Changes in biological characteristics during the cellular aging of ligament fibroblasts derived from patients with prolapsus uteri.
Prolapsus uteri in pelvic support disorders are common in elderly women. The etiology is unclear and more likely to be multifactorial. We examined changes in biological characteristics and responsiveness to growth factors during the in vitro cellular aging of cardinal ligamental fibroblasts derived from patients with prolapsus uteri (HPLiF), and compared them with those of cells from age-matched control subjects (HCLiF). HPLiF and HCLiF had almost the same in vitro life span and the age-related patterns of biological parameters were essentially the same. However, the saturation density was significantly higher in HPLiF than in HCLiF. Furthermore, the high proliferative activity of HPLiF to serum mitogens, especially to platelet-derived growth factor, was retained throughout the in vitro life span. p53 protein levels in HPLiF increased at late passages, but were significantly less than in aged HCLiF. These results indicate that the higher proliferative activity in prolapsus fibroblasts may result from the decreased expression of p53 protein and may lead to a decrease in the synthesis and deposition of extracellular matrix components. These results support the hypothesis that functional alterations in ligament fibroblasts are involved in the mechanism of the development of prolapsus uteri.
Yamamoto
M
M
Department of Cell Biology, Tokyo Metropolitan Institute of Gerontology, 35-2 Sakae-cho, Itabashi-ku, 173, Tokyo, Japan.
Akazawa
K
K
Aoyagi
M
M
Yamamoto
K
K
D000368:Aged; D000369:Aged, 80 and over; D016022:Case-Control Studies; D016922:Cellular Senescence / Q000235:genetics / Q000502:physiology; D004247:DNA / Q000096:biosynthesis; D005260:Female; D005347:Fibroblasts / Q000378:metabolism / Q000473:pathology; D015870:Gene Expression; D016158:Genes, p53; D006801:Humans; D066298:In Vitro Techniques; D008022:Ligaments / Q000378:metabolism / Q000473:pathology*; D008875:Middle Aged; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism; D014596:Uterine Prolapse / Q000235:genetics / Q000378:metabolism / Q000473:pathology*
D012333:RNA, Messenger; D016159:Tumor Suppressor Protein p53; D004247:DNA