Activation of telomerase and expression of human telomerase reverse transcriptase in coronary atherosclerosis

Liu, Shih-Chi; Wang, Shoei‐Shen; Wu, Mu-Zon; Wu, Deng-Chyang; Yu, Fang‐Jung; Chen, Wen‐Jone; Chiang, Fu-Tien; Yu, Meng-Fen

doi:10.1016/j.carpath.2005.05.006

Cited by 25 publications

(20 citation statements)

References 42 publications

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“…Recently, reactivation of telomerase activity was observed in vascular smooth muscle cells but not in areas of monocyte-macrophage infiltrations in human atherosclerotic coronary plaque from heart transplant recipients (27). Different mechanism of inflammation in transplanted hearts and in acute coronary syndrome might explain the different pattern of telomerase reactivation in our and in their study.…”

Section: Discussionmentioning

confidence: 82%

High Telomerase Activity in Neutrophils From Unstable Coronary Plaques

Narducci

Grasselli

Biasucci

et al. 2007

Journal of the American College of Cardiology

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Section: Discussionmentioning

confidence: 82%

High Telomerase Activity in Neutrophils From Unstable Coronary Plaques

Narducci

Grasselli

Biasucci

et al. 2007

Journal of the American College of Cardiology

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“…In response to hypoxia and during hypertension, telomerase is selectively activated in human and rat vascular smooth muscle cells, and its down-regulation suppresses their proliferative response (25,26). Telomerase activity is also induced in atherosclerotic coronary arteries, a finding correlated with the induction of TERT (27). Some inflammatory stimuli, including LPS and TNF-a, could activate telomerase and TERT expression, via NF-kB signaling in response to LPS in macrophages of human atherosclerotic lesions (28).…”

Section: Discussionmentioning

confidence: 87%

Telomerase and Telomere Length in Pulmonary Fibrosis

Liu

Ullenbruch

Choi

et al. 2013

Am J Respir Cell Mol Biol

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In addition to its expression in stem cells and many cancers, telomerase activity is transiently induced in murine bleomycin (BLM)-induced pulmonary fibrosis with increased levels of telomerase transcriptase (TERT) expression, which is essential for fibrosis. To extend these observations to human chronic fibrotic lung disease, we investigated the expression of telomerase activity in lung fibroblasts from patients with interstitial lung diseases (ILDs), including idiopathic pulmonary fibrosis (IPF). The results showed that telomerase activity was induced in more than 66% of IPF lung fibroblast samples, in comparison with less than 29% from control samples, some of which were obtained from lung cancer resections. Less than 4% of the human IPF lung fibroblast samples exhibited shortened telomeres, whereas less than 6% of peripheral blood leukocyte samples from patients with IPF or hypersensitivity pneumonitis demonstrated shortened telomeres. Moreover, shortened telomeres in lategeneration telomerase RNA component knockout mice did not exert a significant effect on BLM-induced pulmonary fibrosis. In contrast, TERT knockout mice exhibited deficient fibrosis that was independent of telomere length. Finally, TERT expression was up-regulated by a histone deacetylase inhibitor, while the induction of TERT in lung fibroblasts was associated with the binding of acetylated histone H3K9 to the TERT promoter region. These findings indicate that significant telomerase induction was evident in fibroblasts from fibrotic murine lungs and a majority of IPF lung samples, whereas telomere shortening was not a common finding in the human blood and lung fibroblast samples. Notably, the animal studies indicated that the pathogenesis of pulmonary fibrosis was independent of telomere length.

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“…While a link between age and hTERT activity has not previously been tested in human arteries, a few studies have shown age-related declines in hTERT activity in human WBCs (27,42). Interestingly, Liu et al (35) found greater hTERT expression and activity in atherosclerotic arteries compared with nonatherosclerotic controls, and a recent study by Kroenke et al (31) has associated increased WBC hTERT activity with greater CVD risk. We reported no difference in active hTERT with advancing age in human arteries.…”

Section: Discussionmentioning

confidence: 99%