MicroRNAs are responsible for regulating autophagy, concluded a joint research team from the universities of Monash in Australia and Cambridge in the UK.
A disorder in autophagy can lead to the aggregation of toxic proteins in the body, and may cause Parkinson and Huntington disease that causes a gradual neurodegeneration. Autophagy is the body's way of removing and recycling damaged cells and is crucial for clearing toxic proteins from cells.
Findings on how autophagy is regulated by microRNAs urged the research team to use a worm known as "Caenorhabditis elegans" in experiments that may help reach a possible treatment for diseases caused by autophagy disorders.
MicroRNAs were discovered for the first time in this free-living worm that lives independently from other living organisms in moist soil environments. Its lifespan ranges from three to four weeks, and has over 19,000 genes. Later, the same protein had been discovered in humans. It is a small non-coding ribonucleic acid molecule that forms 1 to 5 percent of the human genome, and accounts for 30 percent of the gene expression of proteins.
During the study recently published in the e-Life journal, researchers found that microRNAs protects from toxic proteins by controlling the expression of the TBC-7 protein in worms. This later is responsible for regulating autophagy.
The researchers removed microRNA in the worm and looked at the effect. They noticed a further aggregation of toxic proteins responsible for Parkinson and Huntington, which indicates that this protein is primordial to clean toxic proteins.
Researchers then conducted more experiments that showed that the microRNA regulates a related pathway to control autophagy in human cells. They found that when human cells are supplied with a molecule called interferon-b, its pathway is upregulated revealing a way of treating autophagy disorders.
In a report published Sunday on the university's website, Associate Professor Roger Pocock, from the Monash University said: "We have provisionally patented our findings and are in discussions with pharmaceutical companies about translating the research. We will further test it in pre-clinical models for Huntington's and Parkinson's disease."