骨母细胞特异性因子2介导间充质干细胞调控瘢痕疙瘩样瘤体生长的研究

目的探讨骨母细胞特异性因子2(Periostin)调控瘢痕疙瘩间充质干细胞(KMLSCs)对体外及裸鼠体内瘢痕疙瘩样瘤体生长的影响。方法从瘢痕疙瘩中分离培养KMLSCs,设置实验Periostin干扰组、空载体组和未转染组,根据干预目的构建Periostin慢病毒载体并转染对应组细胞。利用Western Blot技术体外检测各组细胞Periostin、α平滑肌肌动蛋白(α-SMA)和血管内皮生长因子(VEGF)的表达情况;制备丝素蛋白-壳聚糖支架复合体,与细胞共培养后,扫描电镜观察支架的结构、KMLSCs的生长情况。建立裸鼠皮下瘢痕疙瘩样瘤体移植模型,移植8周后取出瘤体,测量3组肿瘤体积,通过荧光共聚焦技术检测各组组织中Periostin、α-SMA、VEGF以及Western Blot技术评估Erk的表达情况。结果体外培养的3组KMLSCs中Periostin在空载体组和未转染组有表达,而干扰组则表达微弱;同时3组细胞均不表达α-SMA和VEGF。制备的支架复合体呈多孔结构,KMLSCs在复合体支架中生长良好;各分组瘤体移植模型在体内裸鼠皮下成活良好。干扰组中Periostin表达下调后,瘤体体积显著减小,同时α-SMA、VEGF、Erk表达减弱,差异有统计学意义(P 0. 05),并呈现一致性。结论 Periostin可能通过调控KMLSCs的功能,参与了模型中瘢痕疙瘩样肿块的生长。     

核结合因子a1在成骨细胞分化和骨形成中的作用

核结合因子a1(corebindingfactora1,Cbfa1)是近年来发现的一个成骨细胞特异性转录因子,在转录水平与多种成骨细胞相关基因的启动子相结合调控其表达,Cbfa1在间充质干细胞向成骨细胞分化及成骨细胞产生细胞外基质矿化成骨过程起重要作用。抑制或增强Cbfa1的表达均将引起相应表型的变化。     

Semaphorins家族在骨自身动态平衡及代谢性骨病中的重要角色

背景：骨的形成是一个动态的过程,破骨细胞和成骨细胞参与该动态过程。Semaphorin家族最早是作为轴突导向分子而被发现,其在许多不同组织里面表达并调节很多生理过程,近来更发现其在调节破骨细胞和成骨细胞方面发挥了重要作用。目的：总结Semaphorin家族各因子在骨动态平衡中发挥的作用。方法：应用计算机检索PubMed和Web of science数据库中1993年6月至2014年1月关于Semaphorin家族各因子调控骨代谢的文章,以“semaphorin,sema”为检索词进行检索;排除与研究内容无关和内容重复的文章,保留48篇文章进行综述。结果与结论：semaphorins在骨的细胞生物学方面是一类新型的调控分子,研究显示semaphorins通过一些特殊的机制很活跃的参与了骨的重塑过程,semaphorin家族蛋白在骨自身动态平衡中很关键,这些发现给治疗骨质疏松、骨硬化症、关节假体旁骨溶解等骨病提供了一种新颖的方法及治疗靶点。 中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程全文链接：     

骨髓间充质干细胞诱导成骨细胞模型中活化转录因子4基因的表达

背景:研究发现活化转录因子4为近调控成骨细胞分化和功能的活化因子,在成骨细胞分化过程中起着至关重要的作用。目的:探索SD大鼠骨髓间充质干细胞成骨诱导过程中活化转录因子4基因的表达变化及其意义。方法:以全骨髓贴壁法培养SD大鼠骨髓间充质干细胞,传代至第3代细胞时加入成骨诱导剂,在诱导的第0,1,4,7,10,13,16,19天分别采用PT-PCR,Western blot动态监测活化转录因子4基因及蛋白的表达变化,以未进行成骨诱导细胞做对照。结果与结论:RT-PCR结果显示,活化转录因子4 mRNA的表达随着细胞成骨分化程度加剧而升高,16 d达到峰值。Western blot分析结果显示,活化转录因子4蛋白表达量随着骨髓间充质干细胞骨化程度加剧,表达水平亦呈上升趋势,于16 d达到高峰,19 d维持在高水平状态。实验组各时间点活化转录因子4 mRNA和活化转录因子4蛋白表达与对照组相比差异有均有显著性意义(P0.05)。结果表明诱导成骨细胞中活化转录因子4表达增强,提示活化转录因子4的增强与骨髓间充质干细胞成骨分化能力呈正相关。     

