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| Biomechanics in bone tissue engineering.
May 15, 2010 at 6:42 AM
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| | Biomechanics in bone tissue engineering. Comput Methods Biomech Biomed Engin. 2010 May 12;:1 Authors: Pioletti DP Biomechanics may be considered as central in the development of bone tissue engineering. The initial mechanical aspects are essential to the outcome of a functional tissue engineering approach; so are aspects of interface micromotion, bone ingrowths inside the scaffold and finally, the mechanical integrity of the scaffold during its degradation. A proposed view is presented herein on how biomechanical aspects can be synthesised and where future developments are needed. In particular, a distinction is made between the mechanical and the mechanotransductional aspects of bone tissue engineering: the former could be related to osteoconduction, while the latter may be correlated to the osteoinductive properties of the scaffold. This distinction allows biomechanicians to follow a strategy in the development of a scaffold having not only mechanical targets but also incorporating some mechanotransduction principles. PMID: 20467959 [PubMed - as supplied by publisher] | | |
| Improved myocardial performance in infarcted rat heart by co-injection of basic fibroblast growth factor with temperature-responsive Chitosan hydrogel.
May 15, 2010 at 6:42 AM
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| | Improved myocardial performance in infarcted rat heart by co-injection of basic fibroblast growth factor with temperature-responsive Chitosan hydrogel. J Heart Lung Transplant. 2010 May 11; Authors: Wang H, Zhang X, Li Y, Ma Y, Zhang Y, Liu Z, Zhou J, Lin Q, Wang Y, Duan C, Wang C BACKGROUND: Basic fibroblast growth factor (bFGF) stimulates neoangiogenesis. The sustained release of bFGF by using biomaterials helped to enhance its angiogenic activity in vivo. In this study we investigated the effects of co-injection of bFGF with temperature-responsive chitosan hydrogel on myocardial performance in a rat model of infarction. METHODS: Myocardial infarction was induced in rats using coronary artery ligation. Temperature-responsive chitosan hydrogel was prepared and injected intramyocardially into the left ventricular wall of rat infarction models alone or together with bFGF. Detailed histologic analysis and echocardiography were used to determine the structural and functional consequences 4 weeks after injection. RESULTS: Heart function improved significantly in the chitosan+bFGF group compared with the phosphate-buffered saline (PBS)+bFGF group with regard to left ventricular ejection fraction (LVEF) and LV fractional shortening (LVFS) 4 weeks! after transplantation (p < 0.05, n = 8 per group). In addition, arteriole densities within the infarcted area improved significantly (p < 0.01) in the chitosan+bFGF group (259 +/- 22/mm(2)) compared with the PBS+bFGF group (95 +/- 18/mm(2); n = 8 per group) at 4 weeks after transplantation. Infarct size and fibrotic area decreased significantly (p < 0.05) in the chitosan+bFGF group (39.64 +/- 1.75% and 25.09 +/- 3.31%, respectively) compared with the PBS+bFGF group (48.91 +/- 1.39% and 48.0 +/- 3.83%, respectively; n = 8 per group). No significant difference (p > 0.05) was noted between the PBS and PBS+bFGF groups. CONCLUSIONS: Co-injection of bFGF with temperature-responsive chitosan hydrogels enhanced the effects of bFGF on arteriogenesis, ventricular remodeling and cardiac function. Our findings suggest a new approach to improve infarcted repairs in the prevention of adverse remodeling after myocardial infarction. PMID: 20466563 [PubMed - as supplied by publisher] | | |
| Collagen-Hyaluronic Acid Scaffolds for Adipose Tissue Engineering.
May 15, 2010 at 6:42 AM
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| | Collagen-Hyaluronic Acid Scaffolds for Adipose Tissue Engineering. Acta Biomater. 2010 May 10; Authors: Davidenko N, Campbell JJ, Thian ES, Watson CJ, Cameron RE Three-dimensional (3D) in vitro models of the mammary gland require a scaffold matrix that supports the development of adipose stroma within a robust freely permeable matrix. 3D porous collagen-hyaluronic acid (HA: 7.5 and 15%) scaffolds were produced by controlled freeze-drying technique and cross-linking with 1-ethyl-3-(3-dimethylaminopropyl)-carbodiimide hydrochloride. All scaffolds displayed uniform, interconnected pore structure (total porosity approximately 85%). Physical and chemical analysis showed no signs of collagen denaturation during the formation process. The values of thermal characteristics indicated that cross-linking occurred and that its efficiency was enhanced by the presence of HA. Although the cross-linking reduced the swelling of the strut material in water, the collagen-HA matrix as a whole tended to swell more and show higher dissolution resistance than pure collagen samples. The compressive modulus and elastic collapse stress were higher ! for collagen-HA composites. All the scaffolds were shown to support the proliferation and differentiation 3T3-L1 preadipocytes while collagen-HA samples maintained a significantly increased proportion of cycling cells (Ki-67+). Furthermore, collagen-HA composites displayed significantly raised Adipsin gene expression with adipogenic culture supplementation for 8 days versus control conditions. These results indicate that collagen-HA scaffolds may offer robust, freely permeable 3D matrices that enhance mammary stromal tissue development in vitro. PMID: 20466086 [PubMed - as supplied by publisher] | | |
| Characterization of a Biodegradable Electrospun Polyurethane Nanofiber Scaffold: Mechanical Properties and Cytotoxicity.
