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Liver CRP production linked to atherosclerosis
September 29, 2005Tsukuba, Japan -New research shows that levels of C-reactive protein (CRP), produced by the liver and not at the lesion site, correlate with the degree of atherosclerosis. The paper by Sun et al., "C-reactive protein in atherosclerotic lesions: its origin and pathophysiological significance," appears in the October issue of The American Journal of Pathology and is accompanied by a commentary.
C-reactive protein (CRP) is a hallmark of inflammation and tissue damage, as in arthritis or infection. It is also widely touted as a marker for cardiovascular disease, with doctors using patient CRP levels to improve risk assessment. However, whether CRP is merely a risk marker or is actually a contributing factor of cardiovascular disease has remained controversial.
To address these issues, Dr. Jianglin Fan's group examined the role of CRP in two rabbit models of atherosclerosis: high cholesterol diet or LDL receptor deficiency. Rabbits represent highly suitable models as they quickly form atherosclerotic plaques in response to high serum cholesterol, and rabbit CRP shares 70% homology with human CRP.
As expected, hypercholesterolemic rabbits developed atherosclerotic plaques. Upon further examination, serum CRP levels were found to positively correlate with plaque size. CRP was found in plaques of various stages, including early and advanced lesions, but it did not appear to associate with macrophages, as had been suggested. Similar results were seen in human aortic lesions.
To determine where CRP protein was being produced, CRP mRNA levels were measured by Northern blot and real-time RT-PCR. CRP mRNA was only detected in liver obtained from atherosclerotic rabbits but was undetectable in vascular cells or macrophages. Again, results were confirmed in human specimens: insignificant mRNA levels found in atherosclerotic aorta compared to high levels in liver. Finally, in vitro analysis revealed that hepatocytes, but not macrophages, expressed CRP mRNA following stimulation by inflammatory molecules.
These data highlight a powerful role for the liver in generating the CRP that is associated with atherosclerotic lesions. Nonetheless, we are still left wondering whether CRP is a cause, result, or both of heart disease, as presence at the scene of a crime is not necessarily evidence of guilt. Thus, CRP could be an innocent bystander, a victim, or possibly an atheroprotective force. Sun and colleagues acknowledge that "further studies will be required to clarify whether decreasing CRP alone without changing the plasma cholesterol level can be beneficial for the treatment of atherosclerosis."
This study uncovers new approaches for the treatment of atherosclerosis. In the future, Dr. Fan hopes to "test whether any therapeutic inhibition of CRP levels can be beneficial for [coronary heart disease] patients or preventive from coronary artery syndrome or plaque rupture. Importantly, we will target the liver rather than the vascular wall (such as macrophages) for the inhibition of CRP."
American Journal of Pathology
As expected, hypercholesterolemic rabbits developed atherosclerotic plaques. Upon further examination, serum CRP levels were found to positively correlate with plaque size. CRP was found in plaques of various stages, including early and advanced lesions, but it did not appear to associate with macrophages, as had been suggested. Similar results were seen in human aortic lesions.
To determine where CRP protein was being produced, CRP mRNA levels were measured by Northern blot and real-time RT-PCR. CRP mRNA was only detected in liver obtained from atherosclerotic rabbits but was undetectable in vascular cells or macrophages. Again, results were confirmed in human specimens: insignificant mRNA levels found in atherosclerotic aorta compared to high levels in liver. Finally, in vitro analysis revealed that hepatocytes, but not macrophages, expressed CRP mRNA following stimulation by inflammatory molecules.
These data highlight a powerful role for the liver in generating the CRP that is associated with atherosclerotic lesions. Nonetheless, we are still left wondering whether CRP is a cause, result, or both of heart disease, as presence at the scene of a crime is not necessarily evidence of guilt. Thus, CRP could be an innocent bystander, a victim, or possibly an atheroprotective force. Sun and colleagues acknowledge that "further studies will be required to clarify whether decreasing CRP alone without changing the plasma cholesterol level can be beneficial for the treatment of atherosclerosis."
This study uncovers new approaches for the treatment of atherosclerosis. In the future, Dr. Fan hopes to "test whether any therapeutic inhibition of CRP levels can be beneficial for [coronary heart disease] patients or preventive from coronary artery syndrome or plaque rupture. Importantly, we will target the liver rather than the vascular wall (such as macrophages) for the inhibition of CRP."
American Journal of Pathology
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Healthy neighborhoods may be associated with lower diabetes risk
Individuals living in neighborhoods conducive to physical activity and providing access to healthy foods may have a lower risk of developing type 2 diabetes in a five-year period, according to a report in the October 12 issue of Archives of Internal Medicine, one of the JAMA/Archives journals.
Liver cells grown from patients' skin cells
Scientists at The Medical College of Wisconsin in Milwaukee have successfully produced liver cells from patients' skin cells opening the possibility of treating a wide range of diseases that affect liver function.
National report shines light on lupus 50-year treatment drought
Today, The Lewin Group, a national health care consulting firm, issued recommendations on ways to overcome the barriers that have obstructed lupus drug development resulting in no new drug approval for this disease in more than 50 years - since the Eisenhower Administration.
Calcium scans may be effective screening tool for heart disease
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