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1.
The use of hydrogel in cartilage tissue engineering is especially popular due to its high hydrophilic property which is similar to native cartilage matrix. Alginate hydrogel was used as a transient scaffold material to facilitate chondrocyte proliferation into a three‐dimensional scaffold‐free living hyaline cartilaginous graft (LhCG). As LhCG is purely cell‐based and has a marked resemblance to native hyaline cartilage, it served as an excellent in vitro platform for studying the endochondral ossification pathway. Due to the complexity of events involved throughout endochondral ossification, this study only focuses on early stages of the process where it involves chondrocyte hypertrophy and blood vessel invasion. Human umbilical vein endothelial cells (HUVECs) were selected as the target cells for possible endothelialization in the LhCG template. They were seeded onto the LhCG construct and subjected to vascular endothelial growth factor (VEGF) treatment. Results suggested that VEGF is indeed a potent driving force for initiation of the endochondral pathway. It alone is sufficient to induce hypertrophy in chondrocytes and the corresponding expression of osteogenic genes with or without the presence of HUVECs in the LhCG template. On the other hand, the effect of HUVECs in the LhCG system was less evident. It is hypothesized that this is attributed to the preservation of anti‐angiogenic properties in primary chondrocytes from the LhCG construct, inhibiting HUVECs from endothelialization in the LhCG+HUVEC construct. Based on the outcome from this study, it is recommended that hypertrophy in chondrocytes should be induced prior to endothelial cell introduction so that the microenvironment will be altered to favor angiogenesis within the cartilaginous template. © 2013 Society of Chemical Industry  相似文献   
2.
Tissue engineering strategies promote bone regeneration for large bone defects by stimulating the osteogenesis route via intramembranous ossification in engineered grafts, which upon implantation are frequently constrained by insufficient integration and functional anastomosis of vasculature from the host tissue. In this study, we developed a hybrid biomaterial incorporating decellularized cartilage extracellular matrix (CD-ECM) as a template and silk fibroin (SF) as a carrier to assess the bone regeneration capacity of bone marrow-derived mesenchymal stem cells (hBMSC’s) via the endochondral ossification (ECO) route. hBMSC’s were primed two weeks for chondrogenesis, followed by six weeks for hypertrophy onto hybrid CD-ECM/SF or SF alone scaffolds and evaluated for the mineralized matrix formation in vitro. Calcium deposition biochemically determined increased significantly from 4-8 weeks in both SF and CD-ECM/SF constructs, and retention of sGAG’s were observed only in CD-ECM/SF constructs. SEM/EDX revealed calcium and phosphate crystal localization by hBMSC’s under all conditions. Compressive modulus reached a maximum of 40 KPa after eight weeks of hypertrophic induction. μCT scanning at eight weeks indicated a cloud of denser minerals in groups after hypertrophic induction in CD-ECM/SF constructs than SF constructs. Gene expression by RT-qPCR revealed that hBMSC’s expressed hypertrophic markers VEGF, COL10, RUNX2, but the absence of early hypertrophic marker ChM1 and later hypertrophic marker TSBS1 and the presence of osteogenic markers ALPL, IBSP, OSX under all conditions. Our data indicate a new method to prime hBMSC’S into the late hypertrophic stage in vitro in mechanically stable constructs for ECO-mediated bone tissue regeneration.  相似文献   
3.
Osteoarthritis (OA) is the most common type of arthritis and is associated with wear and tear, aging, and inflammation. Previous studies revealed that several antimicrobial peptides are up-regulated in the knee synovium of patients with OA or rheumatoid arthritis. Here, we investigated the functional effects of cathelicidin-related antimicrobial peptide (Cramp) on OA pathogenesis. We found that Cramp is highly induced by IL-1β via the NF-κB signaling pathway in mouse primary chondrocytes. Elevated Cramp was also detected in the cartilage and synovium of mice suffering from OA cartilage destruction. The treatment of chondrocytes with Cramp stimulated the expression of catabolic factors, and the knockdown of Cramp by small interfering RNA reduced chondrocyte catabolism mediated by IL-1β. Moreover, intra-articular injection of Cramp into mouse knee joints at a low dose accelerated traumatic OA progression. At high doses, Cramp affected meniscal ossification and tears, leading to cartilage degeneration. These findings demonstrate that Cramp is associated with OA pathophysiology.  相似文献   
4.
