Effects of ageing on proliferative ability, and the expressions of secreted protein, acidic and rich in cysteine (SPARC) and osteoprotegerin (osteoclastogenesis inhibitory factor) in cultures of human periodontal ligament cells.
Secreted protein, acidic and rich in cysteine (SPARC) has been suggested to play an important role in wound repair and mineralization. Osteoprotegerin/osteoclastogenesis inhibitory factor (OPG/OCIF) is a secreted protein that inhibits the maturation, activity and survival of osteoclasts. An examination of the changes in expression of these proteins as well as their proliferative ability according to ageing in cultured cells may elucidate characteristic changes in periodontal tissues induced by ageing. In the present study, proliferative ability and the expression of SPARC and OPG/OCIF were compared between cultures of human periodontal ligament (HPL) cells obtained from young and senior donors (in vivo cellular ageing) as well as in cultures of HPL cells at early and late passages (in vitro cellular ageing). Cumulative population doubling levels and cell population doubling time of HPL cells from young donors were greater and shorter, respectively, than those of HPL cells from senior donors. Levels of SPARC mRNA in HPL cells increased with cellular ageing in vivo. No change in the levels of OPG/OCIF mRNA in HPL cells with cellular ageing in vivo was observed. The changes in proliferative ability and the mRNA levels of SPARC and OPG/OCIF with cellular ageing in vitro were similar to those with ageing in vivo. This study demonstrated for the first time a relationship between in vivo and in vitro cellular ageing in the functional changes in HPL cells. These findings suggest that the impairment of periodontal ligament repair with ageing is due to the decrease in proliferative ability in HPL cells with ageing. Furthermore, the increase in SPARC with ageing may be related to changes in metabolism of periodontal ligament that occur with ageing.
Shiba
H
H
Department of Periodontology and Endodontology, Hiroshima University Faculty of Dentistry, 1-2-3, Kasumi, Minami-ku, 734-8553, Hiroshima, Japan.
Nakanishi
K
K
Sakata
M
M
Fujita
T
T
Uchida
Y
Y
Kurihara
H
H
D000328:Adult; D000375:Aging / Q000378:metabolism*; D002455:Cell Division; D002478:Cells, Cultured; D005260:Female; D005347:Fibroblasts / Q000166:cytology / Q000378:metabolism; D006023:Glycoproteins / Q000235:genetics / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D015676:Osteonectin / Q000235:genetics / Q000378:metabolism*; D053244:Osteoprotegerin; D010513:Periodontal Ligament / Q000166:cytology / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D018160:Receptors, Cytoplasmic and Nuclear / Q000235:genetics / Q000502:physiology*; D018124:Receptors, Tumor Necrosis Factor
D006023:Glycoproteins; D015676:Osteonectin; D053244:Osteoprotegerin; D012333:RNA, Messenger; D018160:Receptors, Cytoplasmic and Nuclear; D018124:Receptors, Tumor Necrosis Factor; C506030:TNFRSF11B protein, human