Upregulation of heparin-binding growth-associated molecule after spinal cord injury in adult rats
Abstract
AIM:
To investigate whether traumatic spinal cord injury (SCI) induces changes of gene expression of heparin-binding growth-associated molecule (HB-GAM).
METHODS:
In a spinal cord transection model, HB-GAM expression and cellular localization were examined using Northern blot, RT-PCR, immunohistochemistry and immunofluorescence double-labeling methods.
RESULTS:
HB-GAM mRNA was significantly upregulated in spinal cord tissues rostral and caudal to the injury at 7 d after SCI. HB-GAM gene expression was markedly increased at 3 d, peaked at 7 d, and declined to the baseline level at 28 d post-injury. During its peak expression, HB-GAM was co-localized in astrocytes, oligodendrocytes, and neurons in spinal cord tissues within 7 mm from the site of spinal transection.
CONCLUSION:
SCI induces HB-GAM expression at both mRNA and protein levels in areas close to the injury. Both neurons and glial cells expressed HB-GAM implying that HB-GAM played a role in the process of injury and/or repair following SCI.
Keywords:
To investigate whether traumatic spinal cord injury (SCI) induces changes of gene expression of heparin-binding growth-associated molecule (HB-GAM).
METHODS:
In a spinal cord transection model, HB-GAM expression and cellular localization were examined using Northern blot, RT-PCR, immunohistochemistry and immunofluorescence double-labeling methods.
RESULTS:
HB-GAM mRNA was significantly upregulated in spinal cord tissues rostral and caudal to the injury at 7 d after SCI. HB-GAM gene expression was markedly increased at 3 d, peaked at 7 d, and declined to the baseline level at 28 d post-injury. During its peak expression, HB-GAM was co-localized in astrocytes, oligodendrocytes, and neurons in spinal cord tissues within 7 mm from the site of spinal transection.
CONCLUSION:
SCI induces HB-GAM expression at both mRNA and protein levels in areas close to the injury. Both neurons and glial cells expressed HB-GAM implying that HB-GAM played a role in the process of injury and/or repair following SCI.