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Seminar(July 05, 2017)
2017-09-11 | Author: | From:

Speaker: Shu-Sheng Wang (Associate Professor, Department of Cell and Molecular Biology, Department of Ophthalmology, Tulane University, US)      

TitleRole of noncoding RNAs in angiogenesis 

Time: July 05 (Wednesday) 2017, 15:00pm

Venue: Conference room 237, 2nd floor, main building, KIZ main campus

Everyone is welcome! 

Introduction of the speaker:

Shusheng Wang, PhD. Associate Professor. The long term goal of my research is to elucidate the epigenetic mechanisms of retinal vascular development and disease, focusing on noncoding RNAs and chromatin remodeling factors. As a tenured associate professor in the Department of Cell and Molecular Biology and the Department of Ophthalmology at Tulane University, my research focuses on two closely related areas. The first area is to study noncoding RNA regulation of retinal vascular development and disease, and to develop therapeutics of wet age-related macular degeneration (AMD). Our NIH-sponsored research has shown that microRNAs miR-126 and miR-23~24~27 family members are critical for ocular vascular development and pathology.We have led the way in studying miRNAs in ocular disease processes. We found that let-7 family members contribute to non-proliferative diabetic retinopathy but repress pathological ocular angiogenesis; miR-146 is upregulated during retinal pigment epithelial (RPE)/Choroidal aging; miR-143/145 is required for regulating intraocular pressure (IOP) in vivo. The second area is to study the mechanism and pathogenesis of dry AMD. Our recently published work has suggested that necroptosis, rather than apoptosis, is a major mechanism for oxidative stress-induced death of RPE cells. Besides research, I have been actively involved in teaching and serving the scientific community. I have provided advanced mentoring to 10 graduate students and postdoctoral fellows and ~30 undergraduate students to prepare them for research careers. I have developed the expertise, leadership and motivation to lead successful projects and make breakthrough discoveries. The renewal R01 application is based on my finished R01 that generated 25 papers (including several high profile papers), and exciting preliminary data that miR-24 inhibits epithelial mesenchymal transition and fibrosis in RPE cells. The proposed project will uncover the mechanisms of miRNAs in choroidal neovascularization and fibrosis in AMD, and provide proof-of-concept for miRNA-based therapeutics for the devastating AMD disease.  

  Key Laboratory of Animal Models and Human Disease Mechanisms 

  Laboratory of tumor signal transduction 

Laboratory of oncobiology 


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