Immunostaining and transcriptional enhancement of interleukin-1 receptor type I in the rat dental follicle.
Interleukin-1alpha (IL-1alpha) enhances the gene expression of colony-stimulating factor-one (CSF-1) in dental follicle cells. In turn, CSF-1 appears to be a critical molecule in stimulating the cellular events of eruption that require the presence of the follicle. Chronologically, the maximal transcription and translation of CSF-1 in the follicle occurs early postnatally, followed by a decline later. Thus, in this study, immunostaining for the interleukin-1 receptor type I (IL-1RI) was used to determine if it paralleled the CSF-1 localization and chronology. The results showed that IL-1RI is primarily localized in the dental follicle, with maximal immunostaining early postnatally and a greatly reduced staining by day 10. In conjunction with this, molecules that enhance the gene expression of IL-1alpha epidermal growth factor (EGF) and transforming growth factor-beta1 (TGF-beta1) were also shown to enhance the expression of IL-1RI, but IL-1alpha did not increase the gene expression of IL-1RI. After injections of EGF at different times postnatally the mRNA of IL-1RI increased over comparable controls. Between days 2 and 5 the IL-1RI mRNA in the follicle decreased. In combination the results suggest that, as the expression of IL-1alpha is enhanced in the stellate reticulum either by EGF or TGF-beta1, these two molecules could also enhance the expression of IL-1RI in the dental follicle such that more receptors would be available to respond to the increased IL-1alpha secreted. The maximal presence of the receptors (IL-1RI) in the dental follicle early postnatally, followed by their subsequent decline, parallels the rise and fall of CSF-1 in the follicle. Thus, regulation of the IL-1RI and IL-1RI gene expression might be a means of regulating changes in CSF-1 in the follicle.
Wise
G E
GE
Department of Veterinary Anatomy and Cell Biology, School of Veterinary Medicine, Louisiana State University, Baton Rouge 70803-8408, USA.
Zhao
L
L
D000375:Aging / Q000235:genetics; D000818:Animals; D004396:Coloring Agents; D003795:Dental Sac / Q000378:metabolism / Q000648:ultrastructure*; D004658:Enamel Organ / Q000378:metabolism / Q000648:ultrastructure; D004815:Epidermal Growth Factor / Q000032:analysis / Q000235:genetics; D005786:Gene Expression Regulation; D007124:Immunoenzyme Techniques; D007375:Interleukin-1 / Q000032:analysis / Q000235:genetics; D016173:Macrophage Colony-Stimulating Factor / Q000235:genetics; D016133:Polymerase Chain Reaction; D014176:Protein Biosynthesis; D012333:RNA, Messenger / Q000032:analysis / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D017472:Receptors, Interleukin-1 / Q000032:analysis* / Q000235:genetics; D014078:Tooth Eruption / Q000235:genetics; D014158:Transcription, Genetic; D016212:Transforming Growth Factor beta / Q000032:analysis / Q000235:genetics
D004396:Coloring Agents; D007375:Interleukin-1; D012333:RNA, Messenger; D017472:Receptors, Interleukin-1; D016212:Transforming Growth Factor beta; D004815:Epidermal Growth Factor; D016173:Macrophage Colony-Stimulating Factor