Low-power infrared laser on telomere maintenance in an experimental model of arthritis.

Abstract

Telomere shortening accelerated by inflammation and oxidative stress is a critical factor in arthritic joint degradation. While photobiomodulation (PBM) is known to mitigate inflammation, its impact on nuclear mechanisms governing genomic stability remains poorly understood. This study evaluated the effects of low-power infrared laser on the temporal expression of key telomere maintenance genes (TRF1, TRF2, POT1, and TIN2) in zymosan-induced arthritis. Experimental arthritis was induced via bilateral intra-articular injection of zymosan into the talocrural and subtalar joints of C57BL/6 mice. PBM was initiated 5 h post-induction using a low-power infrared laser (830 nm, 10 mW, 200 mW/cm², 3 and 30 J/cm², 0.15 and 1.5 J, 15 and 150 s). Joint tissues were harvested at 24, 48, and 72 h to determine relative mRNA expression levels using RT-qPCR. Zymosan administration alone triggered an acute, compensatory upregulation of all evaluated telomere maintenance genes within 24 h. PBM significantly altered this transcriptional kinetic profile in a time- and fluence-dependent manner. At 24 and 48-hour time points, laser treatment induced a pronounced downregulation of telomere maintenance genes. Conversely, a striking transcriptional rebound occurred at 72 h in the high-fluence group, yielding a highly significant upregulation of TRF2, POT1, and TIN2 relative to untreated arthritic controls. By regulating telomere maintenance kinetics, PBM could prevent replicative senescence and the senescence-associated secretory phenotype. Mapping this the temporal window, number of laser exposures, and dosing parameters could provide a mechanistic framework for optimizing clinical PBM protocols to preserve genomic stability, extend cellular longevity, and restore tissue homeostasis in arthritic diseases.