张彦定
主要进行器官发育的分子机制和利用干细胞进行器官再生的研究工作。
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- 姓名:张彦定
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学术头衔:
博士生导师
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学科领域:
生物化学
- 研究兴趣:主要进行器官发育的分子机制和利用干细胞进行器官再生的研究工作。
张彦定教授(博士生导师)。1982年福建师范大学本科毕业(1985年获硕士/2005年获博士学位)。1985年至今,福建师大生命科学学院任助教,讲师,副教授,教授。其间多次出国深造,分别在澳大利亚Flinders大学,美国犹他(Utah)大学,美国哈佛大学和美国Tulane大学进修和合作研究。现任生命科学学院院长,福建省发育与神经生物学重点实验室主任,福建省生物医学工程学会理事长,福建省生物化学及分子生物学学会常务理事,福建省遗传学会副理事长,福建省细胞生物学学会常务理事。承担“发育生物学”,“分子生物学”和“分子生物学实验技术”等本科和研究生教学,省级“分子生物学”精品课程负责人, 国家级生物学实验教学中心主任。主要进行器官发育的分子机制和利用干细胞进行器官再生的研究工作。曾获国家教委科技进步二等奖,福建省科技进步三等奖。先后主持国家自然科学基金项目6项和省部级科技项目多项。在国内外学术刊物发表论文50多篇,其中有20多篇被SCI收录。
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581
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成果数
15
【期刊论文】Induction of human keratinocytes into enamel-secreting ameloblasts
张彦定, Bingmei Wang a, , Liwen Li a, Shengrong Du a, Chao Liu b, Xin Lin a, b, YiPing Chen a, *, Yanding Zhang a
Developmental Biology 344(2010)795-799,-0001,():
-1年11月30日
Mammalian tooth development relies heavily on the reciprocal and sequential interactions between cranial neural crest-derived mesenchymal cells and stomadial epithelium. During mouse tooth development, odontogenic potential, that is, the capability to direct an adjacent tissue to form a tooth, resides in dental epithelium initially, and shifts subsequently to dental mesenchyme. Recent studies have shown that mouse embryonic dental epithelium possessing odontogenic potential is able to induce the formation of a bioengineered tooth crown when confronted with postnatal mesenchymal stem cells of various sources. Despite many attempts, however, postnatal stem cells have not been used successfully as the epithelial component in the generation of a bioengineered tooth. We show here that epithelial sheets of cultured human keratinocytes, when recombined with mouse embryonic dental mesenchyme, are able to support tooth formation. Most significantly, human keratinocytes, recombined with mouse embryonic dental mesenchyme in the presence of exogenous FGF8, are induced to express the dental epithelial marker PITX2 and differentiate into enamel-secreting ameloblasts that develop a human–mouse chimeric whole tooth crown. We conclude that in the presence of appropriate odontogenic signals, human keratinocytes can be induced to become odontogenic competent; and that these are capable of participating in tooth crown morphogenesis and differentiating into ameloblasts. Our studies identify human keratinocytes as a potential cell source for in vitro generation of bioengineered teeth that may be used in replacement therapy.
Bioengineered tooth, Human keratinocyte stem cell, Mouse dental mesenchyme, FGF8
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【期刊论文】Mesenchyme is Responsible for Tooth Suppression in the Mouse Lower Diastema
张彦定, G.H. Yuan?, L. Zhang?, Y.D. Zhang, M.W. Fan, Z. Bian, and Z. Chen*
J Dent Res 87(4): 386-390, 2008,-0001,():
-1年11月30日
Between the incisor and molars in each dental quadrant, mice have a toothless gap (diastema) that may contain vestigial tooth primordia. It is still not clear whether suppression of odonto genesis in the mouse lower diastema can be attributed to epithelium, mesenchyme, or both. Therefore, using recombination experiments with mouse tissues from E11.5 and E13.5 stages, we investigated whether the epithelium or mesenchyme is responsible for the suppression of odontogenesis. Five groups of recombinants were established and cultured under mouse kidney capsules. The results demonstrated that at E11.5, the lower diastemal epithelium and mesenchyme possessed odontogenic potential and competence, respectively; at E13.5, both the lower diastemal epithelium and mesenchyme had odontogenic competence, while the lower diastemal mesen-chyme did not possess odontogenic potential. On the basis of comparison of the odontogenic capabilities between the lower diastemal and molar tooth primordia, we conclude that mesenchyme is responsible for tooth regression in the mouse lower diastema. Abbreviations used in this paper: E, embryonic day; Dia, diastema; Mol, molar; BA1, first branchial arch; BA2, second branchial arch; MS, mesial segment; R2, lower second rudimentary segment; M1, first lower molar.
