%0 Journal Article
%T Effects of bFGF on the Modulation of Apoptosis in Gingival Fibroblasts with Different Host Ages
%A Kotaro Tanimoto
%A Satoru Ohkuma
%A Yuki Tanne
%A Ryo Kunimatsu
%A Naoto Hirose
%A Tomomi Mitsuyoshi
%A Yuki Yoshimi
%A Shaoching Su
%A Kazuo Tanne
%J International Journal of Dentistry
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/619580
%X The purpose of this study was to investigate the effects of basic fibroblast growth factor (bFGF) treatment on the proliferation and apoptosis of cultured gingival fibroblasts (GFs). Human GFs were isolated from the palatal gingival tissues of 16 healthy volunteers ranging in the age from 9 to 35 years old. Cultured GFs were subjected to the analyses for cell proliferation by ELISA assay, gene expression by RT-PCR analysis, and apoptosis potency by caspase-3 assay. The cell proliferation activity and gene expression of type-I collagen and caspase-3 activity were enhanced significantly by the treatment with bFGF in cultured GFs. Furthermore, the activity of caspase-3 in cultured GFs from young subjects was significantly higher than that in GFs from adults. It is shown that bFGF significantly enhances the gene expression of type-I collagen in cultured fibroblasts from human gingival tissues. It also demonstrated that bFGF modulates the apoptosis of periodontal fibroblasts, and the effect is higher in young subjects, indicating a significant role of bFGF in the prevention of scar formation during wound healing. 1. Introduction Basic fibroblast growth factor (bFGF) is a multigene family member of structurally related peptide growth factors, and its function is mediated through high-affinity receptors [1]. It is well known that bFGF is a multifunctional cytokine to participate in the process of wound healing, cell proliferation, and apoptosis [2¨C4]. Wound healing can be divided into three consecutive, partly overlapping phases: inflammation, proliferation, and tissue remodeling [5]. The macrophage plays a pivotal role in the transition between wound inflammation and repair, since this cell both scavenges tissue debris and releases a plethora of biologically active substances that include growth factors like bFGF. During the remodeling phase, the number of blood vessels declines and apoptosis of fibroblasts results in scar tissue with a low cell density [6]. Apoptosis is a requisite event for maintaining kinetic homeostasis in continuously renewing tissues such as oral mucosa and skin, and it is suggested to play a crucial role in the repair of connective tissues. Nevertheless, apoptosis is often involved in pathogenetic pathways [7]. Regarding the mechanism of apoptosis induced by bFGF treatment, it has recently been demonstrated that bFGF plays an important role in apoptosis during development of the neural retina. The apoptosis of fibroblasts treated with bFGF was enhanced in both in vivo and in vitro experiments [8, 9]. In dentistry, bFGF was reported to
%U http://www.hindawi.com/journals/ijd/2013/619580/