益骨胶囊含药血清对大鼠成骨细胞IL-6 mRNA及其蛋白表达的影响

目的：从mRNA及蛋白水平探讨益骨胶囊含药血清对成骨细胞表达IL-6的影响。方法：分离、培养新生SD大鼠成骨细胞，传代后分为3组即含药血清组；空白血清组；DMEM组。采用RT-PCR法检测IL-6 mRNA相对表达量，用放射免疫法检测成骨细胞培养上清中的IL-6含量。结果：益骨胶囊含药血清组IL-6 mRNA相对表达量显著低于对照组（P<0.05）；益骨胶囊含药血清组IL-6蛋白表达量也低于对照组（P<0.05）。结论：益骨胶囊含药血清能下调成骨细胞IL-6 mRNA 表达；亦能在蛋白水平降低成骨细胞分泌骨吸收因子IL-6，这可能是益骨胶囊防治骨质疏松症的机制之一。     

活性维生素D3联合力学拉伸对成骨细胞MC3T3-E1增殖、分化及OPG和RANKL表达的影响

目的体外模拟成骨细胞在体内的生存环境,考察活性维生素D3(VD3)、力学拉伸以及两者联合对成骨细胞MC3T3-E1增殖、分化及破骨细胞抑制因子(OPG)和破骨细胞分化因子(RANKL)表达的影响。方法将10 nmol/L VD3、间断性力学拉伸以及两者联合作用于成骨细胞。流式细胞术检测细胞增殖。荧光探针试剂盒检测碱性磷酸酶(ALP)活性。实时定量PCR检测核心转录因子Runx2、OPG、RANKL mRNA水平,Western blotting检测其蛋白表达。结果 VD3抑制成骨细胞增殖,力学拉伸不能改变这种抑制效应。力学拉伸和VD3单独作用成骨细胞均能增加ALP活性及提高ALP、Runx2 mRNA水平,但当联合刺激后这些指标均降低,且成强度依赖性。力学拉伸增加OPG/RANKL比值,增强成骨作用,联合VD3后,OPG/RANKL比值下降。结论力学拉伸能有效诱导成骨分化,增加骨形成。VD3与力学拉伸联合抑制成骨细胞增殖和分化,并通过增加RANKL表达而影响骨重建。研究结果为骨质疏松及相关骨疾病的理论和治疗提供有意义的探索。     

活性维生素D3联合力学拉伸对成骨细胞MC3T3-E1增殖、分化及OPG和RANKL表达的影响（英文）

目的体外模拟成骨细胞在体内的生存环境,考察活性维生素D3(VD3)、力学拉伸以及两者联合对成骨细胞MC3T3-E1增殖、分化及破骨细胞抑制因子(OPG)和破骨细胞分化因子(RANKL)表达的影响。方法将10 nmol/L VD3、间断性力学拉伸以及两者联合作用于成骨细胞。流式细胞术检测细胞增殖。荧光探针试剂盒检测碱性磷酸酶(ALP)活性。实时定量PCR检测核心转录因子Runx2、OPG、RANKL mRNA水平,Western blotting检测其蛋白表达。结果 VD3抑制成骨细胞增殖,力学拉伸不能改变这种抑制效应。力学拉伸和VD3单独作用成骨细胞均能增加ALP活性及提高ALP、Runx2 mRNA水平,但当联合刺激后这些指标均降低,且成强度依赖性。力学拉伸增加OPG/RANKL比值,增强成骨作用,联合VD3后,OPG/RANKL比值下降。结论力学拉伸能有效诱导成骨分化,增加骨形成。VD3与力学拉伸联合抑制成骨细胞增殖和分化,并通过增加RANKL表达而影响骨重建。研究结果为骨质疏松及相关骨疾病的理论和治疗提供有意义的探索。     

