Cargando…
Young bone marrow Sca‐1 cells protect aged retina from ischaemia‐reperfusion injury through activation of FGF2
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‐rep...
Autores principales: | , , , , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2018
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6237572/ https://www.ncbi.nlm.nih.gov/pubmed/30255622 http://dx.doi.org/10.1111/jcmm.13905 |
_version_ | 1783371210757767168 |
---|---|
author | Shao, Zhengbo Wu, Jie Du, Guoqing Song, Huifang Li, Shu‐Hong He, Sheng Li, Jiao Wu, Jun Weisel, Richard D. Yuan, Huiping Li, Ren‐Ke |
author_facet | Shao, Zhengbo Wu, Jie Du, Guoqing Song, Huifang Li, Shu‐Hong He, Sheng Li, Jiao Wu, Jun Weisel, Richard D. Yuan, Huiping Li, Ren‐Ke |
author_sort | Shao, Zhengbo |
collection | PubMed |
description | 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 (FGF2) 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 FGF2 and Akt signalling pathways. |
format | Online Article Text |
id | pubmed-6237572 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-62375722018-12-01 Young bone marrow Sca‐1 cells protect aged retina from ischaemia‐reperfusion injury through activation of FGF2 Shao, Zhengbo Wu, Jie Du, Guoqing Song, Huifang Li, Shu‐Hong He, Sheng Li, Jiao Wu, Jun Weisel, Richard D. Yuan, Huiping Li, Ren‐Ke J Cell Mol Med Original Articles 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 (FGF2) 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 FGF2 and Akt signalling pathways. John Wiley and Sons Inc. 2018-09-25 2018-12 /pmc/articles/PMC6237572/ /pubmed/30255622 http://dx.doi.org/10.1111/jcmm.13905 Text en © 2018 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Shao, Zhengbo Wu, Jie Du, Guoqing Song, Huifang Li, Shu‐Hong He, Sheng Li, Jiao Wu, Jun Weisel, Richard D. Yuan, Huiping Li, Ren‐Ke Young bone marrow Sca‐1 cells protect aged retina from ischaemia‐reperfusion injury through activation of FGF2 |
title | Young bone marrow Sca‐1 cells protect aged retina from ischaemia‐reperfusion injury through activation of FGF2 |
title_full | Young bone marrow Sca‐1 cells protect aged retina from ischaemia‐reperfusion injury through activation of FGF2 |
title_fullStr | Young bone marrow Sca‐1 cells protect aged retina from ischaemia‐reperfusion injury through activation of FGF2 |
title_full_unstemmed | Young bone marrow Sca‐1 cells protect aged retina from ischaemia‐reperfusion injury through activation of FGF2 |
title_short | Young bone marrow Sca‐1 cells protect aged retina from ischaemia‐reperfusion injury through activation of FGF2 |
title_sort | young bone marrow sca‐1 cells protect aged retina from ischaemia‐reperfusion injury through activation of fgf2 |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6237572/ https://www.ncbi.nlm.nih.gov/pubmed/30255622 http://dx.doi.org/10.1111/jcmm.13905 |
work_keys_str_mv | AT shaozhengbo youngbonemarrowsca1cellsprotectagedretinafromischaemiareperfusioninjurythroughactivationoffgf2 AT wujie youngbonemarrowsca1cellsprotectagedretinafromischaemiareperfusioninjurythroughactivationoffgf2 AT duguoqing youngbonemarrowsca1cellsprotectagedretinafromischaemiareperfusioninjurythroughactivationoffgf2 AT songhuifang youngbonemarrowsca1cellsprotectagedretinafromischaemiareperfusioninjurythroughactivationoffgf2 AT lishuhong youngbonemarrowsca1cellsprotectagedretinafromischaemiareperfusioninjurythroughactivationoffgf2 AT hesheng youngbonemarrowsca1cellsprotectagedretinafromischaemiareperfusioninjurythroughactivationoffgf2 AT lijiao youngbonemarrowsca1cellsprotectagedretinafromischaemiareperfusioninjurythroughactivationoffgf2 AT wujun youngbonemarrowsca1cellsprotectagedretinafromischaemiareperfusioninjurythroughactivationoffgf2 AT weiselrichardd youngbonemarrowsca1cellsprotectagedretinafromischaemiareperfusioninjurythroughactivationoffgf2 AT yuanhuiping youngbonemarrowsca1cellsprotectagedretinafromischaemiareperfusioninjurythroughactivationoffgf2 AT lirenke youngbonemarrowsca1cellsprotectagedretinafromischaemiareperfusioninjurythroughactivationoffgf2 |