𝔖 Bobbio Scriptorium
✦   LIBER   ✦

Overexpression of Bcl-2 is neuroprotective after experimental brain injury in transgenic mice

✍ Scribed by Nakamura, Michio; Raghupathi, Ramesh; Merry, Diane E.; Scherbel, Uwe; Saatman, Kathryn E.; Mcintosh, Tracy K.

Publisher
John Wiley and Sons
Year
1999
Tongue
English
Weight
425 KB
Volume
412
Category
Article
ISSN
0021-9967

No coin nor oath required. For personal study only.

✦ Synopsis

The cell death regulatory protein, Bcl-2, has been suggested to participate in the pathophysiology of various neurological disorders, including traumatic brain injury (TBI). The cognitive function and histopathologic sequelae after controlled cortical impact brain injury were evaluated in transgenic (TG) mice that overexpress human Bcl-2 protein (n ϭ 13) and their wild type (WT) controls (n ϭ 9). Although brain-injured Bcl-2 TG mice exhibited similar posttraumatic deficits in a Morris water maze (MWM) test of spatial memory as their WT counterparts at 1 week postinjury, the preinjury learning ability of Bcl-2 TG mice was impaired significantly compared with their WT littermates (P Ͻ 0.05). In contrast, histopathologic analysis revealed significantly attenuated tissue loss in the ipsilateral hemisphere (p Ͻ 0.01) and decreased tissue loss in ipsilateral hippocampal area CA3 (P Ͻ 0.001) and the dentate gyrus (P Ͻ 0.01) in brain-injured Bcl-2 TG mice compared with brain-injured WT mice. Immunohistochemical evaluation of glial fibrillary acidic protein also revealed a significant decrease in reactive astrocytosis in the ipsilateral dorsal thalamus (P Ͻ 0.05) and the ventral thalamus (P Ͻ 0.01) in brain-injured Bcl-2 TG mice. These results suggest that overexpression of Bcl-2 protein may play a protective role in neuropathologic sequelae after TBI.

📜 SIMILAR VOLUMES

Inhibition of cell death by lens-specifi
Inhibition of cell death by lens-specific overexpression of bcl-2 in transgenic mice
✍ Fromm, Larry ;Overbeek, Paul A. 📂 Article 📅 1997 🏛 John Wiley and Sons 🌐 English ⚖ 367 KB 👁 1 views

Previous studies on cell cycle regulation in the ocular lens using transgenic mice have shown that inactivation of the retinoblastoma tumor suppressor protein (pRb) can cause postmitotic lens fiber cells to enter the cell cycle. However, when the p53 gene and protein are intact, inactivation of pRb

Twofold overexpression of human ?-amyloi
Twofold overexpression of human ?-amyloid precursor proteins in transgenic mice does not affect the neuromotor, cognitive, or neurodegenerative sequelae following experimental brain injury
✍ Murai, Hisayuki; Pierce, Jean E.S.; Raghupathi, Ramesh; Smith, Douglas H.; Saatm 📂 Article 📅 1998 🏛 John Wiley and Sons 🌐 English ⚖ 270 KB 👁 2 views

By using transgenic mice that overexpress human beta-amyloid precursor proteins (APPs) at levels twofold higher than endogenous APPs, following introduction of the human APP gene in a yeast artificial chromosome (YAC), we examined the effects of controlled cortical impact (CCI) brain injury on neuro

Overexpression of copper/zinc-superoxide
Overexpression of copper/zinc-superoxide dismutase in transgenic mice markedly impairs regeneration and increases development of neuropathic pain after sciatic nerve injury
✍ Katarzyna Kotulska; Marie LePecheur; Wiesław Marcol; Joanna Lewin-Kowalik; Magda 📂 Article 📅 2006 🏛 John Wiley and Sons 🌐 English ⚖ 224 KB

## Abstract Despite the general capacity of peripheral nervous system to regenerate, peripheral nerve injury is often followed by incomplete recovery of function, sometimes with the burden of neuropathic pain. The mechanisms of both regeneration and nociception have not been clarified, but it is kn

Role of the Nrf2-ARE pathway in early br
Role of the Nrf2-ARE pathway in early brain injury after experimental subarachnoid hemorrhage
✍ Gang Chen; Qi Fang; Jian Zhang; Dai Zhou; Zhong Wang 📂 Article 📅 2011 🏛 John Wiley and Sons 🌐 English ⚖ 795 KB

## Abstract The nuclear factor erythroid 2‐related factor 2 and antioxidant‐response element (Nrf2‐ARE) pathway is a key regulator for modulating inflammation and oxidative damage, which are involved in the pathogenesis of early brain injury (EBI) after subarachnoid hemorrhage (SAH). Previous studi

Genetic disruption of cyclooxygenase-2 d
Genetic disruption of cyclooxygenase-2 does not improve histological or behavioral outcome after traumatic brain injury in mice
✍ Muzamil Ahmad; Marie E. Rose; Vincent Vagni; Raymond P. Griffith; C. Edward Dixo 📂 Article 📅 2008 🏛 John Wiley and Sons 🌐 English ⚖ 335 KB

## Abstract Increasing evidence suggests a role for cyclooxygenase‐2 (COX‐2) in traumatic brain injury (TBI). In the present study, the role of COX‐2 in TBI was investigated using COX‐2 gene‐disrupted (COX‐2 null) mice and wild‐type (WT) controls that were subjected to the controlled cortical impac