血管内皮生长因子165/骨形态发生蛋白改善缺氧复氧状态下成骨细胞损伤

背景：研究发现,血管内皮生长因子165和骨形态发生蛋白两种因子在缺氧复氧过程中相互作用,通过调节细胞内信号通路的活化,参与骨细胞损伤的修复过程。目的：进一步探究血管内皮生长因子165/骨形态发生蛋白与缺氧复氧成骨细胞损伤的关系分析。方法：取成骨细胞,建立缺氧复氧损伤模型,建模前后Real-Time PCR法和免疫印迹法检测血管内皮生长因子165、骨形态发生蛋白2的mRNA及蛋白表达。分别给予建模后成骨细胞不同质量浓度(10,20,40ng/mL)血管内皮生长因子165或骨形态发生蛋白2处理12,24,36,48,72 h,CCK-8法检测细胞增殖,DAPI检测细胞凋亡。结果与结论：(1)与建模前相比,建模后成骨细胞中血管内皮生长因子165、骨形态发生蛋白2的mRNA和蛋白表达量显著降低(P <0.05);(2)成骨细胞增殖率随着血管内皮生长因子165质量浓度的升高而明显升高(P <0.05);成骨细胞凋亡率随着血管内皮生长因子165质量浓度的升高而明显降低(P <0.05);(3)成骨细胞增殖率随着骨形态发生蛋白2质量浓度的升高而明显升高(P <0.05);成骨...     

内质网应激介导成骨细胞凋亡在骨溶解骨组织中的作用及机制

背景：磨损微粒能够在体外诱导成骨细胞凋亡,但是发生骨溶解的骨组织中是否也存在成骨细胞的凋亡以及骨组织中的成骨细胞凋亡信号通过何种途径进行传导目前尚不清楚。 目的：分析内质网应激反应在骨溶解骨组织中成骨细胞凋亡和骨溶解发生发展中的作用。 方法：制备磨损微粒诱导骨溶解动物模型。实验分为4组：空白对照组只接受PBS的刺激;磨损微粒组只接受纳米合金粉末悬液的刺激;内质网应激阳性对照组接受纳米合金粉末+毒胡萝卜素的刺激;内质网应激抑制组接受纳米合金粉末悬液及造模后当时、造模后1,2,3和5 d分别腹腔注射4-苯基丁酸。通过甲苯胺蓝染色、苏木精-伊红染色和碱性磷酸酶染色观察骨溶解的病理变化;分析骨溶解颅骨组织中成骨细胞分化成熟情况;Western Blot方法检测骨溶解颅骨组织内内质网应激反应标志蛋白的表达变化;TUNEL和Caspase-3免疫组织化学方法检测骨溶解颅骨组织内成骨细胞的凋亡情况。 结果与结论：磨损微粒能够在体外诱导小鼠颅骨骨溶解的发生、加重炎症细胞的浸润以及抑制成骨细胞分化成熟,同时磨损微粒还可以上调成骨细胞内质网应激反应标志蛋白以及促进骨溶解骨组织中成骨细胞的凋亡。经内质网应激抑制剂(4-苯基丁酸)的治疗后,骨溶解症状明显缓解,骨侵蚀和炎症浸润显著降低,成骨细胞的分化成熟得到改善,凋亡的成骨细胞急剧减少,内质网应激标志蛋白的表达逐渐减弱。表明内质网应激反应参与骨溶解的形成并在骨溶解的发生发展中发挥重要作用。提示内质网应激可作为一种新的治疗靶点,为临床逆转或治疗骨溶解和无菌性松动提供新的思路和方法。 中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程全文链接：     

Upregulation of Periostin expression in the pathogenesis of ameloblastoma

Ameloblastoma(AB) is an aggressive and slow-growing tumor with high recurrence rate, which arises from odontogenic epithelium. AB mostly shows osteolytic growth, but the specific pathogenesis is not yet clear. Periostin is a considered a prominent oncogene, which was mainly produced by osteoblasts and their precursors cells, it have been proved that Periostin play an important role in bone lysis. However, the precise role of Periostin in AB progression remains unknown. In this article, the surgical specimens from cases of AB were collected, and the Periostin expression was tested and the results were analyzed for possible correlations with clinical characteristics. In addition, the proliferation、cell cycle and migration of AM-1 cells were evaluated after transfection of siPeriostin. The results showed that Periostin levels were significantly higher in patients with AB than in controls. Moreover, Periostin levels in patients with AB were significantly associated with the number of disease. Furthermore, the results suggested that Periostin expression significantly promoted the proliferation and migration, in addition to cell cycle progression of AM-1 cells. The present study demonstrated that Periostin may be important in the pathogenesis and progression of AB and indicated its potential therapeutic value.     

