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Researchers' Description Of The Regulation Of A New Family Of Ion Channels May Open Doors For Therapies For A Variety Of Conditions

Date:
June 20, 2001
Source:
University Of Washington
Summary:
Researchers have made an important scientific advance by describing the regulatory mechanisms for two members of a new family of ion channels found in non-excitable cells. Their discoveries may pave the way for novel treatments for a variety of conditions, including immune system diseases, blood disorders, liver and kidney failure, strokes, damage from aging, and insulin shock.

Researchers have made an important scientific advance by describing the regulatory mechanisms for two members of a new family of ion channels found in non-excitable cells. Their discoveries may pave the way for novel treatments for a variety of conditions, including immune system diseases, blood disorders, liver and kidney failure, strokes, damage from aging, and insulin shock. Their findings are published in two articles in last week's issue of the journal Nature.

Ion channels are tiny molecular pores in cells. These pores control the entry and exit of substances such as sodium, potassium and calcium into the body's cells.

In electrically excitable cells, such as those in the brain and the heart, ion channels help drive the electrical system that runs the body and generate electrical signals between cells.

At one time, scientists thought only nerve cells had ion channels. Later, ion channels were discovered in the pulsating cells of heart muscle. Now, scientists believe virtually every type of cell has ion channels.

Ion channels in the excitable cells of the brain, nerves and cardiovascular system have been extensively studied. These ion channels are the direct or indirect target of about one-third of all current medications. Malfunctions of these ion channels are at the root of epilepsy as well as heart arrhythmia and some other cardiovascular disorders.

In contrast, much less is known about the ion channels in non-excitable cells, such as blood cells, immune system cells, liver and kidney cells, and the cells lining the inside of blood vessels. The latest findings, appearing in this week's Nature articles, represent a significant advance in understanding how non-excitable cells regulate the inflow and outflow of sodium, calcium and related substances. Information on how these new types of ion channels function may lead to improved therapies for diseases of the blood, kidney, liver, arteries and immune system, as well as better ways to reduce cell damage from stroke, heart attacks, and aging.

The research team was led by Dr. Andrew M. Scharenberg, University of Washington (UW) assistant professor of pediatrics and adjunct assistant professor of immunology; Dr. Ann-Laure Perraud, UW senior fellow in pediatrics, and collaborators Dr. Reinhold Penner at the University of Hawaii, Dr. Maurice Bessman at Johns Hopkins University and Dr. Jean-Pierre Kinet at Harvard Medical School.

Their first paper describes a regulatory mechanism for an ion channel called LTRPC2. This regulatory mechanism involves a small molecule, ADP-ribose, produced by many processes in the body. Previously, ADP-ribose was considered to be a useless byproduct. However, new findings suggest that ADP-ribose is able to control the entry of sodium and calcium into cells that have LTRPC2 channels. This finding holds potential medical significance because ADP-ribose is created in large amounts by the same processes that produce free radicals and reactive oxygen species. Free radicals and reactive oxygen species have been implicated in the cell damage that occurs with aging, stroke, and heart attacks. In some cases this damage has been associated with mechanisms that allow excessive amounts of calcium to enter the cells. The researchers suggest that cells with LTRPC2 ion channels may be susceptible to such damage, and medications designed to block the LTRPC2 channels may help treat these and related conditions.

Their second paper describes the regulatory mechanisms for another ion channel, LTRPC7. This ion channel appears to be controlled by normal levels of the molecule ATP (adenosine triphosphate), the power source for all living cells. This finding suggests that the LTRPC7 ion channel will become more active in situations when the body's cells run low on ATP. This can happen, for example, when the cells are deprived of oxygen or sugar, both of which are necessary for ATP production.

During strokes and heart attacks, when blood flow is interrupted, the surrounding tissues lack oxygen. Lack of sugar to cells occurs dramatically when patients with diabetes receive too much insulin or oral medication. In all these cases --stroke, heart attack, and insulin shock -- tissues can be damaged. This tissue damage has been linked to excessive entry of calcium into cells. Because the LTRPC7 ion channel, which is present in all cells, tends to become more active when ATP levels fall, this ion channel could potentially be a direct mediator of excessive entry of calcium during oxygen or sugar deprivation. Medications designed to block the LTRPC7 ion channel might offer new forms of therapy to reduce tissue damage from stroke, heart attacks, and insulin shock.


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The above story is based on materials provided by University Of Washington. Note: Materials may be edited for content and length.


Cite This Page:

University Of Washington. "Researchers' Description Of The Regulation Of A New Family Of Ion Channels May Open Doors For Therapies For A Variety Of Conditions." ScienceDaily. ScienceDaily, 20 June 2001. <www.sciencedaily.com/releases/2001/06/010605072410.htm>.
University Of Washington. (2001, June 20). Researchers' Description Of The Regulation Of A New Family Of Ion Channels May Open Doors For Therapies For A Variety Of Conditions. ScienceDaily. Retrieved October 22, 2014 from www.sciencedaily.com/releases/2001/06/010605072410.htm
University Of Washington. "Researchers' Description Of The Regulation Of A New Family Of Ion Channels May Open Doors For Therapies For A Variety Of Conditions." ScienceDaily. www.sciencedaily.com/releases/2001/06/010605072410.htm (accessed October 22, 2014).

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