Open AccessMonocyte-derived SDF1 supports optic nerve regeneration and alters retinal ganglion cells’ response to Pten deletion
Author(s) -
Lili Xie,
Ling-Ping Cen,
Yiqing Li,
Hui-ya Gilbert,
Oleksandr Strelko,
Cynthia Berlinicke,
Mihaela Stavarache,
Madeline Ma,
Yong-Ting Wang,
Qing Cui,
Michael G. Kaplitt,
Donald J. Zack,
Larry I. Benowitz,
Yuqin Yin
Publication year - 2022
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.2113751119
Subject(s) - tensin , pten , biology , microbiology and biotechnology , regeneration (biology) , optic nerve , pi3k/akt/mtor pathway , inflammation , stromal cell , retinal ganglion cell , cancer research , immunology , signal transduction , neuroscience
Significance The optic nerve conveys information from retinal ganglion cells (RGCs) to visual processing areas of the brain. Although this pathway normally cannot regenerate when injured nor in degenerative diseases such as glaucoma, this failure can be partially reversed by eliciting a controlled immune reaction in the eye. We show here that the chemokine SDF1 (stromal cell–derived factor 1) is an important contributor to this phenomenon. SDF1 is produced by infiltrative monocytes and acts through its cognate receptor to enhance RGC survival, promote optic nerve regeneration, and sensitize subtypes of RGCs that normally fail to respond to a complementary treatment to exhibit robust, long-distance regeneration. These findings establish SDF1 as an important therapeutic candidate for repairing the injured optic nerve.