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Yusheng Wang, Wenqin Xu; Pay attention to the toxicity of minocycline on photoreceptor cells. Invest. Ophthalmol. Vis. Sci. 2018;59(9):964.
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© ARVO (1962-2015); The Authors (2016-present)
Some patients who use minocycline for the treatment of acne complain of symptoms of darkening of their vision. However, there have no clinical or basic research address the toxicity of minocycline to photoreceptor cells. The objective of this study was to identify the mechanistic effect of minocycline on photoreceptor cell apoptosis.
CCK8 assay, flow cytometry, electron microscope, Ki67 and TUNEL staining have been used to detect the effect of minocycline on 661W cells proliferation and apoptosis. Experimental mice received intravitreous or subretinal injection of minocycline, the pro-apoptosis effect of minocycline in vivo was determined by TUNEL staining of retinal cryosections. ERG also conducted to measure the injury to visual function. The endoplasmic reticulum (ER) stress protein, was illustrated by immunoblot.
In 661W cells, CCK8 and Ki67 staining results demonstrated that minocycline inhibits proliferation, flow cytometry and TUNEL demonstrated that it promotes cell apoptosis. Further, ER stress-PERK-eIF2α-CHOP cascade has been activated, which acted as the key mechanisms underlying apoptosis. In addition, minocycline promoted nuclear translocation of NF-κB, the ER stress pathway could be partly alleviated by inhibiting NF-κB. In vivo study, the apoptosis of photoreceptor cells could be caused by intravitreous or subretinal injection of minocycline, the activation of ER stress-PERK-eIF2α-CHOP-Caspase3 cascade was prominent after intravitreous injection. ERG results showed that cone cells were more susceptible to minocycline than rod cells.
These results demonstrate that minocycline has toxicity on photoreceptor cells, especially cone cells, via ER stress-PERK-eIF2α-CHOP-Caspase3 pathway.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.
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