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893 Low-level laser therapy for the treatment of male and female-pattern hair loss: A review of literature
摘要： Gain-of-function mutations in TRPV3 can result in Olmsted syndrome, characterized by palmoplantar and periorificial keratoderma, itch, and hair loss. The mechanisms underlying these phenotypes are unclear. Here, we engineered the first knock-in mouse model of Trpv3 by introducing a point mutation analogous to that (G568V) found in Olmsted syndrome patients. Homozygous Trpv3 knock-in (Trpv3G568V/G568V) mice exhibit sparse hair within two weeks after birth. Histologically, hair shafts in Trpv3G568V/G568V mice are twisted in the infundibulum, unable to penetrate the skin. Immunofluorescence demonstrated impaired inner root sheath cell differentiation as trichohyalin and KRT71 were diminished in mutant hair follicles. These abnormalities are consistent with the expression pattern of Trpv3, which is predominantly in the proximal region of inner root sheath as demonstrated by in situ hybridization and in a Trpv3 reporter mouse model we engineered. The hair loss phenotype is progressive, and is associated with the lack of typical telogen. After three hair cycles, Trpv3G568V/G568V mice became completely bald. Aberrantly increased proliferation and ectopic expression of epidermal markers, including KRT1 and loricrin, are characteristic of degenerating hair follicles in Trpv3G568V/G568V mice, which gradually lose stem cells, as marked by CD34, NFATc1 and KRT15, and the typical structure of a hair follicle. Findings from this study suggest that Trpv3 is an important regulator of inner root sheath keratinocyte differentiation, whereas hair loss associated with gain-of-function mutations in Trpv3 is caused by impaired proliferation and differentiation programs, leading to the exhaustion of follicular keratinocyte stem cells, and permanent disruption of the hair follicles.
关键词： keratinocyte differentiation,TRPV3,Olmsted syndrome,stem cells,hair loss
更新于2025-09-16 10:30:52
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Effects of Pulsed 810?nm Al‐Ga‐As Diode Laser on Wound Healing Under Immunosuppression: A Molecular Insight
摘要： Background and Objectives: Dysregulated inflammation is one of the major contributing factors for the prevalence of non‐healing chronic wound in immunosuppressed subjects. Photobiomodulation (PBM) has emerged as a potential non‐thermal, light‐based therapeutic healing intervention for the treatment of impaired wounds. Study Design/Materials and Methods: The present study delineates the underlying molecular mechanisms of PBM 810 nm laser‐induced full‐thickness cutaneous wound repair in immunosuppressed rats at continuous and pulsed wave‐mode with power‐density of 40 mW/cm2, fluence 22.6 J/cm2 for 10 minutes daily for 7 post‐wounding days. Molecular markers were assessed using biochemical, assay quantification, enzyme kinetics and immunoblots analyses pertaining to inflammation, oxidative stress, cell survival, calcium signaling, and proliferation cascades. Results: Results distinctly revealed that pulsed 810 nm (10 Hz) PBM potentially influenced the cell survival and proliferation signaling pathway by significantly upregulated phospho‐protein kinase B(phospho‐Akt), phospho‐extracellular‐signal‐regulated kinase 1 (ERK1), transient receptor potential vanilloid‐3 (TRPV3), Ca2+, calmodulin, transforming growth factor‐β1 (TGF‐β1), TGF‐βR3, and Na+/K+‐ATPase pump levels. PBM treatment resulted in reduction of exaggerated inflammatory responses evident by significantly repressed levels of interleukin‐1β (IL‐1β), IL‐6, cyclooxygenase 2 (COX‐2), and substance‐P receptor (SPR), as well as inhibited apoptotic cell death by decreasing p53, cytochrome C, and caspase 3 levels (P < 0.05), which, in turn, effectively augment the wound repair in immunosuppressed rats. PBM treatment also lowered 4‐hydroxynoneal (HNE) adduct level and NADP/NADPH ratio and upregulated the GRP78 expression, which might culminate into reduced oxidative stress and maintained the redox homeostasis. Conclusions: Taken together, these findings would be helpful in better understanding of the molecular aspects involved in pulsed 810 nm laser‐mediated dermal wound healing in immunosuppressed rats through regulation of cell survival and proliferation via Ca2+‐calmodulin, Akt, ERK, and redox signaling.
关键词： immunosuppressed,dermal wound healing,inflammation,TRPV3,cell survival,TGF‐β,proliferation signaling cascade,photobiomodulation
更新于2025-09-11 14:15:04