骨形态发生蛋白

Bone morphogenetic proteins.

作者信息

Chen Di, Zhao Ming, Mundy Gregory R

机构信息

School of Medicine and Dentistry, Department of Orthopaedics, University of Rochester, Rochester, NY 14642, USA.

出版信息

Growth Factors. 2004 Dec;22(4):233-41. doi: 10.1080/08977190412331279890.

Abstract

Bone morphogenetic proteins (BMPs) are multi-functional growth factors that belong to the transforming growth factor beta (TGFbeta) superfamily. The roles of BMPs in embryonic development and cellular functions in postnatal and adult animals have been extensively studied in recent years. Signal transduction studies have revealed that Smad1, 5 and 8 are the immediate downstream molecules of BMP receptors and play a central role in BMP signal transduction. Studies from transgenic and knockout mice and from animals and humans with naturally occurring mutations in BMPs and related genes have shown that BMP signaling plays critical roles in heart, neural and cartilage development. BMPs also play an important role in postnatal bone formation. BMP activities are regulated at different molecular levels. Preclinical and clinical studies have shown that BMP-2 can be utilized in various therapeutic interventions such as bone defects, non-union fractures, spinal fusion, osteoporosis and root canal surgery. Tissue-specific knockout of a specific BMP ligand, a subtype of BMP receptors or a specific signaling molecule is required to further determine the specific role of a BMP ligand, receptor or signaling molecule in a particular tissue. BMPs are members of the TGFbeta superfamily. The activity of BMPs was first identified in the 1960s (Urist, M.R. (1965) "Bone formation by autoinduction", Science 150, 893-899), but the proteins responsible for bone induction remained unknown until the purification and sequence of bovine BMP-3 (osteogenin) and cloning of human BMP-2 and 4 in the late 1980s (Wozney, J.M. et al. (1988) "Novel regulators of bone formation: molecular clones and activities", Science 242, 1528-1534; Luyten, F.P. et al. (1989) "Purification and partial amino acid sequence of osteogenin, a protein initiating bone differentiation", J. Biol. Chem. 264, 13377-13380; Wozney, J.M. (1992) "The bone morphogenetic protein family and osteogenesis", Mol. Reprod. Dev. 32, 160-167). To date, around 20 BMP family members have been identified and characterized. BMPs signal through serine/threonine kinase receptors, composed of type I and II subtypes. Three type I receptors have been shown to bind BMP ligands, type IA and IB BMP receptors (BMPR-IA or ALK-3 and BMPR-IB or ALK-6) and type IA activin receptor (ActR-IA or ALK-2) (Koenig, B.B. et al. (1994) "Characterization and cloning of a receptor for BMP-2 and BMP-4 from NIH 3T3 cells", Mol. Cell. Biol. 14, 5961-5974; ten Dijke, P. et al. (1994) "Identification of type I receptors for osteogenic protein-1 and bone morphogenetic protein-4", J. Biol. Chem. 269, 16985-16988; Macias-Silva, M. et al. (1998) "Specific activation of Smad1 signaling pathways by the BMP7 type I receptor, ALK2", J. Biol. Chem. 273, 25628-25636). Three type II receptors for BMPs have also been identified and they are type II BMP receptor (BMPR-II) and type II and IIB activin receptors (ActR-II and ActR-IIB) (Yamashita, H. et al. (1995) "Osteogenic protein-1 binds to activin type II receptors and induces certain activin-like effects", J. Cell. Biol. 130, 217-226; Rosenzweig, B.L. et al. (1995) "Cloning and characterization of a human type II receptor for bone morphogenetic proteins", Proc. Natl Acad. Sci. USA 92, 7632-7636; Kawabata, M. et al. (1995) "Cloning of a novel type II serine/threonine kinase receptor through interaction with the type I transforming growth factor-beta receptor", J. Biol. Chem. 270, 5625-5630). Whereas BMPR-IA, IB and II are specific to BMPs, ActR-IA, II and IIB are also signaling receptors for activins. These receptors are expressed differentially in various tissues. Type I and II BMP receptors are both indispensable for signal transduction. After ligand binding they form a heterotetrameric-activated receptor complex consisting of two pairs of a type I and II receptor complex (Moustakas, A. and C.H. Heldi (2002) "From mono- to oligo-Smads: the heart of the matter in TGFbeta signal transduction" Genes Dev. 16, 67-871). The type I BMP receptor substrates include a protein family, the Smad proteins, that play a central role in relaying the BMP signal from the receptor to target genes in the nucleus. Smad1, 5 and 8 are phosphorylated by BMP receptors in a ligand-dependent manner (Hoodless, P.A. et al. (1996) "MADR1, a MAD-related protein that functions in BMP2 signaling pathways", Cell 85, 489-500; Chen Y. et al. (1997) "Smad8 mediates the signaling of the receptor serine kinase", Proc. Natl Acad. Sci. USA 94, 12938-12943; Nishimura R. et al. (1998) "Smad5 and DPC4 are key molecules in mediating BMP-2-induced osteoblastic differentiation of the pluripotent mesenchymal precursor cell line C2C12", J. Biol. Chem. 273, 1872-1879). After release from the receptor, the phosphorylated Smad proteins associate with the related protein Smad4, which acts as a shared partner. This complex translocates into the nucleus and participates in gene transcription with other transcription factors (). A significant advancement about the understanding of in vivo functions of BMP ligands, receptors and signaling molecules has been achieved in recent years.

