| Summary: | 碩士 === 國立臺灣大學 === 臨床醫學研究所 === 97 === The structure, development and growth of hair follicles are very complex and depend on intimate epithelial-mesenchymal interaction. The signals from both the epidermis and dermis contribute to the epidermal and dermal interaction. In follicular development, hair growth, hair cycle, and pathological conditions, the mesenchymal cells of hair follicle, namely dermal papilla cells (DPC), play a vital role. For example in the embryonic stage, the dermal cells condensate into dermal papilla (DP) and epidermal cells bud downward to the dermis and further differentiate into follicular structures under the guidance of DP. In pathological conditions, such as alopecia areata and androgenetic alopecia, a huge body of evidence also suggests the function of DPC is compromised and leads to hair loss.
The low level light (LLL) therapy has gained much popularity both in lab researches and clinical applications in recent years. Different from the destructive high energy laser, LLL therapy exerts its effect through direct biomodulation. It has been shown that the LLL therapy is able to promote wound healing, enhance melanocyte regeneration, prevent nerve injury, and facilitate bone repair. The mechanism of the biological effects of LLL therapy has not been investigated in detail.
Recently, FDA approved the use of LLL (LaserComb) in hair loss treatment, but the underlying mechanism is unknown. Our hypothesis is that LLL may reach the effect of hair growth via the interaction with DPC to modulate follicle epithelial-mesenchymal interaction. We irradiated DPC with 625-635nm light emitting diode (LED). In comparison with the untreated group, irradiated DPC have a distinct higher rate of proliferation and enhanced cell viability. Also, the treated group has a significant higher proportion of cells in the S/G2M phases of the cell cycle. The levels of ERK and Akt phosphorylation increased significantly 15 minutes post-irradiation. The addition of either PD98059 or LY294002 reversed the growth increase induced by LLL, which showed that LLL affects the growth of DPC quite specifically through both the ERK and the Akt signaling pathways. The number of outer root sheath keratinocytes (ORSK) co-cultured with irradiated DPC was significantly higher than that of the direct-irradiated and control group. The increased proliferation of ORSK in the co-culture system would be explained by indirect action through increased DPC activation in turn mediating ORSK proliferation. We suggest that LLL irradiation simulates the growth of DPC. Furthermore, DPC may increase ORSK proliferation via secreting soluble factors and then modulate hair follicle epithelial-mesenchymal interaction.
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