Literature DB >> 26528928

Effects of Controlled Cortical Impact on the Mouse Brain Vasculome.

Shuzhen Guo1, Josephine Lok1,2, Song Zhao3, Wendy Leung1, Angel T Som1, Kazuhide Hayakawa1, Qingzhi Wang1, Changhong Xing1, Xiaoying Wang1, Xunming Ji4, Yiming Zhou1, Eng H Lo1.   

Abstract

Perturbations in blood vessels play a critical role in the pathophysiology of brain injury and neurodegeneration. Here, we use a systematic genome-wide transcriptome screening approach to investigate the vasculome after brain trauma in mice. Mice were subjected to controlled cortical impact and brains were extracted for analysis at 24 h post-injury. The core of the traumatic lesion was removed and then cortical microvesels were isolated from nondirectly damaged ipsilateral cortex. Compared to contralateral cortex and normal cortex from sham-operated mice, we identified a wide spectrum of responses in the vasculome after trauma. Up-regulated pathways included those involved in regulation of inflammation and extracellular matrix processes. Decreased pathways included those involved in regulation of metabolism, mitochondrial function, and transport systems. These findings suggest that microvascular perturbations can be widespread and not necessarily localized to core areas of direct injury per se and may further provide a broader gene network context for existing knowledge regarding inflammation, metabolism, and blood-brain barrier alterations after brain trauma. Further efforts are warranted to map the vasculome with higher spatial and temporal resolution from acute to delayed phase post-trauma. Investigating the widespread network responses in the vasculome may reveal potential mechanisms, therapeutic targets, and biomarkers for traumatic brain injury.

Entities:  

Keywords:  extracellular matrix; inflammation; microvessels; neurovascular unit; traumatic brain injury

Mesh:

Year:  2016        PMID: 26528928      PMCID: PMC4931728          DOI: 10.1089/neu.2015.4101

Source DB:  PubMed          Journal:  J Neurotrauma        ISSN: 0897-7151            Impact factor:   5.269


  147 in total

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5.  Annexin A2 Deficiency Exacerbates Neuroinflammation and Long-Term Neurological Deficits after Traumatic Brain Injury in Mice.

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7.  Recombinant annexin A2 inhibits peripheral leukocyte activation and brain infiltration after traumatic brain injury.

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  7 in total

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