Low-power infrared laser modulates telomere length in heart tissue from an experimental model of acute lung injury

Abstract

Acute lung injury and acute respiratory distress syndrome can occur as a result of sepsis. Cardiac dysfunction is a serious component of multi-organ failure caused by severe sepsis. Telomere shortening is related to several heart diseases. Telomeres are associated with the shelterin protein complex, which contributes to the maintenance of telomere length. Low-power infrared lasers modulate mRNA levels of shelterin complex genes. This study aimed to evaluate effects of a low-power infrared laser on mRNA relative levels of genes involved in telomere stabilization and telomere length in heart tissue of an experimental model of acute lung injury caused by sepsis. Animals were divided into six groups, treated with intraperitoneal saline solution, saline solution and exposed to a low-power infrared laser at 10 J cm −2 and 20 J cm −2 , lipopolysaccharide (LPS), and LPS and, after 4 h, exposed to a low-power infrared laser at 10 J cm −2 and 20 J cm −2 . The laser exposure was performed only once. Analysis of mRNA relative levels and telomere length by RT-qPCR was performed. Telomere shortening and reduction in mRNA relative levels of TRF1 mRNA in heart tissues of LPS-induced ALI animals were observed. In addition, laser exposure increased the telomere length at 10 J cm −2 and modulated the TRF1 mRNA relative levels of at 20 J cm −2 in healthy animals. Although the telomeres were shortened and mRNA levels of TRF1 gene were increased in nontreated controls, the low-power infrared laser irradiation increased the telomere length at 10 J cm −2 in cardiac tissue of animals affected by LPS-induced acute lung injury, which suggests that telomere maintenance is a part of the photobiomodulation effect induced by infrared radiation.

Causal relationship between telomere length and sepsis: a bidirectional Mendelian randomization study

“…Existing data suggest a close relationship between TL and inflammation and the immune system, indicating a potential connection between TL and sepsis. An animal experiment’s results have shown that after lipopolysaccharide (LPS)-induced acute lung injury (ALI), telomeres in rat heart tissue exhibited shortening, suggesting that sepsis may affect TL in the chromosomes of the animal’s heart 10 . Recent research assessed variations in leukocyte telomere length (LTL) during 7 days in 40 critically sick patients, finding that LTL shortened in 21 patients, lengthened in 11, and remained unchanged in the rest of the patients.…”