Expression of the basic fibroblast growth factor gene in mild and more severe head injury in the rat.
OBJECTIVE
The goal of this study was to investigate the relationship between basic fibroblast growth factor (bFGF) gene expression and neuropathological changes in the hippocampus after varying degrees of brain injury.


METHODS
Mild and severe brain injury in rats was produced by using Marmarou's method. There were 25 animals in each brain injury group and 25 additional animals served as controls. Basic fibroblast growth factor gene expression was investigated by means of RNA hybridization, in situ hybridization, immunohistochemical analysis, and histological analysis using hematoxylin and eosin staining. A 3.7-kb bFGF messenger (m)RNA was detected in the rat hippocampus in both control and injured rats. In the mild injury group its expression was increased at 12 hours after injury and peaked on the 3rd day. Neuronal degeneration in the hippocampal CA2 and CA3 sectors was maximum on that day. In the severe injury group, the expression of the bFGF gene was the same as that in the mild injury group at corresponding times, but the number of surviving neurons in the CA2 and CA3 sectors was much lower than in the mild injury group. In situ hybridization showed that the main cells that expressed bFGF mRNA were pyramidal and granulocytic neurons in all three experimental groups. The number of neurons expressing bFGF mRNA in the severe injury group was less than that in the mild injury group, but the intensity of expression was greater. Immunohistochemical staining showed that the number of neurons expressing the bFGF protein was less in the severe injury group than in the mild injury group.


CONCLUSIONS
It is concluded that after mild injury there is a close relationship between the expression of the bFGF gene and the degree of histological change in the hippocampus; this indicates that as one of the growth factors, bFGF may participate in the protection and repair processes of neurons following brain injury. In severe injury there is a reduced expression of bFGF. The reason for this appears to be that more of the cells that have the potential to express bFGF have died, reducing the ability to express the bFGF gene. Conversely, it is possible that there may be an intrinsic insufficiency of expression of the gene, compatible with the known vulnerability of the hippocampus to many pathological conditions. Consideration should be given to supplying exogenous bFGF to protect the brain, particularly the hippocampus, after injury.
Yang
S Y
SY
Department of Neurosurgery, Tianjin Medical University General Hospital, People's Republic of China.
Cui
J Z
JZ
D000818:Animals; D001930:Brain Injuries / Q000145:classification / Q000235:genetics* / Q000473:pathology; D002452:Cell Count; D016923:Cell Death; D002470:Cell Survival; D002540:Cerebral Cortex / Q000293:injuries / Q000378:metabolism / Q000473:pathology; D004396:Coloring Agents; D003337:Corpus Callosum / Q000293:injuries / Q000378:metabolism / Q000473:pathology; D004195:Disease Models, Animal; D004801:Eosine Yellowish-(YS); D016222:Fibroblast Growth Factor 2 / Q000032:analysis / Q000235:genetics*; D005456:Fluorescent Dyes; D005786:Gene Expression Regulation; D006416:Hematoxylin; D006624:Hippocampus / Q000293:injuries / Q000378:metabolism / Q000473:pathology; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D008297:Male; D009410:Nerve Degeneration / Q000235:genetics; D009416:Nerve Regeneration / Q000235:genetics; D009474:Neurons / Q000473:pathology; D018696:Neuroprotective Agents / Q000378:metabolism; D009693:Nucleic Acid Hybridization; D017966:Pyramidal Cells / Q000473:pathology; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors
D004396:Coloring Agents; D005456:Fluorescent Dyes; D018696:Neuroprotective Agents; D012333:RNA, Messenger; D016222:Fibroblast Growth Factor 2; D004801:Eosine Yellowish-(YS); D006416:Hematoxylin