Concurrent loss and proliferation of astrocytes following lateral fluid percussion brain injury in the adult rat

Abstract

Astrocyte populations were analyzed over a period of 1 month in the hippocampus following lateral fluid percussion (FP) brain injury. Rats (n = 23) were subjected either to a brain injury of moderate severity, or to anesthesia and surgery without injury (n = 7). At 3 days, 1, 2, or 4 weeks postinjury, subgroups of animals were sacrificed and the brains removed and sectioned for histochemical analysis. The density of astrocytes, identified with gold sublimate staining, decreased significantly in the ipsilateral hippocampus of injured rats 3 days following injury, eventually falling to 64% of the total astrocyte population present in uninjured animals by 1 week postinjury. One month postinjury, the density of hippocampal astrocytes had returned to 85% of the total number of astrocytes observed in the hippocampus of uninjured animals. In order to characterize the post-traumatic formation of new astrocytes, immunohistochemistry was performed using antibodies to proliferating cell nuclear antigen (PCNA) and to glial fibriallary acidic protein (GFAP). Positive immunolabeling for both PCNA and GFAP was most abundant at 3 days following FP brain injury in regions where the blood brain barrier was compromised, and was not detectable by 1 month postinjury. These results indicate that astrocyte proliferation after injury may be evoked by mitogens released from vascular sources, and may be an attempt to compensate for some of the astrocytic cell loss observed after injury.

Post-Traumatic Glioblastoma Multiforme: A Case Report

“…The development of glioblastoma multiforme following a traumatic cerebral contusion is possible [18]. There are several case reports in the literature that discuss posttraumatic gliomas [1][2][3][4][5][6][7][8][9][10][11][12], but some of these cases might only be a statistical coincidence. Hochberg et al [10] demonstrated that severe head injury is a significant risk factor for the development of glial tumors.…”

“…Trauma initiates glial cell proliferation by triggering various growth factors that result in malignant neoplasms. Schiffer et al [23] detected astrocytic proliferation on the ipsilateral injury side in the rat brain two days after trauma, and astrocytic proliferation was demonstrated in regions of fluid percussion injury and deteriorated blood-brain barrier regions [9]. Kernie et al [12] demonstrated significant astrocyte and neural precursor proliferation in response to traumatic brain injury regions at 60 days after trauma, and Propiono bacterium acnes was isolated within the posttraumatic glioma tissue [15].…”

“…Trauma has been implicated as a predisposing factor in patients with malignant gliomas [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16]. However, only a few authors have provided definite evidence for a causative role of trauma in this disease [7,15].…”

Post-Traumatic Glioma: Report of a Case

“…23 However, the presented case show formation of GBM at the site of prior brain injury. 2,3,6,7,[9][10][11][12][13][14][15]18 Trauma and glial scarring are known to be predisposing factors for the development of malignant glial tumors. 25 The development of glioblastoma multiforme following a traumatic cerebral contusion is possible.…”

Sustained Survival and Maturation of Adult Neural Stem/Progenitor Cells after Transplantation into the Injured Brain

“…For example, nerve growth factor (NGF) is increased at 3 days after TBI (Boockvar et al, 2005), and we previously found increased basic fibroblast growth factor (bFGF) and endothelial growth factor (EGF) expression levels at 2 days post-injury (unpublished data). After the regression of this acute phase of inflammation in the injured brain, astrocyte proliferation peaks at approximately 3 days post-TBI, followed by new microvasculature and glia limitans formation in the later stages postinjury (Hill-Felberg et al, 1999). Therefore, the injury response has an early and a late phase, each of which is characterized by its own distinct microenvironment.…”