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Blocking signal-transmitting cellular pores may prevent damage to kidneys
Date:11/15/2013

ka's team to investigate its role in kidney filtration. They were surprised to find that, in addition to TRPC6 channels, TRPC5 channels were also present in podocytes and that their activity was more damaging to the kidney filter, even in the absence of any mutations.

The current article describes a series of experiments by which Greka's team first confirmed the presence of TRPC5 channels in rodent podocytes; they then showed that animals in which TRPC5 expression was knocked out did not experience the type of kidney damage typically caused by a bacterial toxin or by a chemical known to damage podocytes. More detailed studies revealed that those damaging agents cause TRPC5 channels to open in podocytes, admitting excess calcium which causes the cytoskeleton the cells' internal structural support system to collapse, breaking down the filter formed by podocytes.

The researchers went on to show that a recently identified TRPC5 inhibitor, called ML204 discovered in the lab of study co-author Craig Lindsley, PhD, of Vanderbilt University Medical Center blocked the inrush of calcium into podocytes, preventing cytoskeletal breakdown and the damage to the kidney's filtering function. This protective effect was seen not only in cells and tissues but also in living mice.

"Future work needs to focus on optimizing ML204 and other potential TRPC5 blockers to be more potent. But generally our intention is to fervently pursue TRPC5 inhibition as a possible new treatment for the kidney diseases affecting hundreds of millions of people worldwide," says Greka, who is an assistant professor of Medicine at Harvard Medical School.


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Contact: Mike Morrison
mdmorrison@partners.org
617-724-6425
Massachusetts General Hospital
Source:Eurekalert

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