Open AccessYoung bone marrow Sca‐1 cells protect aged retina from ischaemia‐reperfusion injury through activation of FGF 2
Author(s) -
Shao Zhengbo,
Wu Jie,
Du Guoqing,
Song Huifang,
Li ShuHong,
He Sheng,
Li Jiao,
Wu Jun,
Weisel Richard D.,
Yuan Huiping,
Li RenKe
Publication year - 2018
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.13905
Subject(s) - retina , stem cell , biology , bone marrow , pathology , retinal , immunology , microbiology and biotechnology , medicine , neuroscience , biochemistry
Retinal ganglion cell apoptosis and optic nerve degeneration are prevalent in aged patients, which may be related to the decrease in bone marrow ( BM ) stem cell number/function because of the possible cross‐talk between the two organs. This pathological process is accelerated by retinal ischaemia‐reperfusion (I/R) injury. This study investigated whether young BM stem cells can regenerate and repair the aged retina after acute I/R injury. Young BM stem cell antigen 1 positive (Sca‐1 + ) or Sca‐1 − cells were transplanted into lethally irradiated aged recipient mice to generate Sca‐1 + and Sca‐1 − chimaeras, respectively. The animals were housed for 3 months to allow the young Sca‐1 cells to repopulate in the BM of aged mice. Retinal I/R was then induced by elevation of intraocular pressure. Better preservation of visual function was found in Sca‐1 + than Sca‐1 − chimaeras 7 days after injury. More Sca‐1 + cells homed to the retina than Sca‐1 − cells and more cells differentiated into glial and microglial cells in the Sca‐1 + chimaeras. After injury, Sca‐1 + cells in the retina reduced host cellular apoptosis, which was associated with higher expression of fibroblast growth factor 2 ( FGF 2) in the Sca‐1 + chimaeras. Young Sca‐1 + cells repopulated the stem cells in the aged retina and diminished cellular apoptosis after acute I/R injury through FGF 2 and Akt signalling pathways.