scispace - formally typeset
J

Javier Carrasco

Researcher at Autonomous University of Barcelona

Publications -  62
Citations -  3093

Javier Carrasco is an academic researcher from Autonomous University of Barcelona. The author has contributed to research in topics: Metallothionein & Astrocyte. The author has an hindex of 34, co-authored 61 publications receiving 2947 citations. Previous affiliations of Javier Carrasco include Carlos III Health Institute & Scripps Research Institute.

Papers
More filters
Journal ArticleDOI

Strongly compromised inflammatory response to brain injury in interleukin‐6‐deficient mice

TL;DR: It is demonstrated that IL‐6 is crucial for the recruitment of myelo‐monocytes and activation of glial cells following brain injury with disrupted BBB and the opposing effect of IL‐ 6 on MT‐I+II and MT‐III levels in the damaged brain suggests MT isoform‐specific functions.
Journal ArticleDOI

Impaired inflammatory response and increased oxidative stress and neurodegeneration after brain injury in interleukin-6-deficient mice.

TL;DR: The changes in neuronal tissue damage and in brain regeneration observed in IL‐6KO mice are likely caused by the IL-6‐dependent decrease in MT‐I+II expression, indicating IL‐ 6 and MT‐i+II as neuroprotective factors during brain injury.
Journal ArticleDOI

CNS Wound Healing Is Severely Depressed in Metallothionein I- and II-Deficient Mice

TL;DR: It is demonstrated that metallothioneins I and II are essential for a normal wound repair in the CNS, and that their deficiency impairs neuronal survival.
Journal ArticleDOI

Redefining the Role of Metallothionein within the Injured Brain: EXTRACELLULAR METALLOTHIONEINS PLAY AN IMPORTANT ROLE IN THE ASTROCYTE-NEURON RESPONSE TO INJURY*

TL;DR: Evidence is provided for a fundamentally different mode of action relying upon intercellular transfer from astrocytes to neurons, which in turn leads to uptake-dependent axonal regeneration and suggests that the protective functions of MT in the central nervous system should be widened to include extracellular and intra-neuronal roles.
Journal ArticleDOI

Interleukin-6 deficiency reduces the brain inflammatory response and increases oxidative stress and neurodegeneration after kainic acid-induced seizures.

TL;DR: It is demonstrated that interleukin-6 deficiency increases neuronal injury and impairs the inflammatory response after kainic acid-induced seizures, and that reactive astrogliosis and microgliosis were reduced, while morphological hippocampal damage, oxidative stress and apoptotic neuronal death were increased.