Journal of Capital Medical University ›› 2017, Vol. 38 ›› Issue (1): 24-28.doi: 10.3969/j.issn.1006-7795.2017.01.005

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Roles of p75NTR inhibitor on retinal ganglion cells in a rat model of acute ocular hypertension

Wang Xiaolei1, Ma Jianmin2, Meng Zhaoyang1, Yin Yi1, Wang Yanling1   

  1. 1. Department of Ophthalmology, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China;
    2. Department of Ophthalmology, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China
  • Received:2016-11-28 Online:2017-01-21 Published:2017-01-20
  • Supported by:
    This study was supported by Clinical-Basic Cooperation Program from Capital Medical University(14JL32),Beijing Ophthalmology and Visual Sciences Key Laboratory (2015YKSJ02).

Abstract: Objective To explore the role of p75NTR inhibitor on suppressing retinal ganglion cells (RGCs) apoptosis in a rat model of acute ocular hypertension. Methods The acute ocular hypertension (AOH) rat model was established, and animals were divided into control (Ctrl), sham operation, AOH, AOH+TAT-Pep5 treated groups (1,3 and 5d subgroups). Immunofluorescent staining was performed to detect the expression of proNGF and p75NTR. Western blotting was used to detect the protein expression levels of proNGF and cleaved-caspase 3. TUNEL assay was used to detect cell apoptosis. Results The expression of proNGF was increased in acute ocular hypertension model. When the p75NTR was blocked by its inhibitor (TAT-Pep5), the number of death RGCs (TUNEL positive cell number) were less than that of AOH group. The results of Western blotting showed that the protein expression levels of cleaved-caspase 3 could be up-regulated in retina from AOH group or down-regulated in retina from AOH+TAT-Pep5 group when compared with that of Ctrl and AOH groups. Conclusion RGCs injury can increase proNGF expression. p75NTR blockade can potentiate the survival of RGCs.

Key words: acute ocular hypertension, p75NTR, proNGF, TAT-Pep 5 inhibitor, Müller cell

CLC Number: