Abstract
Functional long non-coding RNAs (lncRNAs) have been in the limelight in aging research because short telomeres are associated with higher levels of TERRA (Telomeric Repeat containing RNA). The genomic instability, which leads to short telomeres, is a mechanism observed in cell aging and in a class of cancer cells. Psoriasis, a skin disease, is a disorder of epidermal keratinocytes, with altered telomerase activity. Research on the fraction of nascent RNAs in hybrid with DNA offers avenues for new strategies. Skin and blood samples from patients were fractionated to obtain the RNA associated with DNA as a R-loop structure. The higher amount of TERRA levels attached with each chromosome end was found with psoriasis patients in blood and skin. In addition to telomeric TERRA, we evidenced accumulation of others non-coding RNA, such as non-telomeric TERRA and centromeric transcripts. Increased levels of non-coding RNAs attached to DNA correlates with a decreased in Ribonuclease HII (RNase-HII) transcript which means that overall unresolved DNA–RNA hybrids can ultimately weaken DNA and cause skin lesions. Since the genome is actively transcribed, cellular RNase-HII is essential for removing RNA from the DNA–RNA hybrid in controls of genome stability and epigenome shaping and can be used as a causal prognostic marker in patients with psoriasis.
Highlights
Psoriasis is a chronic, recurrent inflammatory disease of the skin characterized by abnormal proliferation of keratinocytes, vascular hyperplasia, and infiltration of inflammatory cells into the dermis and epidermis [1,2]
Our hypothesis is that altered epigenetic signals are transcripts such as Telomeric Repeat- containing RNAs (TERRA) due to shorter telomere observed in psoriasis lesion
Our results show a higher amount of TERRA molecules attached to the telomeres
Summary
Recurrent inflammatory disease of the skin characterized by abnormal proliferation of keratinocytes, vascular hyperplasia, and infiltration of inflammatory cells into the dermis and epidermis [1,2]. It is generally reported that the central pathogenesis of psoriasis is the dysfunction of T lymphocytes affected by complex interactions between genetic and environmental factors, such as trauma, infections, stress, medications, smoking, and alcohol consumption. The disease affects both men and women [3]. The localization of the skin lesions is determined according to the traumatic triggers, the most frequent local lesions are on the knee, the elbow, and Biomolecules 2022, 12, 368. The abundance of reported familial cases suggests genetics and epigenetics predisposition [8]
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