Abstract
Neuropsychiatric manifestations of systemic lupus erythematosus (SLE), specifically cognitive dysfunction and mood disorders, are widely prevalent in SLE patients, and yet poorly under-stood. TNF-like weak inducer of apoptosis (TWEAK) has previously been implicated in the patho-genesis of neuropsychiatric lupus (NPSLE), and we have recently shown its effects on the transcrip-tome of the cortex of the lupus-prone mice model MRL/lpr. As the hippocampus is thought to be an important focus of NPSLE processes, we explored the TWEAK-induced transcriptional changes that occur in the hippocampus, and isolated several genes (Dnajc28, Syne2, transthyretin) and pathways (PI3K-AKT, as well as chemokine-signaling and neurotransmission pathways) that are most differentially affected by TWEAK activation. While the functional roles of these genes and pathways within NPSLE need to be further investigated, an interesting link between neuroinflammation and neurodegeneration appears to emerge, which may prove to be a promising novel direction in NPSLE research.
| Original language | English |
|---|---|
| Article number | 1172 |
| Journal | Genes |
| Volume | 12 |
| Issue number | 8 |
| DOIs | |
| State | Published - 29 Jul 2021 |
Bibliographical note
Publisher Copyright:© 2021 by the authors. Licensee MDPI, Basel, Switzerland.
Funding
Funding: This research received no external funding. D.A.I. was supported by the Texas A&M University System Chancellor’s Research Initiative (CRI) funding for the Center for Computational Systems Biology at the Prairie View A&M University.
| Funders | Funder number |
|---|---|
| Prairie View A&M University | |
| Cancer research institute | |
| Texas A and M University |
Keywords
- Akt2
- Dnajc28
- Fn14
- Hippocampus
- Neuropsychiatric lupus
- PI3K-AKT pathway
- Syne2
- TNF-like weak inducer of apoptosis, TWEAK
- Tnfrsf12a
- Tnfsf12
- Transthyretin