Mouse diastema, odontogenic competence, odontogenic potential, recombination, tooth rudiments.,
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【期刊论文】Expression Survey of Genes Critical for Tooth Development in the Human Embryonic Tooth Germ
张彦定, Dahe Lin, Yide Huang, , Fenglei He, Shuping Gu, Guozhong Zhang, YiPing Chen, * and Yanding Zhang, *
DEVELOPMENTAL DYNAMICS 236: 1307-1312, 2007,-0001,():
-1年11月30日
In the developing murine tooth, the expression patterns of numerous regulatory genes have been examined and their roles have begun to be revealed. To unveil the molecular mechanisms that regulate human tooth morphogenesis, we examined the expression patterns of several regulatory genes, including BMP4, FGF8, MSX1, PAX9, PITX2, and SHOX2, and compared them with that found in mice. All of these genes are known to play critical roles in murine tooth development. Our results show that these genes exhibit basically similar expression patterns in the human tooth germ compared with that in the mouse. However, slightly different expression patterns were also observed for some of the genes at certain stages. For example, MSX1 expression was detected in the inner enamel epithelium in addition to the dental mesenchyme at the bell stage of the human tooth. Moreover, FGF8 expression remained in the dental epithelium at the cap stage, while PAX9 and SHOX2 expression was detected in both dental epithelium and mesenchyme of the human tooth germ. Our results indicate that, although slight differences exist in the gene expression patterns, the human and mouse teeth not only share considerable homology in odontogenesis but also use similar underlying molecular networks. Developmental Dynamics 236: 1307-1312, 2007.
human tooth germ, gene expression, trans, c, r, i, p, t, ional factors, growth factors
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张彦定, Yiqiang Song, ? Zunyi Zhang, ?? Xueyan Yu, Minquan Yan, Xiaoyun Zhang, ? Shuping Gu, Thomas Stuart, Chao Liu, Jakob Reiser, Yanding Zhang, and Yiping Chen, *
DEVELOPMENTAL DYNAMICS 235: 1334-1344, 2006,-0001,():
-1年11月30日
RNA interference (RNAi) has recently become a powerful tool to silence gene expression in mammalian cells, but its application in assessing gene function in mammalian developing organs remains highly limited. Here we describe several unique developmental properties of the mouse molar germ. Embryonic molar mesenchyme, but not the incisor mesenchyme, once dissociated into single cell suspension and re-aggregated, retains its odontogenic potential, the capability of a tissue to instruct an adjacent tissue to initiate tooth formation. Dissociated molar mesenchymal cells, even after being plated in cell culture, retain odontogenic competence, the capability of a tissue to respond to odontogenic signals and to support tooth formation. Most interestingly, while dissociated epithelial and mesenchymal cells of molar tooth germ are mixed and re-aggregated, the epithelial cells are able to sort out from the mesenchymal cells and organize into a well-defined dental epithelial structure, leading to the formation of a well-differentiated tooth organ after sub-renal culture. These unique molar developmental properties allow us to develop a strategy using a lentivirus-mediated RNAi approach to silence gene expression in dental mesenchymal cells and assess gene function in tooth development. We show that knockdown of Msx1 or Dlx2 expression in the dental mesenchyme faithfully recapitulates the tooth phenotype of their targeted mutant mice. Silencing of Barx1 expression in the dental mesenchyme causes an arrest of tooth development at the bud stage, demonstrating a crucial role for Barx1 in tooth formation. Our studies have established a reliable and rapid assay that would permit large-scale analysis of gene function in mammalian tooth development. Developmental Dynamics 235: 1334-1344, 2006.
RNAi, lentivirus, gene function, tooth development, Barx1, Dlx, Msx1
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【期刊论文】Shox2-deficient mice exhibit a rare type of incomplete clefting of the secondary palate
张彦定, Ling Yu, *, Shuping Gu, ?, Sylvia Alappat, Yiqiang Song, Mingquan Yan, Xiaoyun Zhang, Guozhong Zhang, Yiping Jiang, Zunyi Zhang, Yanding Zhang and YiPing Chen,
,-0001,():
-1年11月30日
The short stature homeobox gene SHOX is associated with idiopathic short stature in humans, as seen in Turner syndrome and Leri-Weill dyschondrosteosis, while little is known about its close relative SHOX2. We report the restricted expression of Shox2 in the anterior domain of the secondary palate in mice and humans. Shox2-/-mice develop an incomplete cleft that is confined to the anterior region of the palate, an extremely rare type of clefting in humans. The Shox2-/-palatal shelves initiate, grow and elevate normally, but the anterior region fails to contact and fuse at the midline, owing to altered cell proliferation and apoptosis, leading to incomplete clefting within the presumptive hard palate. Accompanied with these cellular alterations is an ectopic expression of Fgf10 and Fgfr2c in the anterior palatal mesenchyme of the mutants. Tissue recombination and bead implantation experiments revealed that signals from the anterior palatal epithelium are responsible for the restricted mesenchymal Shox-expression. BMP activity is necessary but not sufficient for the induction of palatal Shox2 expression. Our results demonstrate an intrinsic requirement for Shox2 in palatogenesis, and support the idea that palatogenesis is differentially regulated along the anteroposterior axis. Furthermore, our results demonstrate that fusion of the posterior palate can occur independently of fusion in the anterior palate.
