Lysophosphatidic acid as a CSF lipid in posthemorrhagic hydrocephalus that drives CSF accumulation via TRPV4-induced hyperactivation of NKCC1.
Trine L Toft-BertelsenDagne BarbuskaiteEva Kjer HeerfordtSara Diana LolansenSøren Norge AndreassenNina RostgaardMarkus Harboe OlsenNicolas H NoragerTenna CapionMartin Fredensborg RathMarianne JuhlerNanna MacAulayPublished in: Fluids and barriers of the CNS (2022)
Together, our data reveal that a serum lipid present in brain pathologies with hemorrhagic events promotes CSF hypersecretion and ensuing brain water accumulation via its direct action on TRPV4 and its downstream regulation of NKCC1. TRPV4 may therefore be a promising future pharmacological target for pathologies involving brain water accumulation.
Keyphrases
- resting state
- white matter
- neuropathic pain
- functional connectivity
- cerebrospinal fluid
- cerebral ischemia
- fatty acid
- single cell
- subarachnoid hemorrhage
- gene expression
- diabetic rats
- multiple sclerosis
- spinal cord injury
- machine learning
- dna methylation
- current status
- big data
- brain injury
- endothelial cells
- deep learning