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IFN‐γ‐induced BACE1 expression is mediated by activation of JAK2 and ERK1/2 signaling pathways and direct binding of STAT1 to BACE1 promoter in astrocytes
Abstract
β‐Site APP cleaving enzyme 1 (BACE1) is an essential enzyme for the production of β amyloid. Since we found that injection of interferon‐γ (IFN‐γ) into young mouse brains increased BACE1 expression in astrocytes, we investigated molecular mechanisms underlying this process by cloning a putative BACE1 promoter. BACE1 promoter activity was differentially regulated by IFN‐γ in a region specific manner and down‐regulated by an inhibitor of Janus kinase 2 (JAK2). A dominant negative mutant of signal transducer and activator of transcription 1 (STAT1) expression suppressed BACE1 promoter activity, and this was rescued by transfecting wild type STAT1. Electrophoretic mobility shift assay and promoter activity assays indicated that STAT1 binds directly to the putative STAT1 binding sequence of BACE1 promoter. Because IFN‐γ treatment induced STAT1 phosphorylation, we examined whether the expression of a suppressor of cytokine signaling (SOCS), negative regulator of JAK2, suppresses BACE1 promoter activity. The results show that SOCS1 or SOCS3 expression suppressed BACE1 promoter by blocking phosphorylation of Tyr701 residue in STAT1. Also, because IFN‐γ treatment specifically potentiated extracellular signal regulated MAP kinase (ERK) 1/2 activation, pretreatment of mitogen‐activated or extracellular signal‐regulated protein kinase (MEK) inhibitor, PD98059, significantly attenuated IFN‐γ‐induced BACE1 promoter activity and protein expression through blocking phosphorylation of Ser727 residue in STAT1, suggesting that ERK1/2 is associated with IFN‐γ‐induced STAT1 signaling cascade. Taken together, our results suggest that IFN‐γ activates JAK2 and ERK1/2 and then phosphorylated STAT1 binds to the putative STAT1 binding sequences in BACE1 promoter region to modulate BACE1 protein expression in astrocytes. © 2006 Wiley‐Liss, Inc.
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The action of STAT1 can be inhibited by SOCS1 and 3, which prevent phosphorylation of STAT1 on the Tyrosine 701 residue.
“This action of STAT1 can be inhibited by suppressor of cytokine signaling (SOCS) 1 and 3, which prevent phosphorylation of STAT1 on the Tyrosine 701 residue.”
From BACE1: More than just a β‐secretase (2022) · cites this paper as [52]
Phosphorylation of STAT1 leads to its binding of the BACE1 promoter, increasing BACE1 gene expression.
“The phosphorylation of STAT1 leads to its binding of the BACE1 promoter, increasing BACE1 gene expression.”
From BACE1: More than just a β‐secretase (2022) · cites this paper as [52]
The pro-inflammatory cytokine interferon-gamma causes an increase in BACE1 through subsequent JAK2 and MAP kinase signaling causing phosphorylation of STAT1.
“The pro‐inflammatory cytokine interferon‐gamma (IFNy) causes an increase in BACE1 through subsequent Janus Kinase 2 (JAK2) and mitogen activated protein (MAP) kinase signaling causing phosphorylation of STAT1.”
From BACE1: More than just a β‐secretase (2022) · cites this paper as [52]
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Vassar, R., Bennett, B. D., Babu-Khan, S., Kahn, S., Mendiaz, E. A., Denis, P., Teplow, D. B., Ross, S., Amarante, P., Loeloff, R., et al. (1999) · Science · doi:10.1126/science.286.5440.735 · Cited by 3,876 · cited 1×
“…and neuronal loss (Citron, 2004; Selkoe, 1994). b-Amyloid (Ab) is a major constituent of senile plaque and is derived from the sequential proteolytic cleavage of amyloid precursor protein (APP) by b- and g-secretases (Haass and Selkoe, 1993; Hardy and Selkoe, 2002; Vassar and Citron, 2003).”
BackgroundOxidative Damage Is the Earliest Event in Alzheimer Disease
Nunomura, A., Perry, G., Aliev, G., Hirai, K., Takeda, A., Balraj, E. K., Jones, P. K., Ghanbari, H., Wataya, T., Shimohama, S., et al. (2001) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/60.8.759 · Cited by 1,885
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“For example, knock out of the presenilin 1 (PS1) gene, which is a core component of g-secretase complex, resulted in lethality in a mouse model at the embryonic stage (Geling et al., 2002; Shen et al., 1997).”
BackgroundERK1/2 is an endogenous negative regulator of the γsecretase activity
Kim, S., Park, H., Hong, H. S., Baik, E. J., Jung, M. W., & Mook‐Jung, I. (2006) · The FASEB Journal · doi:10.1096/fj.05-4055fje · Cited by 92 · cited 1×
“About 1.2 3 105 cells were seeded in 12-well tissue culture plates and transfected with 0.5 lg BACE1 promoter constructs using Lipofectamine reagent and Plus reagent (Invitrogen, Carlsbad, CA) (Kim et al., 2005). pRL-TK plasmid (0.1 lg) was cotransfected to normalize transfection efficiencies.”
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BACE1: More than just a β‐secretase
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Microglia and Astrocytes in Alzheimer’s Disease: Significance and Summary of Recent Advances
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Metadata
- Authors
- Cho, H. J., Kim, S., Jin, S. M., Hwang, E., Kim, Y. S., Huh, K., & Mook‐Jung, I.
- Venue
- Glia
- Publisher
- Wiley
- Published
- 2006-11-07
- Volume
- 55
- Issue
- 3
- Pages
- 253-262
- ISSN
- 0894-1491
- 1098-1136
- Cited by
- 98
- References
- 4
- Language
- en
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