiomyocyte and different neuronal populations. Recombinant Murine Cardiotrophin-1 is a 21.3 kDa protein consisting of 202 amino acid residues.
Amino Acid Sequence
The ED50 as determined by the dose-dependent proliferation of TF-1 cells was 1.0 ng/ml, corresponding to a specific activity of 1×106 units/mg.
Endotoxin level is <0.1 ng/μg of protein (<1EU/μg).
Centrifuge the vial prior to opening. Reconstitute in water to a concentration of 0.1–1.0 mg/ml. Do not vortex. This solution can be stored at 2–8°C for up to 1 week. For extended storage, it is recommended to further dilute in a buffer containing a carrier protein (example 0.1% BSA) and store in working aliquots at –20°C to –80°C.
Cardiotrophin-1 (CT-1) is a 201 amino acid member of the interleukin-6 superfamily. It was identified by its ability to induce hypertrophic response in cardiac myocytes. CT-1 mRNA levels were found both in cardiac myocytes and in cardiac nonmyocytes. CT-1 was also detected in abundance in normal adult human lung and was expressed in both fetal and adult airway smooth muscle cells. CT-1activates gp130 dependent signaling and stimulates the Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway to transduce hypertrophic and cytoprotective signals in cardiac myocytes. CT-1 has also a neurotrophic function. CT-1 deficiency causes increased motoneuron cell death in spinal cord and brainstem nuclei of mice during a period between embryonic day 14 and the first postnatal week. Moreover, CT-1 is a hepatocyte survival factor that efficiently reduces hepatocellular damage in animal models of acute liver injury. CT-1 expression is augmented after hypoxic stimulation and it can protect cardiac cells when added either prior to simulated ischaemia or at the time of reoxygenation following simulated ischaemia. CT-1 can induce expression of the protective heat shock proteins (hsps) in cardiac cells. Cardiotrophin-1 increased ventricular expression of ANP, brain natriuretic peptide (BNP) and angiotensinogen mRNA. CT-1 levels were significantly elevated in patients with heart failure, patients with dilatative cardiomyopathy, moderate/severe mitral regurgitation, stable and unstable angina and after acute myocardial infarction.