Mouse,, Cleft palate,, Shox2,, Epithelial-mesenchymal interaction
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【期刊论文】Timing of Odontogenic Neural Crest Cell Migration and Tooth-Forming Capability in Mice
张彦定, Yanding Zhang, , Shusheng Wang, Yiqiang Song, Jun Han, Yang Chai, and YiPing Chen, *
DEVELOPMENTAL DYNAMICS 226: 713-718, 2003,-0001,():
-1年11月30日
The mammalian tooth develops through sequential and reciprocal interactions between cranial neural crest (CNC)-derived ectomesenchymal cells and the stomadial epithelium. Classic tissue recombination studies demonstrated that premigratory CNC cells and CNC-derived ectomesenchymal cells possess odontogenic capacity and can respond to oral epithelial signals to form a tooth, suggesting that the CNC cells contributing to odontogenic tissue are not prespecified. Here we show that, in mice, CNC cells have populated the forming first branchial arch before the 9-somite stage and continue to migrate into the arch by the 13-somite stage. Grafts of the first arch from the 10-somite embryo or earlier yielded membranous bone and cysts but no teeth after subrenal culture. However, grafts of the first arch with its dorsally adjacent tissue containing migrating neural crest cells from the same age embryos gave rise to teeth. In contrast, teeth formed in first arch grafts that do not contain migrating neural crest cells from embryos with 12 or more somites. Interestingly, the acquisition of tooth forming capability in the first arch coincides with the onset of Fgf8 expression in the oral epithelium. These results suggest that there exists a population of odontogenic neural crest cells that migrates into the first arch between the 10- and 12-somite stages. These cells either possess odontogenic potential and are able to initiate tooth development, or can respond to odontogenic signals derived from the oral epithelium to support tooth formation. Developmental Dynamics 226: 713-718, 2003.
neural crest, tooth development, odontogenic potential, mouse embryo
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张彦定, Yanding Zhang, *, Zunyi Zhang, ?, Xiang Zhao, Xueyan Yu, , Yueping Hu, Benedicto Geronimo, Sigurd H. Fromm and YiPing Chen, §
Development 127, 1431-1443 (2000),-0001,():
-1年11月30日
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【期刊论文】Conservation of early odontogenic signaling pathways in Aves
张彦定, YiPing Chen*?, Yanding Zhang*?, Ting-Xing Jiang?, Amanda J. Barlow§, Tara R. St. Amand?, Yueping Hu?, Shaun Heaney*, Philippa Francis-West§, Cheng-Ming Chuong?, and Richard Maas*
10044-10049 u PNAS u August 29, 2000 u vol. 97 u no. 18,-0001,():
-1年11月30日
Teeth have been missing from birds (Aves) for at least 60 million years. However, in the chick oral cavity a rudiment forms that resembles the lamina stage of the mammalian molar tooth germ. We have addressed the molecular basis for this secondary loss of tooth formation in Aves by analyzing in chick embryos the status of molecular pathways known to regulate mouse tooth development. Similar to the mouse dental lamina, expression of Fgf8, Pitx2, Barx1, and Pax9 defines a potential chick odontogenic region. However, the expression of three molecules involved in tooth initiation, Bmp4, Msx1, and Msx2, are absent from the presumptive chick dental lamina. In chick mandibles, exogenous bone morphogenetic protein (BMP) induces Msx expression and together with fibroblast growth factor promotes the development of Sonic hedgehog expressing epithelial structures. Distinct epithelial appendages also were induced when chick mandibular epithelium was recombined with a tissue source of BMPs and fibroblast growth factors, chick skin mesenchyme. These results show that, although latent, the early signaling pathways involved in odontogenesis remain inducible in Aves and suggest that loss of odontogenic Bmp4 expression may be responsible for the early arrest of tooth development in living birds.
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张彦定
,-0001,():
-1年11月30日
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