May 15, 2010 at 6:42 AM
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| | Characterization of a Biodegradable Electrospun Polyurethane Nanofiber Scaffold: Mechanical Properties and Cytotoxicity. Acta Biomater. 2010 May 10; Authors: Yeganegi M, Kandel RA, Santerre JP The current study analyzes the biodegradation of a polycarbonate polyurethane scaffold intended for the growth of a tissue engineered annulus fibrosus (AF) disc component. Electrospun scaffolds with random and aligned nanofiber configurations were fabricated using a biodegradable polycarbonate-urethane (PU) with and without an anionic surface modifier (anionic dihydroxyl oligomer (ADO)), and the mechanical behavior of the scaffolds was examined during a four week biodegradation study. Both the tensile strength and initial modulus of aligned scaffolds (sigma =14+/-1 MPa, E=46+/-3 MPa) were found to be higher than those of random fiber scaffolds (sigma =1.9+/-0.4 MPa, E=2.1+/-0.2 MPa) prior to degradation. Following initial wetting of the scaffold, the initial modulus of the aligned samples showed a significant decrease (dry: 46+/-3 MPa, prewetted: 9+/-1 MPa, p<0.001). The modulus remained relatively constant during the remainder of the four week incubation perio! d (aligned at four weeks: 8.0+/-0.3 MPa). The tensile strength for aligned fibre scaffolds was affected in the same manner. Similar changes were not observed for the initial modulus of the random scaffold configuration. Biodegradation of the scaffold in the presence of cholesterol esterase (a monocyte derived enzyme) yielded a 0.5 mg/week weight loss. The soluble and non-soluble degradation products were found to be non-toxic to bovine AF cells grown in vitro. The consistent rate of material degradation along with stable mechanical properties comparable to those of native AF tissue, and the absence of cytotoxic effects, make this polymer a suitable biomaterial candidate for further investigation into its use for tissue-engineering annulus fibrosus. PMID: 20466079 [PubMed - as supplied by publisher] | | |
| Cardiospheres and tissue engineering for myocardial regeneration: potential for clinical application.
May 15, 2010 at 6:42 AM
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| | Cardiospheres and tissue engineering for myocardial regeneration: potential for clinical application. J Cell Mol Med. 2010 May 12; Authors: Gaetani R, Rizzitelli G, Chimenti I, Barile L, Forte E, Ionta V, Angelini F, Sluijter JP, Barbetta A, Messina E, Frati G Tissue engineering is an increasingly expanding area of research in the cardiovascular field that involves engineering, chemistry, biology and medicine. Cardiac Tissue Engineering (CTE) aims to regenerate myocardial damage by combining cells, matrix, biological active molecules and physiologic stimuli. The rationale behind CTE applications is that in order to regenerate the ventricular wall after a myocardial infarction it is necessary to combine procedures that regenerate both cardiomyocytes and the extracellular matrix. The application of (stem) cells together with a matrix could represent an environment protected from the inflammatory and pro-apoptotic signals, a stemness/survival reservoir slowly releasing cells and factors promoting tissue regeneration and angiogenesis. This review will focus on the applications and advantages that CTE application could offer compared to conventional cell therapy. PMID: 20465579 [PubMed - as supplied by publisher] | | |
| Toward engineering a human neoendothelium with circulating progenitor cells.
