International journal of biological macromolecules · 2019
Insulin-like growth factor 1 exhibits the pro-autophagic and anti-apoptotic activity on T cells of oral lichen planus.
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Wang Fang, Tan Ya-Qin, Zhang Jing, Zhou Gang
Аннотация
BACKGROUND: Oral lichen planus (OLP) is an autoimmune mucocutaneous disease characterized by T cell infiltrating in microenvironment. T cell-mediated immune dysfunctions are of importance in the pathogenesis of OLP. Insulin-like growth factor 1 (IGF1) has profound effects on maintenance of immune functions; however, its specific mechanism in OLP remains unknown. This study aims to explore how IGF1 regulates T-cell immune functions in OLP.
METHODS: IGF1 in OLP lesions was stained by immunohistochemistry and immunofluorescence. Additionally, proliferation, apoptosis and autophagy of T cells were examined after stimulation with IGF1 for 24 h, respectively. Z-VAD-FMK, a pan-caspase inhibitor, was used to explore IGF1-mediated crosstalk between apoptosis and autophagy. The modulation of IGF1 on ERK and PI3K/mTOR pathway was also analyzed.
RESULTS: IGF1 was increased in OLP lesions and was remarkably co-located with T cells. IGF1 significantly enhanced T-cell proliferation, suppressed apoptosis and induced autophagic flux. Moreover, autophagy was induced by apoptosis inhibitor, Z-VAD-FMK, thereby reducing death of T cells. IGF1 could facilitate Z-VAD-FMK-induced autophagy and then decrease proportion of apoptotic T cells. IGF1-treated T cells also showed elevated phosphorylation of ERK, PI3K and mTOR.
CONCLUSIONS: IGF1 inhibited apoptosis and promoted autophagy in T cells, potentially contributing to the pathogenesis of OLP.
METHODS: IGF1 in OLP lesions was stained by immunohistochemistry and immunofluorescence. Additionally, proliferation, apoptosis and autophagy of T cells were examined after stimulation with IGF1 for 24 h, respectively. Z-VAD-FMK, a pan-caspase inhibitor, was used to explore IGF1-mediated crosstalk between apoptosis and autophagy. The modulation of IGF1 on ERK and PI3K/mTOR pathway was also analyzed.
RESULTS: IGF1 was increased in OLP lesions and was remarkably co-located with T cells. IGF1 significantly enhanced T-cell proliferation, suppressed apoptosis and induced autophagic flux. Moreover, autophagy was induced by apoptosis inhibitor, Z-VAD-FMK, thereby reducing death of T cells. IGF1 could facilitate Z-VAD-FMK-induced autophagy and then decrease proportion of apoptotic T cells. IGF1-treated T cells also showed elevated phosphorylation of ERK, PI3K and mTOR.
CONCLUSIONS: IGF1 inhibited apoptosis and promoted autophagy in T cells, potentially contributing to the pathogenesis of OLP.