Abstract:
:When pregnant mice were exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), the average time to eye opening in the offspring was shortened by about a day. How acceleration of eye opening by TCDD occurs remains unknown. To reveal the underlying mechanisms of the accelerated eye opening, pregnant mice were intraperitoneally injected with corn oil or TCDD at GD (gestation day) 11, and tissues around the eye of neonatal mice were subject to proteome analysis and RT-PCR. Upon TCDD administration, translationally controlled tumor protein (TCTP) and 60S acidic ribosomal protein p2 (RLA2) were reduced, while stathmin 1(STMN1) was increased, at both protein and mRNA levels. One hypothetical mechanism for eye opening is the proliferation of corneal epithelial cells before eye opening. STMN1, but not TCTP and RLA2, was up-regulated in immortalized human corneal epithelial cells (HCE-T) by TCDD, which promoted proliferation of HCE-T probably by accelerating the G1/S transition. Down-regulation of STMN1 by the antisense oligonucleotide technology inhibited proliferation of HCE-T, suggesting that STMN1, of which expression is enhanced by TCDD, may be involved in accelerated eye opening, probably by stimulating proliferation of corneal epithelial cells.
journal_name
Toxicol Lettjournal_title
Toxicology lettersauthors
Gin DW,Kim HR,Lee DM,Lee SH,Seong AR,Hwang JA,Park JHdoi
10.1016/j.toxlet.2010.04.001subject
Has Abstractpub_date
2010-07-01 00:00:00pages
87-94issue
2eissn
0378-4274issn
1879-3169pii
S0378-4274(10)01259-2journal_volume
196pub_type
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