M
Mingli Qu
Researcher at Peking Union Medical College
Publications - 31
Citations - 593
Mingli Qu is an academic researcher from Peking Union Medical College. The author has contributed to research in topics: Corneal epithelium & Cornea. The author has an hindex of 12, co-authored 28 publications receiving 430 citations.
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Journal ArticleDOI
Substance P Promotes Diabetic Corneal Epithelial Wound Healing Through Molecular Mechanisms Mediated via the Neurokinin-1 Receptor
Lingling Yang,Guohu Di,Xia Qi,Mingli Qu,Yao Wang,Haoyun Duan,Patrik Danielson,Lixin Xie,Qingjun Zhou +8 more
TL;DR: The results suggest that SP-NK-1 receptor signaling plays a critical role in the maintenance of corneal epithelium homeostasis, and that SP signaling through the NK-1 receptors contributes to the promotion of diabetic corneAL epithelial wound healing by rescued activation of Akt, EGFR, and Sirt1, improvement of mitochondrial function, and increased ROS scavenging capacity.
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Macrophage depletion impairs corneal wound healing after autologous transplantation in mice.
TL;DR: Macrophage depletion significantly impairs wound healing after autologous corneal transplantation through at least partially impacting on angiogenesis and wound closure.
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Trichostatin A Inhibits Transforming Growth Factor-β–Induced Reactive Oxygen Species Accumulation and Myofibroblast Differentiation via Enhanced NF-E2-Related Factor 2-Antioxidant Response Element Signaling
Lingling Yang,Mingli Qu,Yao Wang,Haoyun Duan,Peng Chen,Ye Wang,Weiyun Shi,Patrik Danielson,Qingjun Zhou +8 more
TL;DR: This study provides the first evidence implicating that TSA inhibits TGF-β–induced ROS accumulation and myofibroblast differentiation via enhanced Nrf2-ARE signaling.
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ROCK inhibitor Y-27632 increases the cloning efficiency of limbal stem/progenitor cells by improving their adherence and ROS-scavenging capacity.
TL;DR: Rho-associated coiled-coil kinase (ROCK) inhibitor Y-27632 increased the cloning efficiency of rabbit limbal stem/progenitor cells by improving their adherence and ROS scavenging capacity.
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TGFβ mediated transition of corneal fibroblasts from a proinflammatory state to a profibrotic state through modulation of histone acetylation
Qingjun Zhou,Lingling Yang,Yao Wang,Mingli Qu,Peng Chen,Ye Wang,Lixin Xie,Jing Zhao,Yiqiang Wang +8 more
TL;DR: TGFβ suppressed the production of proinflammatory factors and enhanced the expression of matrix remodeling genes of corneal fibroblasts in the transition from the proinflammatory state to the profibrotic state, and the dual roles of TGFβ on the phenotype regulations of cornea fibro Blasts were mediated by altered histone acetylation.