Prevalence of Telomerase in Coronary Artery Atherosclerosis

Summary: Telomerase detected in atherosclerotic plaque tissue, likely to be related to restenosis.

Interestingness: 3

Paper by Madhu Gupta, Marie R Shogreen, Gregory A Braden, Wain L White and David C Sane in the Journal of Anti-Aging Medicine, Volume 3, Issue 1, Spring 2000.


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They measured the presence of telomerase in the bits cut out of 23 people that had directional coronary atherectomy (DCA). The bits cut out are blockages of the coronary artery and the DCA cuts it out. They correlated the tissues in which they detected telomerase with those that had restenosis, which is when the blockage/narrowing of the artery reappears.

They detected telomerase in 8 out of the 23 total, in 5 out of the 7 people who later developed restenosis, and on 2 out of the 10 who didn't (p < 0.05). Results were inconclusive for restenosis in the other 6. There was no correlation between what the people had come in for and the presence of telomerase.

They mention that atherosclerotic plaques have a monoclonal population of smooth muscle cells, but I don't know what other type you could have inside one person. They offer three explanations for the 35% detection rate of telomerase, that is, how come it's not 100%:

• that the tissue is maintaining its telomeres by means other than telomeres
• that the tissue is senescent or closer to senescence, with some evidence coming from studies on replicative capacity of muscle cells from plaque-derived tissue compared to healthy arteries. The presence of telomerase would probably be induced by cells having replicated beyond the normal senescent stage by a viral infection or broken tumor-suppressors, and that this would activate telomerase. These cells would then be better able to cause restenosis. I have no idea how much reality there is to that idea of telomerase reactivation.
• that there was no telomerase in the smooth-muscle cells at all, and instead the telomerase was detected from other cells in the tissue cut out. This could be from vascular stem cells, or from non-related cells like endothelial cells, lymphocytes or macrophages.

They also mention that the telomerase could be driving the hyperplasia not by replication but by stopping apoptosis.

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Abstract follows:

Telomerase is an essential enzyme for maintaining the telomeres of chromosomes and thereby enhancing the sustained replication of cells. Because atherosclerosis and restenosis are characterized by cellular proliferation, we determined whether telomerase enzyme activity was present in coronary artery tissue from 23 patients undergoing directional coronary atherectomy. Telomerase activity was determined from detergent lysates of the atherectomy tissue using an enzyme-linked immunoadsorbent assay (ELISA)-based modification of the Telomere Repeat Amplification Protocol. The presence of telomerase activity was correlated with the occurrence of coronary artery restenosis. Eight of the 23 samples (35%) were positive for telomerase. Seventeen of the 23 patients had adequate clinical follow-up to judge restenosis status. Of these, 7 had restenosis and 5 of these 7 had detectable telomerase. Of the 10 patients without restenosis, 8 were telomerase negative (p <= 0.05). We have shown, for the first time, that telomerase is found in 35% of atherosclerotic tissues. There was a strong trend toward an association between telomerase presence and restenosis in patients for whom follow-up data were available. The presence of telomerase in atherosclerotic tissue may enable a robust, sustained cellular proliferation in response to vascular injury that culminates in restenosis.