Identification and detection of the periostin gene in cardiac development

Periostin, a member of the fasciclin gene family, acts as a cell adhesion molecule through binding to cell surface integrins. Periostin expression has previously been shown to increase substantially following transforming growth factor beta (TGF-beta) and bone morphogenetic protein stimulation. As these molecules are indispensable for cardiac development, we sought to clone the chicken ortholog of periostin and evaluate its spatiotemporal expression pattern during heart morphogenesis. We show by Northern analysis, whole mount and section in situ hybridization experiments that periostin is predominantly expressed in the developing endothelium of the ventricular trabeculae as well as in the endothelium and mesenchyme of the outflow tract and atrioventricular endocardial cushions. Cardiac expression continues into fetal development where periostin is seen predominantly in the valve leaflets and supporting chordae tendinae.     

Roles of Periostin in Symptom Manifestation and Airway Remodeling in a Murine Model of Allergic Rhinitis

Purpose

Periostin was originally identified as a secreted factor during screening of a mouse osteoblastic library. In a recent study, periostin was found to directly regulate eosinophil accumulation in allergic mucosal inflammation. Chronic eosinophilic inflammation is related to the development of remodeling. The present study examined the expression of periostin and evaluated its role in the inflammatory process and remodeling associated with allergic rhinitis.

Methods

A murine model of allergic rhinitis was established in periostin knockout mice. We analyzed the expression of periostin, manifestation of nasal symptoms, eosinophilic inflammation, and subepithelial fibrosis as well as the expression of MMP-2, TIMP-1, and type 1 collagen in nasal tissue.

Results

Periostin was mainly distributed in the subepithelial tissue of the nasal mucosa. The subepithelial tissue was thinner in the knockout group than in the control group. No differences in the expression of MMP-2 or TIMP-1 were found in the knockout group. However, after a month of allergen challenge, type I collagen in the nasal tissue was lower in the knockout group than in the control group. The number of eosinophils and the symptom score were also lower in the knockout group.

Conclusions

Periostin is expressed in nasal tissues of murine models of allergic rhinitis. Periostin deficiency may affect the remodeling of nasal tissue with reduced subepithelial fibrosis, and lead to less eosinophilic inflammation.     

Periostin expression and epithelial-mesenchymal transition in cancer: a review and an update

Periostin, also called osteoblast-specific factor 2, is a secreted cell adhesion protein, which shares a homology with the insect cell adhesion molecule fasciclin I. It has been shown to be an important regulator of bone and tooth formation and maintenance, and of cardiac development and healing. Recent studies revealed that periostin plays an important role in tumor development and is upregulated in a wide variety of cancers such as colon, pancreatic, ovarian, breast, head and neck, thyroid, and gastric cancer as well as in neuroblastoma. Periostin binding to the integrins activates the Akt/PKB- and FAK-mediated signaling pathways which lead to increased cell survival, angiogenesis, invasion, metastasis, and importantly, epithelial-mesenchymal transition of carcinoma cells. In this review we summarize recent clinicopathological studies that have investigated periostin expression in lung, kidney, prostate, liver cancer, and malignant pleural mesothelioma and discuss the role of periostin isoforms in tumorigenesis and their potential as targets for stroma-targeted anticancer therapy.     

Periostin is expressed within the developing teeth at the sites of epithelial-mesenchymal interaction.

Periostin was originally isolated as an osteoblast-specific factor that functions as a cell adhesion molecule for preosteoblasts and is thought to be involved in osteoblast recruitment, attachment, and spreading. The protein was renamed "periostin" because of its expression in the periosteum and periodontal ligament, indicating a potential role in bone and maintenance of tooth structure. Periostin has structural similarity to insect fasciclin-I and can be induced by TGF-beta and Bmp2. Because tooth and periodontium development is a well-described genetic model for organogenesis governed by a reciprocal set of epithelial-mesenchymal interactions, thought to be controlled by various TGF-beta superfamily members, we investigated whether periostin is present during tooth morphogenesis. Both periostin mRNA and protein expression were analyzed throughout normal tooth development (embryonic day [E] 9.5-newborn) and within both Bmp4- and Msx2-null embryos. Periostin mRNA is initially present within the E9.5 first branchial arch epithelium and then shifts to underlying ectomesenchyme. Both mRNA and protein are asymmetrically localized to the lingual/palatal and buccal side during the early epithelial-mesenchymal interactions. Periostin is also present in dental papilla cells and within the trans-differentiating odontoblasts during the bell and hard tissue formation stages of tooth development. We suggest that periostin plays multiple roles as a primary responder molecule during tooth development and may be linked to deposition and organization of other extracellular matrix adhesion molecules during maintenance of the adult tooth, particularly at the sites of hard-soft tissue interface.     