目的:探究南极磷虾油(Antarctic krill oil,AKO)对骨质疏松模型小鼠骨折愈合的促进作用。方法:采用C57BL/6J雌性小鼠,通过双侧去卵巢术建立骨质疏松模型;随后行右胫开放性骨折手术并随机分为一般性骨折对照组、骨质疏松性骨折模型组、阳性对照组、AKO组。于骨折后5、11、24、35、56 d取材,动态分析AKO对小鼠血清相关指标、骨痂组织形态学、显微结构和生物力学以及软骨内成骨关键基因表达的影响。结果:酶联免疫吸附测定结果表明AKO能显著升高血清中血管内皮生长因子(vascular endothelial growth factor,VEGF)质量浓度及骨碱性磷酸酶活力;骨痂苏木精-伊红染色及微型计算机断层扫描结果显示AKO能够促进软骨痂向硬骨痂转化,并改善骨痂微结构,加速骨痂重塑;生物力学检测结果显示AKO可增强骨性骨痂生物力学性能;实时荧光定量聚合酶链式反应结果显示,AKO可显著提高血管入侵相关因子(VEGF、血小板衍生生长因子和血管紧张素1)的mRNA表达(P<0.05),显著降低软骨细胞增殖和肥大相关基因(聚集蛋白聚糖A g g r e c a n和Col10a)的表达(P<0.05),显著升高软骨基质降解因子MMP-13以及骨生成相关基因(Col1a、骨钙素和骨形态发生蛋白2)的表达(P<0.05),提示AKO可通过调控软骨内成骨关键基因的表达,加速软骨内骨化进程。结论:AKO通过促进软骨内成骨及骨痂重塑,加速骨质疏松模型小鼠骨折愈合,提高愈合质量。  相似文献   
5.
Improvements in medical care, nutrition and social care are resulting in a commendable change in world population demographics with an ever increasing skew towards an aging population. As the proportion of the world’s population that is considered elderly increases, so does the incidence of osteodegenerative disease and the resultant burden on healthcare. The increasing demand coupled with the limitations of contemporary approaches, have provided the impetus to develop novel tissue regeneration therapies. The use of stem cells, with their potential for self-renewal and differentiation, is one potential solution. Adipose-derived stem cells (ASCs), which are relatively easy to harvest and readily available have emerged as an ideal candidate. In this review, we explore the potential for ASCs to provide tangible therapies for craniofacial and long bone skeletal defects, outline key signaling pathways that direct these cells and describe how the developmental signaling program may provide clues on how to guide these cells in vivo. This review also provides an overview of the importance of establishing an osteogenic microniche using appropriately customized scaffolds and delineates some of the key challenges that still need to be overcome for adult stem cell skeletal regenerative therapy to become a clinical reality.  相似文献   
6.
7.
In a previous study using transgenic mice ectopically expressing Hoxa2 during chondrogenesis, we associated the animal phenotype to human idiopathic proportionate short stature. Our analysis showed that this overall size reduction was correlated with a negative influence of Hoxa2 at the first step of endochondral ossification. However, the molecular pathways leading to such phenotype are still unknown. Using protein immunodetection and histological techniques comparing transgenic mice to controls, we show here that the persistent expression of Hoxa2 in chondrogenic territories provokes a general down-regulation of the main factors controlling the differentiation cascade, such as Bapx1, Bmp7, Bmpr1a, Ihh, Msx1, Pax9, Sox6, Sox9 and Wnt5a. These data confirm the impairment of chondrogenic differentiation by Hoxa2 overexpression. They also show a selective effect of Hoxa2 on endochondral ossification processes since Gdf5 and Gdf10, and Bmp4 or PthrP were up-regulated and unmodified, respectively. Since Hoxa2 deregulation in mice induces a proportionate short stature phenotype mimicking human idiopathic conditions, our results give an insight into understanding proportionate short stature pathogenesis by highlighting molecular factors whose combined deregulation may be involved in such a disease.  相似文献   
8.
