Muscle contractures in patients with cerebral palsy and acquired brain injury are associated with extracellular matrix expansion, pro‐inflammatory gene expression, and reduced rRNA synthesis

2018 ◽  
Vol 58 (2) ◽  
pp. 277-285 ◽  
Author(s):  
Ferdinand Von Walden ◽  
Stefan Gantelius ◽  
Chang Liu ◽  
Hanna Borgström ◽  
Lars Björk ◽  
...  
Keyword(s):  
Gene Expression ◽  
Extracellular Matrix ◽  
Cerebral Palsy ◽  
Brain Injury ◽  
Acquired Brain Injury ◽  
Rrna Synthesis ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene ◽  
Matrix Expansion ◽  
Extracellular Matrix Expansion

scholarly journals Surface Texturization of Breast Implants Impacts Extracellular Matrix and Inflammatory Gene Expression in Asymptomatic Capsules

2020 ◽  
Vol 145 (3) ◽  
pp. 542e-551e
Author(s):  
Isabelle Brigaud ◽  
Charles Garabédian ◽  
Nathalie Bricout ◽  
Laurent Pieuchot ◽  
Arnaud Ponche ◽  
...  
Keyword(s):  
Gene Expression ◽  
Extracellular Matrix ◽  
Breast Implants ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene

scholarly journals Peripheral loss of EphA4 ameliorates TBI-induced neuroinflammation and tissue damage

2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Elizabeth A. Kowalski ◽  
Jiang Chen ◽  
Amanda Hazy ◽  
Lauren E. Fritsch ◽  
Erwin Kristobal Gudenschwager-Basso ◽  
...  
Keyword(s):  
Gene Expression ◽  
Brain Injury ◽  
Tissue Damage ◽  
Injury Severity ◽  
Cortical Lesion ◽  
Lesion Volume ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene ◽  
Anti Inflammatory

Abstract Background The continuum of pro- and anti-inflammatory response elicited by traumatic brain injury (TBI) is suggested to play a key role in the outcome of TBI; however, the underlying mechanisms remain ill -defined. Methods Here, we demonstrate that using bone marrow chimeric mice and systemic inhibition of EphA4 receptor shifts the pro-inflammatory milieu to pro-resolving following acute TBI. Results EphA4 expression is increased in the injured cortex as early as 2 h post-TBI and on CX3CR1gfp-positive cells in the peri-lesion. Systemic inhibition or genetic deletion of EphA4 significantly reduced cortical lesion volume and shifted the inflammatory profile of peripheral-derived immune cells to pro-resolving in the damaged cortex. These findings were consistent with in vitro studies showing EphA4 inhibition or deletion altered the inflammatory state of LPS-stimulated monocyte/macrophages towards anti-inflammatory. Phosphoarray analysis revealed that EphA4 may regulate pro-inflammatory gene expression by suppressing the mTOR, Akt, and NF-κB pathways. Our human metadata analysis further demonstrates increased EPHA4 and pro-inflammatory gene expression, which correlates with reduced AKT concurrent with increased brain injury severity in patients. Conclusions Overall, these findings implicate EphA4 as a novel mediator of cortical tissue damage and neuroinflammation following TBI.

Sign in / Sign up

Export Citation Format

Share Document