Fractional Subnanosecond Nd:YAG Laser Improves Matrix Architecture in Ultraviolet-Aged Facial Retaining Ligaments in Rats.

Facial retaining ligaments maintain soft-tissue position and support the lower face, but whether fractional subnanosecond Nd:YAG laser treatment can improve the matrix architecture of ultraviolet (UV)-aged ligament tissue remains unclear. We evaluated whether laser-associated matrix alteration was accompanied by coordinated changes in LATS1-YAP-IQGAP1-NFAT1 signaling and collagen type I-dominant remodeling. Male Sprague-Dawley rats were allocated to non-UV control, UV-aged, and UV-aged plus laser groups (n = 5 per group). After UV-aging induction, the laser group received a single fractional 1064 nm, 450 ps (subnanosecond) Nd:YAG treatment at 3.8 J/cm2 and 10 Hz using a 6 × 6 mm spot, with a measured pulse energy of 1.07 J and a calculated irradiance of 8.44 GW/cm2; 30 stacks, corresponding to 30 laser shots delivered to the same target area, were applied over 3 s. UV exposure increased cytosolic pLATS1/LATS1, cytosolic pYAP, and ELISA-detected IQGAP1-associated pYAP signals while reducing nuclear YAP; laser treatment partially reversed these changes. Concurrently, laser treatment decreased ELISA-detected IQGAP1-associated pNFAT1 signals, restored nuclear NFAT1 localization, and reduced cytosolic pNFAT1. Quantitative immunofluorescence, histomorphometric, and ultrastructural analyses showed restoration of the collagen type I signal and collagen type I/III ratio and improvements in collagen density, coherency, angular deviation, and collagen bundle diameter. Laser treatment restored the expression of tendon/ligament-lineage markers, including scleraxis, mohawk homeobox, and tenomodulin; UV-induced elevations in osteogenic markers (RUNX2, SP7, and ALPL) were not significantly attenuated. Overall, fractional subnanosecond Nd:YAG laser treatment partially improved the matrix architecture of UV-aged rat facial retaining ligaments. These exploratory findings support an association model linking laser-associated matrix remodeling with coordinated changes in LATS1-YAP-IQGAP1-NFAT1 signaling, lineage-marker recovery, and collagen type I-dominant realignment, but do not establish a causal signaling sequence or functional mechanical strengthening.