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
- induced apoptosis
- white matter
- bone marrow
- resting state
- binding protein
- acute myeloid leukemia
- stem cells
- spinal cord
- lps induced
- long non coding rna
- mesenchymal stem cells
- multiple sclerosis
- genome wide
- patient safety
- signaling pathway
- quality improvement
- palliative care
- immune response
- copy number
- cell proliferation
- endoplasmic reticulum stress
- functional connectivity
- brain injury
- blood brain barrier
- dna methylation
- real time pcr
- smoking cessation