Retinoic acid promotes migration of MC3T3-E1 osteoblast-like cells via RARα signaling-mediated upregulation of profilin-1 expression

• Material Type: 博士論文
• Title: Retinoic acid promotes migration of MC3T3-E1 osteoblast-like cells via RARα signaling-mediated upregulation of profilin-1 expression
• Author/Editor: 犬伏, 正和
• Author Heading: 犬伏, 正和
• Alternative Title: レチノイン酸はRARαシグナル経路を介してprofilin-1遺伝子発現調節によりMC3T3-E1骨芽細胞様細胞遊走能を向上させる
• Degree grantor/type: 大阪歯科大学
• Date Granted: 2019-12-25
• Dissertation Number: 乙第1623号
• Degree Type: 博士（歯学）
• Text Language Code: eng
• Subject Heading: Retinoic acid (RA); profilin-1; RARα; MC3T3-E1 osteoblast-like cells
• Target Audience: 一般
• Note (General): Retinoic acid (RA) is a vitamin A metabolite required for growth and development of the mammalian body.1–3 In skeletal biology studies, RA promoted bone development and antler bone regeneration.1,4 However, a study in humans showed that serum RA levels outside the normal range elevated the risk of hip fracture.5 In animal studies, doses of RA or injection of vitamin A affected bone mass in a site-specific manner.6,7 Thus, the role of RA in bone health is dependent on cell type, cell function, and tissue. RA binds to heterodimers of retinoic acid receptors (RARs) and retinoid X receptors (RXRs).2,8,9 Upon binding, RARs are translocated to the nucleus where they regulate the transcription of various target genes. This intracellular signaling is the primary biological pathway activated by all-trans-RA.9 There are three subtypes of RAR, α, β and γ, that exhibit specific functions and different localizations in mammalian tissues and cells. The roles of these three subtypes in bone remodeling have been investigated in knockout mouse studies.1,10 Deficiency of RARγ is associated with trabecular bone loss through increased bone resorption. Interestingly, RARα-knockout mice showed normal bone mass and remodeling.1 Therefore, among the RAR subtypes, RARγ is considered the main subtype for maintenance of bone mass.The relationships among bone formation, mineralization, and RA have been extensively investigated in osteoblasts, as bone-forming cells that migrate to resorbing lacunae.1,11–13 Some studies have indicated that addition of RA inhibited osteoblast differentiation, while others have suggested that RA promotes differentiation and bone formation in vivo.14–16 Thus, knowledge on the effects of RA on bone formation in vitro remains inadequate. Consequently, the role of RA both in vivo and in vitro is still under debate. During bone remodeling, osteoblasts associate with one another by moving from their original location to sites of resorbing lacunae on the bone surface. When these cells become condensed within the primordia, they shift from a fibroblastic morphology to a cuboidal morphology and begin to secrete components of the extracellular matrix. Thus, the cells are in direct contact with not only the extracellular environment, but also the neighboring cells. This contact between cells requires cell migration, which is under the control of cytoskeletal actin dynamics.17–19 At present, the relationship between RA and cell migration is well known. In the present study, we examined the relationship between RA and migration of MC3T3-E1 osteoblast-like cells (OBs). The effect of RA on cell migration was found to be mediated by upregulated mRNA expression of certain migration-related genes, mainly profilin-1 (PFN1).; 2019年度
• Access Restrictions: インターネット公開
• Rights (production): CC BY-NC-ND
• Data Provider (Database): 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）; https://irdb.nii.ac.jp
• Original Data Provider (Database): 大阪歯科大学 : 大阪歯科大学学術リポジトリ

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