Mouse Spinal Cord Vascular Transcriptome Analysis Identifies CD9 and MYLIP as Injury-Induced Players.
Isaura MartinsDalila Neves-SilvaMariana Ascensão-FerreiraAna Filipa DiasDaniel RibeiroAna Filipa IsidroRaquel QuitériaDiogo Paramos-de-CarvalhoNuno L Barbosa-MoraisLeonor SaúdePublished in: International journal of molecular sciences (2023)
Traumatic spinal cord injury (SCI) initiates a cascade of cellular events, culminating in irreversible tissue loss and neuroinflammation. After the trauma, the blood vessels are destroyed. The blood-spinal cord barrier (BSCB), a physical barrier between the blood and spinal cord parenchyma, is disrupted, facilitating the infiltration of immune cells, and contributing to a toxic spinal microenvironment, affecting axonal regeneration. Understanding how the vascular constituents of the BSCB respond to injury is crucial to prevent BSCB impairment and to improve spinal cord repair. Here, we focus our attention on the vascular transcriptome at 3- and 7-days post-injury (dpi), during which BSCB is abnormally leaky, to identify potential molecular players that are injury-specific. Using the mouse contusion model, we identified Cd9 and Mylip genes as differentially expressed at 3 and 7 dpi. CD9 and MYLIP expression were injury-induced on vascular cells, endothelial cells and pericytes, at the injury epicentre at 7 dpi, with a spatial expression predominantly at the caudal region of the lesion. These results establish CD9 and MYLIP as two new potential players after SCI, and future studies targeting their expression might bring promising results for spinal cord repair.
Keyphrases
- spinal cord
- spinal cord injury
- neuropathic pain
- poor prognosis
- stem cells
- genome wide
- high glucose
- traumatic brain injury
- physical activity
- induced apoptosis
- transcription factor
- oxidative stress
- brain injury
- dna methylation
- optical coherence tomography
- signaling pathway
- blood brain barrier
- drug induced
- nk cells
- long non coding rna
- human health
- rna seq
- climate change
- cell cycle arrest