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Query: UMLS:C0848237 (
acute stress
)
4,619
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The [3H]-flunitrazepam receptor density, measured ex vivo in synaptosomes at 4 degrees C, increased by about 30% because of
acute stress
in chicks. This increase was first reported to be a receptor recruitment due to the fact that the increase induced by subsolubilizing concentrations of Triton X-100 was not additive to the receptor increase induced by
acute stress
[J Neural Transm 87 (1992) 97]. In synaptosomal membranes from stressed chicks, the incorporation of alkaline phosphatase or ATP into the lumen abolished or increased, respectively, the receptor unmasking after incubation at 4 and 37 degrees C, suggesting that phosphorylation plays a role in the recruitment mechanism. Moreover, both colchicine and vinblastine, but not taxol, abolished the recruitment induced by stress at 37 degrees C only in synaptosomes, suggesting that micrutubule depolymerization plays a role in the masking of receptors. Furthermore, both cytochalasins C and D induced an increase of the receptor density, abolished by N-ethylmaleimide, in both the stressed and nonstressed conditions, suggesting that microfilament depolymerization induced the exposure to the radioligand of a cytosolic vesicular receptor pool, which had not
fused
yet with the postsynaptic membrane.
...
PMID:Effects of phosphorylation and cytoskeleton-affecting reagents on GABA(A) receptor recruitment into synaptosomes following acute stress. 1217 45
Our previous study had shown that chronic corticosterone (CORT) exposure causes excessive fat deposition in chicken liver, yet it remains unknown whether it is associated with inflammation and fibrosis. In general, heat shock proteins (HSPs) are activated in response to
acute stress
to play a cytoprotective role, and this activation is associated with m
6
A-mediated post-transcriptional regulation. However, changes of HSPs and the m
6
A methylation on their mRNAs in response to chronic CORT treatment in chicken liver have not been reported. In this study, chronic CORT exposure induced inflammation and fibrosis in chicken liver, associated with significantly modulated expression of HSPs that was significantly upregulated at mRNA level yet downregulated at protein level. Concurrently, m
6
A methyltransferases METTL3 content was upregulated together with the level of m
6
A methylation on HSPs transcripts. The m
6
A-seq analysis revealed 2-6 significantly (P < 0.05) hypermethylated m
6
A peaks in the mRNA of 4 different species of HSPs in CORT-treated chicken liver. HSP90B1 transcript had 6 differentially methylated m
6
A peaks among which peaks on exon 16 and exon 17 showed 3.14- and 4.72-fold of increase, respectively. Mutation of the 8 predicted m
6
A sites on exon 16 and exon 17 resulted in a significant (P < 0.05) increase in eGFP-
fused
content of HSP90B1 exon 16 and exon 17 fragment in 293 T cells, indicating a possible role of m
6
A in post-transcriptional regulation of HSPs. In conclusion, chronic CORT exposure induces inflammation and fibrosis in chicken liver along with an increase in the levels and m6A methylation of several HSPs mRNAs; HSPs levels were however reduced under the indicated conditions. Results presented suggest that the reduction in HSPs levels may be associated with m6A methylation in CORT-exposed chickens.
...
PMID:Chronic corticosterone exposure induces liver inflammation and fibrosis in association with m
6
A-linked post-transcriptional suppression of heat shock proteins in chicken. 3174 45
