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A study published online in the journal Proceedings of the National Academy of Sciences suggests that a gene called Hu antigen R (HuR) plays a critical role in inducing and mediating an inflammatory response in cells experiencing mechanical and chemical stresses. The study was supported by the National Institutes of Health.

The findings may open up new possibilities for developing treatments of metabolic diseases associated with inflammation, such as atherosclerosis. Atherosclerosis typically occurs in branched or curved regions of arteries where plaques form because of cholesterol build-up. Inflammation can alter the structure of plaques so that they become more likely to rupture, causing a blood vessel blockage and leading to heart attack or stroke.

“This is the first systematic study showing that HuR not only responds to external stimuli as a stress-sensitive gene, but it also regulates other stress-sensitive genes,” said senior author Gang Bao, the Robert A. Milton Chair in Biomedical Engineering in the Wallace H. Coulter Department of Biomedical Engineering at Georgia Tech and Emory University.

The study results show that HuR promotes the expression of genes that support atherosclerosis and inhibits the expression of genes that combat atherosclerosis.

“We found that suppressing expression of HuR inhibited the inflammatory response of cells, which shows that designing drugs that block HuR function may reduce the risk of plaques rupturing,” explained Bao.

Bao guided Won Jong Rhee, a former postdoctoral fellow in his laboratory, to conduct a series of experiments investigating the biology, behavior and pathways of HuR.

The researchers first studied how the HuR gene responds to different flow environments and chemical treatments. They exposed human umbilical vein endothelial cells to disturbed flow — which occurs in artery regions where plaques form — and found that the cells expressed higher levels of HuR than when they experienced a static or laminar flow environment. This finding was validated in tissue experiments with results showing increased amounts of HuR in regions of a mouse aorta that were exposed to disturbed flow.

Then the researchers treated endothelial cells with statins, medications used to treat atherosclerosis by reducing the number of cholesterol-containing low-density lipoprotein (LDL) molecules in the blood and inhibiting inflammation. The results indicated a decreased level of HuR with statin treatment.

After establishing HuR as a stress-sensitive gene regulated by external stimuli, including flow and statin treatment, the researchers conducted experiments to determine whether HuR regulates the expression of other stress-sensitive genes. They found that reducing the level of HuR in cells increased the levels of two genes that combat atherosclerosis — Kruppel-like factor 2 (Klf2) and endothelial nitric oxide synthase (eNOS). The reduction in HuR also decreased the expression of bone morphogenic protein-4 (BMP-4), a gene that supports atherosclerosis.

Reducing the level of HuR in cells also significantly inhibited many inflammatory responses of the endothelial cells, including the expression of two potential atherosclerosis drug targets: inter-cellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1).

Though this study showed that HuR plays a critical role in inducing and mediating an inflammatory response in cells subjected to a stressful environment, the underlying mechanism for this regulation is still not known.

“HuR protein often binds to messenger RNAs to increase their stability and translation, but we found that regulation of other stress-sensitive genes by HuR was not due to changes in mRNA stability by direct protein binding,” explained Bao.

To uncover the pathways that lead to HuR's stress sensitivity, the researchers conducted a series of studies to reveal that HuR functions by adding a phosphate group to the transcriptional factor nuclear factor kappa B (NFkB) and its inhibitor IkBa. Additional research is underway to reveal what mRNAs HuR binds to and the mechanisms used to respond to mechanical and chemical stresses. Identifying the triggers for inflammation and unraveling the details of inflammatory pathways may eventually furnish new therapeutic targets.

Hanjoong Jo, the Coulter Department's Ada Lee and Pete Correll Professor in Biomedical Engineering, Kyunghwa Chang, graduate student Chih-Wen Ni and research scientist Zhilan Zheng also contributed to this research.

This project is supported by the National Institutes of Health (NIH) (Award Nos. HL80711, CA119338 and HL70531). The content is solely the responsibility of the principal investigator and does not necessarily represent the official view of the NIH.

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More than likely, if you have ever taken niacin before, you have already been introduced to its side effects: the redness, the hot flashes, the stomach ache, and, of course, the flushing. The side effects can be pretty nasty, and some cases, some people may surrender taking niacin in favor of something else to lower their cholesterol. The good news is that the side effects don't last forever. However, what can you do in the meantime to reduce those bothersome side effects? This article may be able to provide the relief you are looking for.

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A study published this week in the Journal of the American Medical Association suggests that heart attack patients who have no health insurance, or who have health insurance but also have financial concerns, significantly delay going to the hospital for treatment. Since time is of the essence when you are having a heart attack, this delay greatly increases the risk of sustaining permanent cardiac damage, or worse.

The investigators studied records from 3721 patients admitted to 25 American hospitals for heart attacks between 2005 and 2008. Of these patients, 738 were uninsured, and 689 had insurance but also had financial worries. The researchers found that patients without health insurance or who had financial worries were significantly more likely, compared to insured patients who reported no financial worries, to delay their arrival at the hospital by six hours or more.

The key to surviving a heart attack without sustaining permanent heart damage is immediate medical care. If the blocked coronary artery which is causing the heart attack can be re-opened (by angioplasty or by clot-busting drugs) within a few hours, most of the permanent cardiac damage can be avoided. The earlier you get treatment, the better. However, if therapy is delayed for six hours or more, significant and permanent cardiac damage becomes much more likely.

Too many patients who are suffering an acute heart attack already delay getting themselves to a hospital, due to wishful thinking or denial – hoping their acute symptoms are from “something I ate,” or just hoping the symptoms will go away. It is now apparent that people who have financial concerns are even more likely to critically delay receiving vital treatment.

If you think you might be having a heart attack, please do not let wishful thinking – or financial concerns – prevent you from taking the action you need to take to save your heart, and prevent permanent disability or death. If you experience any symptoms suggestive of heart attack, especially if you know you have risk factors for heart disease, you should get medical help as soon as possible. Generally, this is best done by calling 911.

And especially if you have those risk factors, it is important that you know how to tell if you might be having a heart attack.

Sources:

Smolderen KG, Spertus JA, Nallamothu BK, et al. Health Care Insurance, Financial Concerns in Accessing Care, and Delays to Hospital Presentation in Acute Myocardial Infarction. JAMA. 2010;303(14):1392-1400.

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For people at extremely high risk of psychosis, taking fish oil supplements may help cut the odds of developing psychotic disorders. That's the finding of a new study that focused on 81 individuals at “ultra-high risk” for psychosis (defined as a loss of contact with reality). All participants had mild psychotic symptoms, transient psychosis, or a family history of psychotic disorders, in addition to a decrease in functioning.

For 12 weeks, 41 of the study members took daily fish oil supplements containing 1.2 grams of omega-3 fatty acids, while the other 41 participants took a placebo. By the end of the study, two percent of those taking fish oil supplements had transitioned to a psychotic disorder, compared to 27.5 percent in the placebo group. The supplements also appeared to significantly reduce symptoms and improve functioning.

It's possible that omega-3 fatty acids could have a positive effect on chemical signaling in the brain, according to the study's authors. Although it's too soon to recommend the use of fish oil supplements to reduce psychosis risk, the authors note that intervention with at-risk individuals has “the potential to prevent full-blown psychotic disorders.”