Periostin表达对鼻咽癌细胞体外侵袭行为的影响

探讨Periostin表达对体外鼻咽癌（NPC）细胞侵袭行为的影响及其机制。 方法 采用Western blotting检测激光捕获显微切割纯化的鼻咽癌间质和正常鼻咽黏膜间质、鼻咽癌低转移潜能细胞系6-10B和高转移潜能细胞系5-8F及NIH 3T3成纤维细胞中Periostin的表达水平。应用阳性脂质体法将pCMV-neo-Periostin质粒瞬时转染到NIH 3T3细胞,运用Western blotting检测转染前后NIH 3T3细胞中Periostin的表达水平,利用Boyden小室穿膜侵袭实验检测Periostin蛋白对肿瘤细胞的体外侵袭能力的影响,明胶酶谱法检测其对基质金属蛋白酶（MMPs）活性的影响。 结果 Periostin在纯化的鼻咽癌间质中高表达,在纯化的正常鼻咽黏膜间质中及高转移细胞系5-8F中弱表达,在低转移细胞系6-10B及NIH 3T3细胞中不表达。瞬时转染过表达Periostin的NIH 3T3细胞中Periostin的表达明显增强。Boyden小室实验提示,分泌蛋白Periostin可明显增强鼻咽癌细胞6-10B的体外侵袭能力,转染组穿膜的细胞数与空白对照组及未转染对照组比较,明显增多(P<0.01);转染组与6-10B细胞共培养后,培养上清中MMPs的活性较对照组明显增强。 结论 Periostin 蛋白能增强鼻咽癌细胞的侵袭能力,其机制可能与上调MMPs的活性有关。     

Relevance of Periostin Splice Variants in Renal Cell Carcinoma

The extracellular matrix N-glycoprotein periostin is thought to enhance tumor invasion. In this study, the expression patterns of periostin and its splice isoforms were investigated in renal cell carcinoma (RCC). Periostin mRNA expression patterns were characterized in 30 fresh-frozen RCCs in normal fetal and adult renal tissues by both isoform-specific and nonspecific RT-PCR and by gene expression array analysis. Its protein expression was analyzed by immunohistochemistry, using tissue microarrays with tissue from 1007 RCC patients. Periostin mRNA in RCC was increased, as observed in both RT-PCR and gene microarray analyses, with significantly higher expression in the clear cell than in the papillary subtype. Four of eight periostin isoforms, identified in fetal kidney by direct sequencing, have not been described to date. Three isoforms could be detected in both RCC and matched non-neoplastic tissue, and one of them was expressed more frequently in RCC. Periostin protein was detected in both mesenchymal cells of the tumor stroma and epithelial tumor cells. Greater amounts of periostin in tumor epithelia correlated with the presence of sarcomatoid differentiation, higher tumor stage, lymph node metastases, and poor overall survival in the clear cell subtype. In conclusion, periostin expression in tumor epithelia may contribute to sarcomatoid differentiation and more aggressive behavior of RCC. The presence of a tumor-associated periostin isoform suggests splice-specific regulation in RCC tissue.Renal cell carcinoma (RCC) is a heterogeneous epithelial tumor with frequent evidence of metastasis at the time of diagnosis. The major histologic subtypes are clear cell, papillary, and chromophobe RCC. Sarcomatoid differentiation is not its own entity and can be observed in all of these subtypes, where its presence is associated with a poor prognosis.^1,2Periostin, also termed osteoblast-specific factor 2, is a secreted matrix N-glycoprotein of 93 kDa.³ The N-terminal region contains four fasciclin-like domains as well as several glycosylation sites. This protein originally was identified in MC3T3-E1 osteoblast-like cells, where it promotes integrin-dependent cell adhesion and motility. It shares homology with the insect cell adhesion molecule fasciclin I, with human β IgH3, and is induced by transforming growth factor-β and bone morphogenic protein-2.^3–5Periostin is thought to promote epithelial-mesenchymal transition (EMT) of carcinoma cells by targeting the cross-talk between epidermal growth factor receptor and integrins at the plasma membrane with consecutive activation of the Akt/protein kinase B pathway.⁶ Through its binding to the integrins α_vβ₃, α_vβ₅, and α_vβ₆ periostin promotes cellular survival, angiogenesis, and resistance to hypoxia-induced cell death.^7–11 Consequently, this protein is considered to be a prognostic marker. Furthermore, periostin was shown to be accessible by the blood stream after ex vivo perfusion and biotinylation of human kidney with tumor and therefore a potential target for stroma-directed tumor therapy.^12,13To date, six different splice isoforms of periostin have been reported, but only four of them (including the full-length variant) have been sequenced and annotated.^13,14 Full-length and isoforms differ in their C-terminal sequences, and the N-terminus is responsible for integrin binding.³ All known isoforms are between 83 and 93 kDa in mass, and vary between 751 and 836 amino acids. The four known splice variants are characterized by an individual presence or absence of cassette exons 17 to 21. They are called isoform 1 (full-length variant with all exons), isoform 2 (absent exons: 17 and 18), isoform 3 (absent exons: 17 and 21), and isoform 4 (absent exons: 17, 18, and 21) with the following UniProtKB/Swiss-Prot accession numbers: {"type":"entrez-nucleotide","attrs":{"text":"D13666","term_id":"393316","term_text":"D13666"}}D13666, {"type":"entrez-nucleotide","attrs":{"text":"D13665","term_id":"393318","term_text":"D13665"}}D13665, {"type":"entrez-nucleotide","attrs":{"text":"AY140646","term_id":"23345099","term_text":"AY140646"}}AY140646, and {"type":"entrez-nucleotide","attrs":{"text":"AY918092","term_id":"62824473","term_text":"AY918092"}}AY918092, respectively.Periostin is expressed mainly in collagen-rich and in fetal tissues such as periosteum, periodontal ligament, placenta, cardiac valves, and vasculature, and is up-regulated by mechanical stress during tissue generation and repair.^3,15–21 Strong protein expression has been observed in lung, breast, ovarian, pancreatic, gastric, thyroid, colon, head and neck, prostate, liver, and other carcinomas, as well as in neuroblastoma, and was related to increased malignant behavior of those tumors.^{7–9,11,21–31} Consequently, the aim of this study was to characterize periostin expression patterns and to analyze periostin isoforms in RCC and in normal renal tissue.     

