title: Expression of transcription factor AP-1 in rat lens epithelial cells during wound repair.
abstract: We examined the spatial and temporal expression patterns of proteins and mRNAs of the components of transcription factor activator protein 1 (AP-1) to examine the activation pattern of lens epithelial cells during lens wound repair following an anterior capsular injury. One eye of adult Wistar rats (n = 106) were used. After making a lens anterior capsule incision with a hypodermic needle, the affected eye was enucleated 0 and 30 min, 1, 3, 5, 8, 10, 15, 20, 24 hr after injury. Forty six globes were processed for in situ hybridization with oligonucleotide probes for c-fos, fosB, c-jun, junB and junD mRNAs, and 60 globes were immunohistochemically analysed using anti-c-Fos and anti-c-Jun antibodies. Normal lens epithelial cells expressed mRNA signals for junD, but not for c-fos, fosB, c-jun, and junB. mRNAs for c-fos, fosB, c-jun, and junB were detected in the whole lens epithelium from the vicinity to the wound to the equator from 30 min to 8 hr post-injury with their peaks after 30 min to 1 hr, but were no longer detected at 10 hr or later. Expression of c-fos mRNA in the equatorial lens cells was more marked than that of c-jun mRNA. Immunohistochemistry showed that c-Fos protein was expressed in the lens epithelial cells in both the anterior and equatorial regions of the injured lens from 1 to 10 hr after injury, and was no longer detected at 12 hr. C-Jun protein was detected only in the equatorial lens cells from 1 to 5 hr after injury, and was no longer detected at 8 hr. Lens epithelial cells except those in the equatorial region did not express c-Jun protein. These findings indicate that transcriptional activation of lens epithelial cells is initiated in the very early phase after the lens injury, i.e. 30 min post-injury, suggesting that AP-1 may play important roles in regulating lens cell behavior during lens wound repair in rats.
authors.affiliation: Department of Ophthalmology, Wakayama Medical University School of Medicine, 811-1 Kimiidera, Wakayama 641-0012, Japan. shizuya@wakayama-med.ac.jp
authors.forename: K
authors.initials: K
authors.lastname: Shirai
authors.forename: Y
authors.initials: Y
authors.lastname: Okada
authors.forename: S
authors.initials: S
authors.lastname: Saika
authors.forename: E
authors.initials: E
authors.lastname: Senba
authors.forename: Y
authors.initials: Y
authors.lastname: Ohnishi
mesh_terms: D000818:Animals; D004847:Epithelial Cells / Q000378:metabolism*; D015870:Gene Expression; D007124:Immunoenzyme Techniques; D017403:In Situ Hybridization; D007903:Lens Capsule, Crystalline / Q000293:injuries / Q000378:metabolism* / Q000473:pathology; D008297:Male; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D018808:Transcription Factor AP-1 / Q000235:genetics / Q000378:metabolism*; D014945:Wound Healing / Q000235:genetics / Q000502:physiology*
chemical_list: D012333:RNA, Messenger; D018808:Transcription Factor AP-1