genetic mechanism helps explain CP

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Genetic Mechanism Helps Explain Chronic Pain Disorders

*Science Daily <http://www.sciencedaily.com/> —* Researchers at the

University of North Carolina at Chapel Hill have discovered that commonly

occurring variations of a gene trigger a domino effect in chronic pain

disorders. The finding might lead to more effective treatments for

temporomandibular joint disorder (TMJD) and other chronic pain conditions.

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Catechol-O-methyltransferase (COMT), an enzyme that metabolizes

neurotransmitters such as epinephrine, norepinephrine and dopamine and that

has been implicated in the modulation of persistent pain, as well as

cognition and mood, is regulated by a gene, also called COMT. Previous

UNC-led research showed that common genetic variants of this gene are

associated with increased pain sensitivity and the likelihood of developing

TMJD.

Now, the researchers have discovered that specific variants of the COMT gene

can dramatically affect the secondary structure of corresponding messenger

RNA - which, in turn, leads to alterations in the amount of enzyme crucial

for regulating pain processing. The discovery is published in the Dec. 22

issue of Science.

" TMJD is a complex pain condition that is frequently associated with other

pain conditions such as fibromyalgia syndrome, chronic headaches and

irritable bowel syndrome, " said Dr. Maixner, director of the Center

for Neurosensory Disorders in UNC's School of Dentistry and a study

co-author.

" This study has identified a new genetic mechanism that influences an

individual's susceptibility to develop chronic pain conditions such as

TMJD, " Maixner said.

The study was conducted to understand the mechanism by which the identified

genetic variants influence enzymatic activity and, ultimately, biological

functions such as pain transmission. The researchers found that three major

variants of COMT show significant differences in how they code for the

secondary structure of messenger RNA, or mRNA. The differences lead to

dramatic alterations in protein expression, which substantially influences

pain sensitivity in humans.

These findings are clinically important because pain conditions resulting

from low COMT activity or elevated catecholamine levels are likely to be

susceptible to treatment with pharmacological agents that block beta 2- and

beta 3-adrenergic receptors, which mediate COMT-dependent pain signaling, or

that control mRNA secondary structure.

" Elucidating the genetic mechanisms that mediate pain perception will

provide new insights into how chronic pain develops and will ultimately

contribute to the identification of unique markers for diagnosing clinical

pain conditions, as well as provide novel targets for the development of

effective individualized therapeutics for TMJD and related conditions, " said

Dr. Nackley Neely, a research assistant professor in the Center for

Neurosensory Disorders and the study's lead author.

" These data have broad medical and evolutionary implications regarding the

analysis of variants common in the human population, " Nackley Neely said.

" It is believed that variants leading to altered protein structure have the

strongest impact on gene function. However, this study demonstrates that

combinations of common genetic variants that influence mRNA secondary

structure may have even stronger effects and, thus, represent another key

factor responsible for disease onset and progression. "

" This study provides additional evidence of a genetic, molecular and

physiological basis for pain perception and human pain conditions and should

help to remove the stigma associated with conditions such as TMJD and

fibromyalgia, " said Dr. Luda Diatchenko, an associate professor in the

center and the study's chief investigator.

Other researchers were Dr. Inna Tchivileva, a postdoctoral research

associate within the Center for Neurosensory Disorders; Satterfield,

a former research assistant within the center; Dr. Olex Korchynskyi, a

former postdoctoral research associate within the UNC-Chapel Hill School of

Medicine's Thurston Arthritis Research Center; Dr. Sergei S. Makarov, a

former associate professor at the Center for Neurosensory Disorders and the

Thurston center and now president and chief executive officer of Attagene

Inc.; and Dr. Svetlana A. Shabalina, a staff scientist with the National

Center for Biotechnology Information.

Funding was provided by the National Institute of Dental and Craniofacial

Research, National Institute of Child Health and Human Development and

National Institute of Neurological Disorders and Stroke, all components of

the National Institutes of Health. Additional support came from the

Intramural Research Program of the National Center for Biotechnology

Information.

Other Center for Neurosensory Disorders research initiatives are currently

under way that further explore the genetic basis of pain: One seven-study, a

$19-million National Institute of Dental and Craniofacial Research-funded

agreement involving multiple institutions and based at the center, will

follow 3,200 health individuals and 200 who have facial pain. Titled OPPERA

(Orofacial Pain: Prospective Evaluation and Risk Assessment), the study is

designed to identify both environmental and genetic factors that increase an

individual's susceptibility to TMJD and other chronic pain conditions.

*Note: This story has been adapted from a news release issued by University

of North Carolina at Chapel Hill*

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