B lymphopoiesis is characterized by pre-B cell marker gene expression in fetal cattle and declines in adults

Fetal cattle B-cell development proceeds via a pre-B cell stage that is characterized by the expression of surrogate light chain and recombination activation genes. In this paper, we identify a new member of bovine pre-B lymphocyte genes, VPREB2. Using RT-qPCR, we assess the expression of VPREB2 and three other surrogate light chain genes as well as RAG1 and RAG2 in fetal and adult cattle tissues. The absence of VPREB1, IGLL1, RAG1 and RAG2 expression in adult tissues and the lack of B-lymphoid differentiation in adult bone marrow - OP9 stromal cell co-culture, suggest a decline of B lymphopoiesis in adult cattle. The marked differences in the expression profiles of VPREB2 and VPREB3 in comparison to those of VPREB1, IGLL1 and RAGs suggest that the biological roles of VPREB2 and VPREB3 are unrelated to the pre-B cells.     

Differential expression and distribution of syndecan-1 and -2 in the developing periodontium of the rat.

Cell surface proteoglycans are known to interact with adhesion molecules, growth factors and a variety of other effector molecules implying their central role in various aspects of cell-cell and cell-matrix interactions. To investigate the expression and distribution of the cell surface proteoglycans syndecan-1 and -2, the developing periodontal tissues of 3-, 5-, and 8-wk-old male Lewis rats, were stained by specific monoclonal antibodies against syndecan-1, or -2 core protein, using immunohistochemical techniques. The results demonstrated that syndecan-1 and -2 were expressed and distributed differentially in several compartments of the developing periodontal tissues at different ages. Expression of syndecan-1 was noted in areas of intense cellular activity such as the developing apical root tip of the tooth and at the crestal bone where new bone formation was taking place. In contrast, syndecan-2 expression and distribution did not exhibit the same patterns as syndecan-1. Syndecan-2 showed significant differences of distribution in hard tissues undergoing maturation at different ages. These findings indicate that syndecan-1 and -2 may have distinctive functions during morphogenesis, organogenesis and differentiation of the periodontium.