Shorter Leukocyte Telomere Length coupled with lower expression of Telomerase Genes in patients with Essential Hypertension

Cheng, Guanghui; Wang, Lina; Dai, Mingkai; Fang, Wei; Xu, Dawei

doi:10.7150/ijms.48456

Cited by 9 publications

(10 citation statements)

References 43 publications

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“…The analysis of this lncRNA on 3 samples of PBMCs via RNA-Flow demonstrated the detection of this RNA was possible in cells derived from blood samples (Fig. 2d ) as previously shown via RT-qPCR 18 , 19 . Quantification in 3 biological samples in PBMCs showed positive cells with average fluorescence intensity of 146 ± 3.2 MFI when compared to control cells with an average mean of 45.7 ± 2.4 MFI.…”

Section: Resultssupporting

confidence: 73%

Quantifying telomeric lncRNAs using PNA-labelled RNA-Flow FISH (RNA-Flow)

Gonzalez-Vasconcellos

Cobos-Fernández

Atkinson

et al. 2022

Commun Biol

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Here we present a method to detect and quantify long non-coding RNAs, in particular those related to telomeres. By coupling the specificity of a peptide nucleic acid (PNA) probe with flow cytometry we have quantified cellular levels of TERRA and TERC lncRNAs in culture cell lines and PBMCs. This easy-to-use method appointed RNA-Flow allows reliable lncRNA quantification with broad applications in basic research and clinical diagnostics. In addition, the staining protocol presented here was proven useful for the detection and quantification of such lncRNAs on unfixed cells using confocal microscopy.

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Section: Resultssupporting

confidence: 73%

Quantifying telomeric lncRNAs using PNA-labelled RNA-Flow FISH (RNA-Flow)

Gonzalez-Vasconcellos

Cobos-Fernández

Atkinson

et al. 2022

Commun Biol

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“…For instance, some previous studies suggested that there was no association between TL and blood pressure (38)(39)(40). A previous meta-analysis of 10 studies indicated a significant negative correlation between TL and hypertension (41), which was also observed in recent studies (42)(43)(44)(45). However, it has also been reported that longer TL is associated with higher blood pressure (46,47).…”

Section: Discussionmentioning

confidence: 62%

Telomere length and the risk of cardiovascular diseases: A Mendelian randomization study

Deng

Li²,

Zhou³

et al. 2022

Front. Cardiovasc. Med.

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BackgroundThe causal direction and magnitude of the associations between telomere length (TL) and cardiovascular diseases (CVDs) remain uncertain due to susceptibility of reverse causation and confounding. This study aimed to investigate the associations between TL and CVDs using Mendelian randomization (MR).Materials and methodsIn this two-sample MR study, we identified 154 independent TL-associated genetic variants from a genome-wide association study (GWAS) consisting of 472,174 individuals (aged 40–69) in the UK Biobank. Summary level data of CVDs were obtained from different GWASs datasets. Methods of inverse variance weighted (IVW), Mendelian Randomization-Egger (MR-Egger), Mendelian Randomization robust adjusted profile score (MR-RAPS), maximum likelihood estimation, weighted mode, penalized weighted mode methods, and Mendelian randomization pleiotropy residual sum and outlier test (MR-PRESSO) were conducted to investigate the associations between TL and CVDs.ResultsOur findings indicated that longer TL was significantly associated with decreased risk of coronary atherosclerosis [odds ratio (OR), 0.85; 95% confidence interval (CI), 0.75–0.95; P = 4.36E-03], myocardial infarction (OR, 0.72; 95% CI, 0.63–0.83; P = 2.31E-06), ischemic heart disease (OR, 0.87; 95% CI, 0.78–0.97; P = 1.01E-02), stroke (OR, 0.87; 95% CI, 0.79–0.95; P = 1.60E-03), but an increased risk of hypertension (OR, 1.12; 95% CI, 1.02–1.23; P = 2.00E-02). However, there was no significant association between TL and heart failure (OR, 0.94; 95% CI, 0.87–1.01; P = 1.10E-01), atrial fibrillation (OR, 1.01; 95% CI, 0.93–1.11; P = 7.50E-01), or cardiac death (OR, 0.95; 95% CI, 0.82–1.10; P = 4.80E-01). Both raw and outlier corrected estimates from MR-PRESSO were consistent with those of IVW results. The sensitivity analyses showed no evidence of pleiotropy (MR-Egger intercept, P > 0.05), while Cochran’s Q test and MR-Egger suggested different degrees of heterogeneity.ConclusionOur MR study suggested that longer telomeres were associated with decreased risk of several CVDs, including coronary atherosclerosis, myocardial infarction, ischemic heart disease, and stroke, as well as an increased risk of hypertension. Future studies are still warranted to validate the results and investigate the mechanisms underlying these associations.

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“…We showed that BPH prostate tissue had the longest telomeres, which might explain why apoptosis and cell death are not initiated. Hyperplasia is caused when cell count increases in the organ, which should cause shorter telomeres in BPH (as cells divide more frequently) as in the literature described (Cheng et al, 2020;Sommerfeld et al, 1996). However, in our and another study, BPH had the longest telomeres compared with normal or cancerous tissue (Heaphy et al, 2010).…”

Section: Discussionmentioning

confidence: 98%

Changes in TP53 gene, telomere length, mitochondrial DNA, and its amount in benign prostatic hyperplasia patients

Zole,

Baumanis,

Freimane

et al. 2024

Preprint

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Benign prostatic hyperplasia (BPH) is a growing issue due to an ageing population; however, there are not enough studies connecting it with ageing hallmarks. Some of the ageing hallmarks are changes in telomere length (TL) and genetic changes like possible mutations in the TP53 gene or mitochondrial genome (mtDNA). Our study investigated these factors to see if they could be linked with BPH. Prostate tissue samples were obtained from 32 patients with BPH (and 30 blood samples). As a healthy control group, age-matching blood DNA samples were used. For mtDNA sequence data comparison, 50 samples of a general Latvian population were used. The full mtDNA genome was sequenced using Next Generation Sequencing (NGS), for TP53 gene - Sanger sequencing, and for mtDNA amount and telomere length - qPCR assay. BPH patients in prostate tissue had much higher TL than in blood cells, and the healthy controls had the shortest telomeres. Also, the mtDNA amount in BPH prostate tissue was the highest compared with blood, and controls had the smallest amount. In the TP53 gene, we did not find any mutations that could be linked to BPH. In the mtDNA genome, we found several unique mutations and heteroplasmic changes, as well as changes that have been linked before with prostate cancer (PC). In conclusion, prolonged telomeres and changes in mtDNA amount might be involved in the development of BPH. Concerning mtDNA genome changes, some of the heteroplasmic or homoplasmic variants might contribute to the development of BPH. More studies should be conducted to prove or disapprove of these connections.

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Shorter Leukocyte Telomere Length coupled with lower expression of Telomerase Genes in patients with Essential Hypertension

Cited by 9 publications

References 43 publications

Quantifying telomeric lncRNAs using PNA-labelled RNA-Flow FISH (RNA-Flow)

Quantifying telomeric lncRNAs using PNA-labelled RNA-Flow FISH (RNA-Flow)

Telomere length and the risk of cardiovascular diseases: A Mendelian randomization study

Changes in TP53 gene, telomere length, mitochondrial DNA, and its amount in benign prostatic hyperplasia patients

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