TLR4 Expression In The Monocytes Of Hypertensive Left Ventricular Hypertrophy Patients

Objective: Hypertension serves as cardiac remodeling and significantly stimulating atherosclerosis. Heart and blood vessel is the mostly easiest injuried target organ. Left ventricular hypertrophy can transform into cardiac failure furthermore. It is an important strategy for preventing and curing cardiovascular disease in recent years to protect directly target organs of heart and blood vessel. We improve the patients of hypertension living level if we would find out some mechanisms in heart and blood vessel's remodeling and prevent them specialy. As far as left ventricular remodeling is concerned , it is a response of heart to enhance after overload. It includes not only hypertrophy of myoctes and apoptosis but also reexpressing of embryo genes and protein , and so on.At present it is unknown that how heart failure come from hypertensive left ventricular remodeling especially hypertrophy. We postulate that TLR4 was involved in the initiation and development of hypertensive left ventricular hypertrophy by providing a cascade of inflammatory response. Human Toll like receptor is a typeⅠtransmembrane receptor and it is a Toll protein homologue of Drosophila. In extracellular portion it contains leucine-rich repeats and in cytoplasmic domain it is significantly similar to the intracellular portion of interleukin-1 receptor.In 1997 Ruslan Medzhitor cloned human Toll like receptor at first that is identified as human Toll like receptor. At the same time they proved that there was a signal transduction pathway of TLR4 and nuclear factor-κB (NF-κB )in human beings. The pathway is still to be a host prevention machanism throughout several billions years. It is probably significant in regulating inflammatory,hyperplasia and apoptosis, from that we can conclude that TLR4 and NF-κB signal pathway is probably a critical pathway leads to ventricular remodeling. In the experiment, the expression of TLR4 is tested in the patients of hypertensive left ventricular hypertrophy. We explore the expression of TLR4 in the left ventricular myocyte of hypertensive patients in order to preliminarily test our hypothesis. Method: There were 18 hypertensive patients with left ventricular hypertrophy who did not suffer from diabetes and acute inflammation. Left ventricular posterior wall thickness at end-diastole was over 12mm. Others 16 hypertensive patients without left ventricular hypertrophy and 16 healthy people served as control groups. Special primer for TLR4 was designed and total RNAs were isolated from monocytes in blood. RT-PCR was used for detection of TLR4 mRNA expression. Results: TLR4 was expressed in the hypertensive left ventricular hypertrophy patients and control groups. By using DNA sequencing, the RT-PCR products were confirmed to be TLR4 cDNA. Contrasting to control groups, the expressing of TLR4 enhanced prominently in the hypertensive left ventricular hypertrophy group(p<0.05) Conclution: The expression of TLR4 enhanced in the monocytes of hypertensive left ventricular hypertrophy patients. The results provide evidence for a link between the immuine receptor TLR4 and left ventricular hypertrophy.