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2017 ; 14
(1
): 215
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DHCR24 exerts neuroprotection upon inflammation-induced neuronal death
#MMPMID29115990
Martiskainen H
; Paldanius KMA
; Natunen T
; Takalo M
; Marttinen M
; Leskelä S
; Huber N
; Mäkinen P
; Bertling E
; Dhungana H
; Huuskonen M
; Honkakoski P
; Hotulainen P
; Rilla K
; Koistinaho J
; Soininen H
; Malm T
; Haapasalo A
; Hiltunen M
J Neuroinflammation
2017[Nov]; 14
(1
): 215
PMID29115990
show ga
BACKGROUND: DHCR24, involved in the de novo synthesis of cholesterol and
protection of neuronal cells against different stress conditions, has been shown
to be selectively downregulated in neurons of the affected brain areas in
Alzheimer's disease. METHODS: Here, we investigated whether the overexpression of
DHCR24 protects neurons against inflammation-induced neuronal death using
co-cultures of mouse embryonic primary cortical neurons and BV2 microglial cells
upon acute neuroinflammation. Moreover, the effects of DHCR24 overexpression on
dendritic spine density and morphology in cultured mature mouse hippocampal
neurons and on the outcome measures of ischemia-induced brain damage in vivo in
mice were assessed. RESULTS: Overexpression of DHCR24 reduced the loss of neurons
under inflammation elicited by LPS and IFN-? treatment in co-cultures of mouse
neurons and BV2 microglial cells but did not affect the production of
neuroinflammatory mediators, total cellular cholesterol levels, or the activity
of proteins linked with neuroprotective signaling. Conversely, the levels of
post-synaptic cell adhesion protein neuroligin-1 were significantly increased
upon the overexpression of DHCR24 in basal growth conditions. Augmentation of
DHCR24 also increased the total number of dendritic spines and the proportion of
mushroom spines in mature mouse hippocampal neurons. In vivo, overexpression of
DHCR24 in striatum reduced the lesion size measured by MRI in a mouse model of
transient focal ischemia. CONCLUSIONS: These results suggest that the
augmentation of DHCR24 levels provides neuroprotection in acute stress
conditions, which lead to neuronal loss in vitro and in vivo.
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