Premium
Molecular mechanisms of spinal cord regeneration
Author(s) -
Echeverri Karen
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.88.3
Subject(s) - spinal cord injury , regeneration (biology) , axolotl , biology , neuroscience , astrogliosis , axon , regenerative medicine , microbiology and biotechnology , astrocyte , spinal cord , glial scar , neuroglia , population , central nervous system , stem cell , medicine , environmental health
Humans have very limited regenerative capacity especially in the central nervous system. In contrast, salamanders like the axolotl can functionally regenerate nervous tissue after injury throughout their life. After spinal cord injury (SCI) in the axolotl a population of cells, called glial cells adjacent to the injury site proliferates and migrates to reconnect the injured spinal cord and direct subsequent axon regeneration. This is in stark contrast to the mammalian response to SCI whereby injured astrocytes become reactive and contribute to glial scar formation and inhibition of axon regeneration. A major gap in knowledge exists regarding the molecular mechanism promoting a pro‐regenerative glial cell response to injury. Previously we identified the transcription factor c‐Fos as an essential regulator of the pro‐regenerative glial cell response to injury. However, c‐Fos functions as an obligate heterodimer with JUN family members to regulate gene expression. In mammalian astrocytes, up‐regulation of c‐Fos and c‐Jun after injury promotes reactive astrogliosis. Here I will present molecular data that identifies the molecular circuitry that must be carefully regulated to direct axolotl glial cells towards a regenerative response. Support or Funding Information Work in the Echeverri lab is funded by grants from NIH NICHD and Regenerative Medicine Minnesota. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .