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Purpose: To investigate the impact of mitochondrial transcription factor A (TFAM), as a modulator of NF-κB, on proliferation of hypoxia-induced human retinal endothelial cell (HREC), and the probable mechanism. Methods: After exposure to hypoxia (1 % O 2 ) for 5 days, cell proliferation and cell cycle of HREC were measured by MTT (3-4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide) assay and flow cytometry. Cell signaling and mitochondrial DNA (mtDNA) copies were determined using real-time polymerase chain reaction and Western blot. NF-κB activity was evaluated by luciferase assay. Results: TFAM expression decreased to 40 % in HREC under hypoxic condition ( p < 0.05). MTT results revealed that TFAM facilitated HREC proliferation under hypoxia ( p < 0.05). Moreover, flow cytometry demonstrated that TFAM promoted HREC proliferation by accelerating cell cycle ( p < 0.05). Western blot and luciferase assay exhibited NF-κB activation in HREC after TFAM overexpression ( p < 0.05). Finally, real-time PCR results showed that mtDNA and targeted genes of NF-κB were upregulated 3-fold in HREC after TFAM transfection under hypoxia ( p < 0.05). Conclusion: These results indicate that NF-κB activated by TFAM protects against hypoxia-induced HREC injury by accelerating cell cycle. The ability of TFAM to enhance NF-κB signaling may be part of the mechanism of hypoxia-induced cell injury. Thus, upregulation of TFAM may help to relieve diabetic retinopathy. Keywords: Mitochondrial transcription factor A, NF-κB, Hypoxia, Human retinal endothelial cell, Diabetic retinopathy

Mitochondrial transcription factor A protects human retinal endothelial cell injury induced by hypoxia