Under pathological conditions, the immune-specialized brain microenvironment contains both resident microglia and bone marrow-derived myeloid cells recruited from peripheral circulation. Due to largely overlapping phenotypic similarities between these ontogenically distinct myeloid populations, studying their individual functions in central nervous system diseases has been challenging. Recently, transmembrane protein 119 (Tmem119) has been reported as a marker for resident microglia which is not expressed by bone marrow-derived myeloid cells. However, several studies have reported the loss or reduction of Tmem119 expression in pathologically activated microglia. Here, we examined whether Tmem119 could be used as a robust marker to identify brain metastasis-associated microglia. In addition, we also compared Tmem119 expression of primary microglia to the immortalized microglia-like BV2 cell line and characterized expression changes after LPS treatment. Lastly, we used a commercially available transgenic mouse line (Tmem119-eGFP) to compare Tmem119 expression patterns to the traditional antibody-based detection methods. Our results indicate that brain metastasis-associated microglia have reduced Tmem119 gene and protein expression.
Keyphrases
- inflammatory response
- poor prognosis
- neuropathic pain
- resting state
- induced apoptosis
- white matter
- binding protein
- acute myeloid leukemia
- lps induced
- stem cells
- dendritic cells
- bone marrow
- oxidative stress
- functional connectivity
- dna methylation
- long non coding rna
- spinal cord injury
- multiple sclerosis
- cell cycle arrest
- immune response
- signaling pathway
- genome wide
- combination therapy
- brain injury
- copy number
- quantum dots