The human TGF-β/SMAD7 signaling has been recognized as an attractive target of heterotopic ossification (HO). Here, we report a successful rational design of cyclic peptides to disrupt the signaling pathway by targeting TGF-β–receptor complex. The intermolecular interaction between TGF-β and its cognate receptor is characterized in detail using molecular dynamics simulation, binding energetic analysis, and alanine scanning. With the computational analysis a binding loop of receptor protein is identified that plays an essential role in the peptide-mediated TGF-β–receptor interaction. Subsequently, the loop is stripped from the protein context to generate a linear peptide segment, which possesses considerable flexibility and intrinsic disorder, and thus would incur a large entropy penalty upon binding to TGF-β. In order to minimize the unfavorable entropic effect, the linear peptide is cyclized by adding a disulfide bond between the N- and C-terminal cysteine residues of the peptide, resulting in a cyclic peptide. In vitro fluorescence anisotropy assays substantiate that the cyclic peptide can bind tightly to TGF-β with determined Kd value of 54 μM. We also demonstrated that structural optimization can further improve the peptide affinity by site-directed mutagenesis of selected residues based on the computationally modeled complex structure of TGF-β with the cyclic peptide.  相似文献   
9.
The patterns of longitudinal and peripheral growth were analyzed in human autopod cartilage anlagen (fetal developmental stage 20th–22nd week) through morphometric assessment of chondrocyte parameter size, shape, alignment and orientation between peripheral and central sectors of the anlage transition zone defined by primary ossification center and the epiphyseal basis. The aim was to correlate the chondrocyte dynamics with the longitudinal and peripheral growth. A further comparison was carried out between the corresponding sectors of the postnatal (3–5 months old) growth plate cartilage documenting: (1) the different chondrocyte framework and the new peripheral mechanism; (2) the opposite direction of fetal periosteal ossification versus the Lacroix bone bark. Measurement of multiple parameters (% lac area, % total matrix area, total lac density and mean single lac area), which characterize the cartilage Anlage growth, suggested the following correlations with chondrocyte duplication rate: (a) slow duplication rate ≈ coupled, intralacunar chondrocytes (in central epiphysis); (b) repeated/frequent cell duplications ≈ clusters (in the basal epiphyseal layer); (c) clusters of chondrocytes before becoming hypertrophic were stacked up on the top of each other (both in the Anlage transition zone or in the columns of metaphyseal growth plate); (d) enhanced osteoclastic resorption of the Lacroix bone bark lower end, extended to the more external metaphyseal trabeculae counterbalancing the discrepancy between the epiphyseal and the diaphyseal circumferential growth.  相似文献   
10.
Growth of the axial and appendicular skeleton depends on endochondral ossification, which is controlled by tightly regulated cell–cell interactions in the developing growth plates. Previous studies have uncovered an important role of a disintegrin and metalloprotease 17 (ADAM17) in the normal development of the mineralized zone of hypertrophic chondrocytes during endochondral ossification. ADAM17 regulates EGF-receptor signaling by cleaving EGFR-ligands such as TGFα from their membrane-anchored precursor. The activity of ADAM17 is controlled by two regulatory binding partners, the inactive Rhomboids 1 and 2 (iRhom1, 2), raising questions about their role in endochondral ossification. To address this question, we generated mice lacking iRhom2 (iR2−/−) with floxed alleles of iRhom1 that were specifically deleted in chondrocytes by Col2a1-Cre (iR1∆Ch). The resulting iR2−/−iR1∆Ch mice had retarded bone growth compared to iR2−/− mice, caused by a significantly expanded zone of hypertrophic mineralizing chondrocytes in the growth plate. Primary iR2−/−iR1∆Ch chondrocytes had strongly reduced shedding of TGFα and other ADAM17-dependent EGFR-ligands. The enlarged zone of mineralized hypertrophic chondrocytes in iR2−/−iR1∆Ch mice closely resembled the abnormal growth plate in A17∆Ch mice and was similar to growth plates in Tgfα−/− mice or mice with EGFR mutations. These data support a model in which iRhom1 and 2 regulate bone growth by controlling the ADAM17/TGFα/EGFR signaling axis during endochondral ossification.  相似文献   
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