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Mitochondrial signaling for histamine releases in laser-irradiated RBL-2H3 mast cells
Zu-Hui Wu1, Yu Zhou, Ji-Yao Chen
1Surface Physics Laboratory (National key laboratory), Department of Physics, Fudan University, Shanghai 200433, China.
Background:
The low power laser irradiation (LPLI) can promote the wound healing, but the mechanism is still not fully understood. We have found in our previous work that the LPLI induces mast cells to release the histamine and thus suggested that the increased histamine release is probably one of the causes for promoting the wound healing since mast cells have been found to play positive roles in the process of wound healing. This study aims to explore the mechanism of histamine release in RBL-2H3 mast cells under laser irradiations.
Materials And Methods:
The wavelength effect of laser irradiations, the permeability function of mitochondrial membrane, the Bcl-2 effect, the cytosolic alkalinization and the increment of intracellular Ca(2+) ([Ca(2+)](i)), on histamine release in RBL-2H3 cells were studied, respectively, with the corresponding fluorescence probes.
Results:
The action bands of laser irradiations were consistent with the absorption bands of cytochrome c oxidase, suggesting that cytochrome c oxidase is the photoacceptor. After laser irradiation, (1) the cytochrome c releases from mitochondrial to cytosol reflecting an increased permeability of mitochondrial membrane, (2) the cytosolic alkalinization appears, (3) [Ca(2+)](i) increases, and (4) finally the enhancement of histamine release occurs. When Bcl-2 was used to inhibit the permeability of mitochondrial membrane these cellular signaling from (1) to (4) were all suppressed obviously.
Conclusion:
As a photoacceptor, cytochrome c oxidase absorbs incident photons and initiates the mitochondrial signaling. When the signals are transferred from the mitochondrial to the cytosol, the cytosolic alkalinization appears leading to the opening of a Ca(2+) channel on the membrane, the transient receptor potential vanilloid (TRPV), and an increment of [Ca(2+)](i). The increased [Ca(2+)](i) consequently mediates an enhanced histamine release. Such a responding chain is a suggested mechanism to understand the histamine release in RBL-2H3 cells under laser irradiations.
