Periodontitis and heart disease: Researchers connect the molecular dots

September 11, 2015, American Society for Microbiology
Confocal fluorosence microscopy: human aortic smooth muscle cells infected with P. gingivalis

Periodontitis is a risk factor for heart disease. Now a team of researchers has shown that a periodontal pathogen causes changes in gene expression that boost inflammation and atherosclerosis in aortic smooth muscle cells. The research is published ahead of print in Infection and Immunity, a journal of the American Society for Microbiology.

The circumstantial evidence that led to this study was ample. The periodontal pathogen, Porphyromonas gingivalis, has also been found in coronary artery plaques of . And in two species of animal models, P. gingivalis has been shown to cause and accelerate formation of coronary and aortic atherosclerosis. The investigators, led by Torbjörn Bengtsson of the Department of Clinical Medicine, School of Health Sciences, Örebro University, Örebro, Sweden, showed how this happens.

They began by culturing human aortic , and infecting them with P. gingivalis. They found that gingipains, virulence factors produced by P. gingivalis, boost expression of the pro-inflammatory angiopoietin 2, while dampening expression of the anti-inflammatory angiopoietin 1 in the smooth muscle cells, with the net effect of increasing inflammation. Inflammation is strongly implicated in atherosclerosis.

"Although unstimulated [aortic smooth muscle cells] produce angiopoietin 2 at a low level, stimulation with wild-type P. gingivalis dramatically increases the of angiopoietin 2 in [aortic smooth muscle cells]," the investigators wrote.

"Angiopoietin 2 directly increases the migration of aortic smooth muscle cells," said first author Boxi Zhang, a PhD student in Bengtsson's laboratory. "The migration of smooth muscle cells is involved in the pathogenesis of atherosclerosis."

As with ginginpains, (TNF), a human-produced inflammatory cytokine and cardiovascular risk factor, also induces and promotes atherosclerosis via the two angiopoietins. However, their research showed that ginginpains operate independently from TNF, said Bengtsson.

"Our research clarifies the mechanism behind the association of periodontitis and cardiovascular disease," said Zhang. "Our aim is to find biomarkers that can help us diagnose and treat both diseases."

Explore further: Linking vascular inflammation to obesity and atherosclerosis

More information: The full study can be read online here.

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JVK
1 / 5 (1) Sep 11, 2015
They found that gingipains, virulence factors produced by P. gingivalis, boost expression of the pro-inflammatory angiopoietin 2, while dampening expression of the anti-inflammatory angiopoietin 1 in the smooth muscle cells, with the net effect of increasing inflammation. Inflammation is strongly implicated in atherosclerosis.


Differences between nutrient-dependent microRNAs and viral microRNAs are the most obvious biomarkers of atherosclerosis and all other pathologies, aren't they?

How else could cell type differentiation be biophysically constrained if not via nutrient-dependent RNA-mediated gene duplication and RNA-mediated amino acid substitutions that determine cell type differences in all cells of all individuals of all species?

How else could microbes be linked from self / non-self recognition to all extant biodiversity if not via metabolic networks and genetic networks?
JVK
1 / 5 (1) Sep 11, 2015
See also: Polymicrobial Infection with Periodontal Pathogens Specifically Enhances MicroRNA miR-146a in ApoE−/− Mice during Experimental Periodontal Disease▿

http://www.ncbi.n...3067556/

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