{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,19]],"date-time":"2026-05-19T01:48:25Z","timestamp":1779155305047,"version":"3.51.4"},"reference-count":20,"publisher":"SAGE Publications","issue":"6","license":[{"start":{"date-parts":[[1997,6,1]],"date-time":"1997-06-01T00:00:00Z","timestamp":865123200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Dent Res"],"published-print":{"date-parts":[[1997,6]]},"abstract":"<jats:p>Colony-stimulating factor-1 (CSF-1) accelerates tooth eruption in rats and is localized in the dental follicle, a loose connective tissue sac that is necessary for eruption to occur. CSF-1 enhances the cellular events that occur in the follicle prior to eruption-namely, an influx of monocytes into the follicle early post-natally to form the osteoclasts needed to resorb bone for the eruption pathway. Because CSF-1 levels are at a peak at day 3 post-natally, and because CSF-1 has an autocrine effect on its own gene expression, the question remains as to what causes the subsequent decline in CSF-1 protein and mRNA after day 3 post-natally. To determine if the autocrine effect is inhibited through the CSF-1 receptor, analysis of the CSF-1 receptor mRNA levels in cultured dental follicle cells reveals that high concentrations of CSF-1 reduce the gene expression of the CSF-1 receptor. Interleukin la, a molecule that enhances CSF-1 gene expression, has no effect on CSF-1 receptor mRNA levels. Immunostaining for the CSF-1 receptor protein shows that it is present in the dental follicle early post-natally and is either absent or greatly reduced by day 10 post-natally. Earlier studies showed that the mRNA levels of the CSF-1 receptor also parallel this time course. Thus, the above results suggest that the feedback inhibition of the autocrine effect of CSF-1 on its own expression is through the effect of CSF-1 inhibiting the translation and transcription of its receptor. In turn, these molecular interactions possibly regulate the cellular events that occur in the follicle prior to and during eruption.<\/jats:p>","DOI":"10.1177\/00220345970760060301","type":"journal-article","created":{"date-parts":[[2009,1,8]],"date-time":"2009-01-08T19:39:42Z","timestamp":1231443582000},"page":"1244-1249","source":"Crossref","is-referenced-by-count":9,"title":["Localization and Expression of CSF-1 Receptor in Rat Dental Follicle Cells"],"prefix":"10.1177","volume":"76","author":[{"given":"G.E.","family":"Wise","sequence":"first","affiliation":[{"name":"Department of Veterinary Anatomy and Cell Biology, School of Veterinary Medicine, Louisiana State University, Baton Rouge, Louisiana 70803-8408, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"L.","family":"Zhao","sequence":"additional","affiliation":[{"name":"Department of Veterinary Anatomy and Cell Biology, School of Veterinary Medicine, Louisiana State University, Baton Rouge, Louisiana 70803-8408, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"suffix":"IV","given":"R.L.","family":"Grier","sequence":"additional","affiliation":[{"name":"Department of Veterinary Anatomy and Cell Biology, School of Veterinary Medicine, Louisiana State University, Baton Rouge, Louisiana 70803-8408, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[1997,6,1]]},"reference":[{"key":"atypb1","doi-asserted-by":"publisher","DOI":"10.1007\/BF00302072"},{"key":"atypb2","doi-asserted-by":"publisher","DOI":"10.3109\/08977199209026928"},{"key":"atypb3","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0714.1980.tb00377.x"},{"key":"atypb4","unstructured":"Cielinski MJ, Jolie M., Wise GE, Ando DG, Marks SC Jr (1994). Colony-stimulating factor-1 (CSF-1) is a potent stimulator of tooth eruption in the rat. In: Biological mechanisms of tooth eruption, resorption and replacement by implants. Davidovitch Z, editor. 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