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Tetracycline administration increases protein (presumably procollagen) synthesis and secretion in periodontal ligament fibroblasts of streptozotocininduced diabetic rats
Author(s) -
Sasaki Takahisa,
Ramamurthy Nungavaram S.,
Yu Zhao,
Golub Lome M.
Publication year - 1992
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/j.1600-0765.1992.tb01747.x
Subject(s) - periodontal fiber , streptozotocin , minocycline , endocrinology , fibroblast , medicine , procollagen peptidase , secretion , hydroxyproline , chemistry , collagenase , perfusion , tetracycline , proline , diabetes mellitus , in vitro , biochemistry , antibiotics , dentistry , enzyme , amino acid
Streptozotocin‐induced, insulin‐deficient diabetic adult rats were daily administrated either minocycline or a chemically‐modified non‐antimicrobial tetracycline (CMT) by oral gavage for a 3‐week time period; untreated diabetic and non‐diabetic rats served as controls. On day 21, all rats received an intravenous injection of 3 H‐proline followed by perfusion fixation with an aldehyde mixture at 20 minutes and 4 hours after isotope injection. The upper and lower mandibles of these rats were dissected and processed for quantitative electron microscopic autoradiography to study 3 H‐proline utilization by fibroblasts in the periodontal ligament (PDL) of molars. In the non‐diabetic controls, at 20 min after 3 H‐proline injection, radioprecursor was incorporated by the Golgi‐RER system of PDL fibroblasts. At the 4‐h time period, most of the label was present over the collagen fibers around these cells. In contrast, PDL fibroblasts in the untreated diabetic rats showed marked abnormalities ultrastructurally and minimal uptake (20 min) and secretion (4 h) of labeled proline. At both time periods, in both minocycline‐ and CMT‐treated diabetic rats, fibroblasts were structurally more normal and the radioprecursor was localized in the fibroblasts and the PDL matrix in a pattern similar to that seen in the control rats. These results suggest that the diabetes‐induced structural abnormalities and suppression of synthesis and secretion of protein (presumably collagen and its precursor) by PDL fibroblasts can be restored to near‐normal by administration of a tetracycline and that this effect is mediated by a non‐antimicrobial property of this family of antibiotics.