We have identified a discrete, focal telomere DNA expansion phenotype in the photoreceptor cell layer of normal, non-neoplastic human retinas. This phenotype is similar to that observed in a subset of human cancers, including a large fraction of tumors of the central nervous system, which maintain their telomeres via the non-telomerase-mediated alternative lengthening of telomeres (ALT) mechanism. We observed that these large, ultra-bright telomere DNA foci are restricted to the rod photoreceptors and are not observed in other cell types. Additionally, focus-positive rod cells are dispersed homogeneously throughout the posterior retinal photoreceptor cell layer and appear to be human-specific. We examined 108 normal human retinas obtained at autopsy from a wide range of ages. These large, ultra-bright telomere DNA foci were not observed in infants before 6 months of age; however, the prevalence of focus-positive rod cells dramatically increased throughout life. To investigate associations between this phenotype and retinal pathology, we assessed adult glaucoma (N = 29) and diabetic retinopathy (N = 38) cases. Focus-positive rod cells were prominent in these diseases. When compared to the normal group, after adjusting for age, logistic regression modeling revealed significantly increased odds of falling in the high category of focus-positive rod cells for glaucoma and diabetic retinopathy. In summary, we have identified a dramatic telomere alteration associated with aging and diseases affecting the retina.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8028494PMC
http://dx.doi.org/10.1111/bpa.12618DOI Listing

Publication Analysis

Top Keywords

telomere dna
16
focus-positive rod
16
rod cells
16
dna expansion
8
expansion phenotype
8
rod photoreceptors
8
associated aging
8
photoreceptor cell
8
cell layer
8
human retinas
8

Similar Publications

IGF2BPs-regulated TIN2 confers the malignant biological behaviors of gastric cancer cells.

Tissue Cell

December 2024

Department of Pathology, The Fourth Hospital of Changsha, Changsha, Hunan 410006, PR China. Electronic address:

Background: Telomere maintenance is an important feature of tumor cells. Telomeric-repeat binding factor 1 interaction nuclear protein 2 (TIN2), a key member of the shelterin proteins, functions in regulating telomere structure, length and function. Our work sought to investigate the role of TIN2 in controlling gastric cancer (GC) malignant biological behaviors.

View Article and Find Full Text PDF

The shelterin complex protects chromosome ends from the DNA damage repair machinery and regulates telomerase access to telomeres. Shelterin is composed of six proteins (TRF1, TRF2, TIN2, TPP1, POT1 and RAP1) that can assemble into various subcomplexes . However, the stoichiometry of the shelterin complex and its dynamic association with telomeres in cells is poorly defined.

View Article and Find Full Text PDF

Transcriptional coupling of telomeric retrotransposons with the cell cycle.

Sci Adv

January 2025

Department of Biochemistry and Molecular Biology, Tulane University School of Medicine, Louisiana Cancer Research Center, 1700 Tulane Avenue, New Orleans, LA 70112, USA.

Unlike most species that use telomerase for telomere maintenance, many dipterans, including , rely on three telomere-specific retrotransposons (TRs)-, , and -to form tandem repeats at chromosome ends. Although TR transcription is crucial in their life cycle, its regulation remains poorly understood. This study identifies the Mediator complex, E2F1-Dp, and Scalloped/dTEAD as key regulators of TR transcription.

View Article and Find Full Text PDF

Current temporal studies of DNA replication are either low-resolution or require complex cell synchronisation and/or sorting procedures. Here we introduce Nanotiming, a single-molecule, nanopore sequencing-based method producing high-resolution, telomere-to-telomere replication timing (RT) profiles of eukaryotic genomes by interrogating changes in intracellular dTTP concentration during S phase through competition with its analogue bromodeoxyuridine triphosphate (BrdUTP) for incorporation into replicating DNA. This solely demands the labelling of asynchronously growing cells with an innocuous dose of BrdU during one doubling time followed by BrdU quantification along nanopore reads.

View Article and Find Full Text PDF

[Peptide regulation of cellular aging.].

Adv Gerontol

January 2025

Saint-Petersburg Institute of Bioregulation and Gerontology, 3 Dinamo av., St. Petersburg 197110, Russian Federation, e-mail:

Cellular aging is the inability of structures to proliferate (further division) and repair damage while maintaining metabolic activity. The key well-known factors of cellular aging are the processes of DNA damage, telomere shortening, the development of oxidative stress and epigenetic changes. The above factors provoke the development of a pro-inflammatory environment, leading to errors in gene expression and metabolic dysregulation, thereby affecting the development of age-related diseases that contribute to pathological changes in the functions of tissues and organs.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!