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Retinoic acid promotes migration of MC3T3-E1 osteoblast-like cells via RARα signaling-mediated upregulation of profilin-1 expression
https://osaka-dent.repo.nii.ac.jp/records/233
https://osaka-dent.repo.nii.ac.jp/records/2334365eca5-0ae5-48b9-bcf5-ba394592a2e4
名前 / ファイル | ライセンス | アクション |
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学位論文 (407.5 kB)
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論文内容要旨・審査結果要旨 (209.3 kB)
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Item type | 学位論文 / Thesis or Dissertation(1) | |||||
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公開日 | 2020-01-20 | |||||
本文言語 | ||||||
言語 | eng | |||||
タイトル | ||||||
タイトル | Retinoic acid promotes migration of MC3T3-E1 osteoblast-like cells via RARα signaling-mediated upregulation of profilin-1 expression | |||||
著者 |
犬伏, 正和
× 犬伏, 正和× Masakazu, Inubushi |
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キーワード | ||||||
主題Scheme | Other | |||||
主題 | Retinoic acid (RA) | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | profilin-1 | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | RARα | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | MC3T3-E1 osteoblast-like cells | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_db06 | |||||
資源タイプ | doctoral thesis | |||||
アクセス権 | ||||||
アクセス権 | open access | |||||
アクセス権URI | http://purl.org/coar/access_right/c_abf2 | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | 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). |
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学位名 | ||||||
学位名 | 博士(歯学) | |||||
学位授与機関 | ||||||
学位授与機関識別子Scheme | kakenhi | |||||
学位授与機関識別子 | 34408 | |||||
学位授与機関名 | 大阪歯科大学 | |||||
学位授与年月日 | ||||||
学位授与年月日 | 2019-12-25 | |||||
学位授与番号 | ||||||
学位授与番号 | 乙第1623号 |