Pial Vessel-Associated Microglia/Macrophages Increase in Female Dahl-SS/Jr Rats Independent of Pregnancy History.
Junie P WarringtonQingmei ShaoAhsia M ClaytonKenji J MaedaAshtin G BeckettMichael R GarrettJennifer M SasserPublished in: International journal of molecular sciences (2022)
As the resident immune cells of the central nervous system, microglia have a wide range of functions such as surveillance, phagocytosis, and signaling through production of chemokines and cytokines. Recent studies have identified and characterized macrophages residing at the meninges, a series of layers surrounding the brain and spinal cord. While perivascular microglia within the brain parenchyma increase following chronic hypertension, there are no reports of changes at the meninges, and specifically, associated with the pial vasculature. Thus, we used female Sprague Dawley and Dahl salt-sensitive (SS/Jr) rat brains, stained for ionized calcium-binding adapter molecule (Iba1), and characterized microglia/macrophages associated with pial vessels in the posterior brain. Results indicate that Iba1 + pial vessel-associated microglia (PVAM) completely surrounded the vessels in brains from the Dahl-SS/Jr rats. PVAM density was significantly higher and distance between PVAMs lower in Dahl-SS/Jr compared to the Sprague Dawley rat brains. Pregnancy history did not affect these findings. While the functional role of these cells are not known, we contextualize our novel findings with that of other studies assessing or characterizing myeloid cells at the borders of the CNS (meninges and choroid plexus) and perivascular macrophages and propose their possible origin in the Dahl-SS/Jr model of chronic hypertension.
Keyphrases
- neuropathic pain
- inflammatory response
- spinal cord
- induced apoptosis
- resting state
- blood pressure
- white matter
- cell cycle arrest
- oxidative stress
- functional connectivity
- preterm birth
- cerebral ischemia
- public health
- emergency department
- endoplasmic reticulum stress
- dendritic cells
- pregnancy outcomes
- acute myeloid leukemia
- cell death
- transcription factor
- cerebrospinal fluid
- patient safety
- brain injury
- drug induced
- electronic health record
- solar cells