"Defective RNA modification, which is also referred to as adenosine deamination, results in a decline in smooth muscle contraction," explain the MedUni Vienna researchers. Consequently, the actin-binding protein filamin A, which plays an important role in organisation of the cytoskeleton and hence muscular contraction, cannot be produced in the correct form (variant R). "At the same time, we were able to show, for the first time, that adenosine deamination plays an important role in smooth muscle, not only in the central nervous system as previously believed" says Jantsch.
It is not yet known what causes RNA modification defects in smooth muscle and this will be the focus of follow-on studies. These might potentially lead to the development of new therapeutic options for improving the treatment of high blood pressure or certain forms of cardiovascular disease that are attributable to defective RNA modification.
Smooth muscle is one of three types of muscle found in humans and animals. It occurs in the walls of all hollow organs (apart from the heart), which are able to contract. For example, these include blood vessels, organs of the digestive tract (bladder, bowel) and the respiratory tract. It is called smooth muscle because of its microscopic structure: whereas skeletal muscle and cardiac muscle exhibit visible horizontal stripes when viewed under the microscope, smooth muscle has no such stripes. Unlike skeletal muscle, it cannot be contracted at will. Instead, its contraction is controlled by muscular mechanisms and also by the nervous system, by hormones, neurotransmitters and other messenger substances.