摘要

骨形态发生蛋白(BMPs)是多功能生长因子,属于转化生长因子β(TGFβ)超家族。近年来,BMPs在胚胎发育以及出生后和成年动物细胞功能中的作用得到了广泛研究。信号转导研究表明,Smad1、5和8是BMP受体的直接下游分子,在BMP信号转导中起核心作用。对转基因和基因敲除小鼠以及BMPs和相关基因发生自然突变的动物和人类的研究表明,BMP信号在心脏、神经和软骨发育中起关键作用。BMPs在出生后的骨形成中也起重要作用。BMP的活性在不同分子水平上受到调节。临床前和临床研究表明,BMP-2可用于各种治疗干预,如骨缺损、骨折不愈合、脊柱融合、骨质疏松症和根管手术。需要对特定的BMP配体、BMP受体亚型或特定信号分子进行组织特异性敲除,以进一步确定BMP配体、受体或信号分子在特定组织中的具体作用。BMPs是TGFβ超家族的成员。BMP的活性最早于20世纪60年代被发现(Urist,M.R.(1965年)“通过自诱导形成骨”,《科学》150,893 - 899),但直到20世纪80年代后期牛BMP-3(骨生成素)的纯化和测序以及人BMP-2和4的克隆,负责骨诱导的蛋白质才得以明确(Wozney,J.M.等人(1988年)“骨形成的新型调节因子:分子克隆和活性”,《科学》242,1528 - 1534;Luyten,F.P.等人(1989年)“骨生成素的纯化和部分氨基酸序列,一种启动骨分化的蛋白质”,《生物化学杂志》264,13377 - 13380;Wozney,J.M.(1992年)“骨形态发生蛋白家族与骨生成”,《分子生殖与发育》32,160 - 167)。迄今为止,已鉴定和表征了约20个BMP家族成员。BMP通过由I型和II型亚型组成的丝氨酸/苏氨酸激酶受体发出信号。已证明三种I型受体可结合BMP配体,即IA型和IB型BMP受体(BMPR-IA或ALK-3以及BMPR-IB或ALK-6)和IA型激活素受体(ActR-IA或ALK-2)(Koenig,B.B.等人(1994年)“来自NIH 3T3细胞的BMP-2和BMP-4受体的表征和克隆”,《分子细胞生物学》14,5961 - 5974;ten Dijke,P.等人(1994年)“成骨蛋白-1和骨形态发生蛋白-4的I型受体的鉴定”,《生物化学杂志》269,16985 - 16988;Macias-Silva,M.等人(1998年)“BMP7 I型受体ALK2对Smad1信号通路的特异性激活”,《生物化学杂志》273,25628 - 25636)。也已鉴定出三种BMP的II型受体,它们是II型BMP受体(BMPR-II)以及II型和IIB型激活素受体(ActR-II和ActR-IIB)(Yamashita,H.等人(1995年)“成骨蛋白-1与激活素II型受体结合并诱导某些激活素样效应”,《细胞生物学杂志》130,217 - 226;Rosenzweig,B.L.等人(1995年)“人骨形态发生蛋白II型受体的克隆和表征”,《美国国家科学院院刊》92,7632 - 7636;Kawabata,M.等人(1995年)“通过与I型转化生长因子-β受体相互作用克隆新型II型丝氨酸/苏氨酸激酶受体”,《生物化学杂志》270,5625 - 5630)。虽然BMPR-IA、IB和II对BMP具有特异性,但ActR-IA、II和IIB也是激活素的信号受体。这些受体在各种组织中差异表达。I型和II型BMP受体对于信号转导都是必不可少的。配体结合后,它们形成由两对I型和II型受体复合物组成的异源四聚体激活受体复合物(Moustakas,A.和C.H. Heldi(2002年)“从单聚体到寡聚体Smads:TGFβ信号转导的核心问题”,《基因与发育》16,67 - 871)。I型BMP受体底物包括一个蛋白质家族,即Smad蛋白,它们在将BMP信号从受体传递到细胞核中的靶基因方面起核心作用。Smad1、5和8以配体依赖性方式被BMP受体磷酸化(Hoodless,P.A.等人(1996年)“MADR1,一种在BMP2信号通路中起作用的与MAD相关的蛋白质”,《细胞》85,489 - 500;Chen Y.等人(1997年)“Smad8介导受体丝氨酸激酶的信号传导”,《美国国家科学院院刊》94,12938 - 12943;Nishimura R.等人(1998年)“Smad5和DPC4是介导BMP-2诱导多能间充质前体细胞系C2C12成骨细胞分化的关键分子”,《生物化学杂志》273,1872 - 1879)。从受体释放后,磷酸化的Smad蛋白与相关蛋白Smad4结合,Smad4作为共享伙伴。该复合物易位到细胞核中并与其他转录因子一起参与基因转录()。近年来,在对BMP配体、受体和信号分子体内功能的理解方面取得了重大进展。

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