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Researchers uncover a gene therapy target for polycystic kidney disease

Researchers at UT Southwestern reported that blocking the expression of PKD1 or PKD2 genes by deleting a binding site for microRNAs prevented the formation and growth of kidney cysts in autosomal dominant polycystic kidney disease (ADPKD) models. These findings were published in Nature Communications and suggested a strategy for gene therapy that could cure or arrest ADPKD.

Researchers uncover a gene therapy target for polycystic kidney disease

ADPKD can be caused by mutations in PKD1 or PKD2 genes. This has been known for over 25 years. Vishal Patel, Associate Professor of Internal Medicine at UTSW and corresponding author of the paper, said that no therapy exists to treat these root causes.

ADPKD is one of the most common human genetic disorders and the most common cause of kidney damage. It affects an estimated 12.5 million people around the world. ADPKD is an inherited condition in which one mutated and one normal copy of PKD1 or PKD2 are passed to patients.

This disease is characterized by the formation of small, fluid-filled sacs called kidney cysts. They form when the levels PKD1 or PKD2 are below a threshold. This can occur when the normal copy of the gene does not produce enough of the proteins Polycystin-1/Polycystin-2.

The messenger ribonucleic acids (mRNA) are responsible for producing or translating proteins. A code region at one end of the mRNA strand protects the gene from degradation and can control the amount of protein made. This region of the mRNA can be blocked by microRNAs, resulting in less protein produced.

PKD1 has a binding site for miR-17. This microRNA is highly expressed in ADPKD models and is active in these models. Dr. Patel and his coworkers wondered if blocking miR-17’s binding site of PKD1 might prevent kidney cyst formation.

Researchers deleted the miR-17 binding sites from PKD1 mRNAs in cell culture and an ADPKD mouse model. They found that the deletion of the binding site improved the stability of the mRNA, increased Polycystin-1 levels, and reduced kidney cyst growth. The group also found that blocking the miR-17 binding site of PKD1 mRNA by using an anti-miR-17 drug following cyst formation decreased cyst growth. This suggests that this interaction may be a promising target in polycystic kidney disease (PKD) treatment.

There are many genetic conditions where one of the copies of the causative genome is mutated, but the other copy remains normal. Dr. Patel indicated that this approach to harnessing a normal copy of the causative gene could be applied to many other diseases besides PKD.

251 thoughts on “Researchers uncover a gene therapy target for polycystic kidney disease”

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