May 15, 2010 at 6:42 AM
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| | Toward engineering a human neoendothelium with circulating progenitor cells. Stem Cells. 2010 Feb;28(2):318-28 Authors: Allen JB, Khan S, Lapidos KA, Ameer GA Tissue-engineered vascular grafts may one day provide a solution to many of the limitations associated with using synthetic vascular grafts. However, identifying a suitable cell source and polymer scaffold to recreate the properties of a native blood vessel remains a challenge. In this work, we assess the feasibility of using endothelial progenitor cells (EPCs) found in circulating blood to generate a functional endothelium on poly(1,8-octanediol-co-citrate) (POC), a biodegradable elastomeric polyester. EPCs were isolated from human blood and biochemically differentiated into endothelial-like cells (HE-like) in vitro. The differentiated cell phenotype and function was confirmed by the appearance of the characteristic endothelial cell (EC) cobblestone morphology and positive staining for EC markers, von Willebrand factor, vascular endothelial cadherin, flk-1, and CD31. In addition, HE-like cells cultured on POC express endothelial nitric oxide synthase at levels co! mparable to aortic ECs. Furthermore, as with mature endothelial cells, HE-like cell populations show negligible expression of tissue factor. Similarly, HE-like cells produce and secrete prostacyclin and tissue plasminogen activator at levels comparable to venous and aortic ECs. When compared to fibroblast cells, HE-like cells cultured on POC show a decrease in the rate of plasma and whole-blood clot formation as well as a decrease in platelet adhesion. Finally, the data show that HE-like cells can withstand physiological shear stress of 10 dynes/cm(2) when cultured on POC-modified expanded poly(tetrafluoroethylene) vascular grafts. Collectively, these data are the foundation for future clinical studies in the creation of an autologous endothelial cell-seeded vascular graft. PMID: 20013827 [PubMed - indexed for MEDLINE] | | |
| Stem/progenitor cells from inflamed human dental pulp retain tissue regeneration potential.
May 15, 2010 at 6:09 AM
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| | Stem/progenitor cells from inflamed human dental pulp retain tissue regeneration potential. Regen Med. 2010 May 14; Authors: Alongi DJ, Yamaza T, Song Y, Fouad AF, Romberg EE, Shi S, Tuan RS, Huang GT Background: Potent stem/progenitor cells have been isolated from normal human dental pulps termed dental pulp stem cells (DPSCs). However, it is unknown whether these cells exist in inflamed pulps (IPs). Aims: To determine whether DPSCs can be identified and isolated from IPs; and if they can be successfully cultured, whether they retain tissue regeneration potential in vivo. Materials & methods: DPSCs from freshly collected normal pulps (NPs) and IPs were characterized in vitro and their tissue regeneration potential tested using an in vivo study model. Results: The immunohistochemical analysis showed that IPs expressed higher levels of mesenchymal stem cell markers STRO-1, CD90, CD105 and CD146 compared with NPs (p < 0.05). Flow cytometry analysis showed that DPSCs from both NPs and IPs expressed moderate to high levels of CD146, stage-specific embryonic antigen-4, CD73 and CD166. Total population doubling of DPSCs-IPs (44.6 +/- 2.9) was lower than that o! f DPSCs-NPs (58.9 +/- 2.5) (p < 0.05), and DPSCs-IPs appeared to have a decreased osteo/dentinogenic potential compared with DPSCs-NPs based on the mineral deposition in cultures. Nonetheless, DPSCs-IPs formed pulp/dentin complexes similar to DPSCs-NPs when transplanted into immunocompromised mice. Conclusion: DPSCs-IPs can be isolated and their mesenchymal stem cell marker profiles are similar to those from NPs. Although some stem cell properties of DPSCs-IPs were altered, cells from some samples remained potent in tissue regeneration in vivo. PMID: 20465527 [PubMed - as supplied by publisher] | | |
| JNK3 mediates paraquat- and rotenone-induced dopaminergic neuron death.
May 15, 2010 at 6:09 AM
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| | JNK3 mediates paraquat- and rotenone-induced dopaminergic neuron death. J Neuropathol Exp Neurol. 2010 May;69(5):511-20 Authors: Choi WS, Abel G, Klintworth H, Flavell RA, Xia Z Mechanistic studies underlying dopaminergic neuron death may identify new drug targets for the treatment of Parkinson disease. Epidemiological studies have linked pesticide exposure to increased risk for sporadic Parkinson disease. Here, we investigated the role of c-Jun-N-terminal kinase 3 (JNK3), a neural-specific JNK isoform, in dopaminergic neuron death induced by the pesticides rotenone and paraquat. The role of JNK3 was evaluated using RNA silencing and gene deletion to block JNK3 signaling. Using an antibody that recognizes all isoforms of activated JNKs, we found that paraquat and rotenone stimulate JNK phosphorylation in primary cultured dopaminergic neurons. In cultured neurons transfected with Jnk3-specific siRNA and in neurons from Jnk3 mice, JNK phosphorylation was nearly abolished, suggesting that JNK3 is the main JNK isoform activated in dopaminergic neurons by these pesticides. Paraquat- and rotenone-induced death of dopaminergic neurons was also s! ignificantly reduced by Jnk3 siRNA or Jnk3 gene deletion, and deletion of the Jnk3 gene completely attenuated paraquat-induced dopaminergic neuron death and motor deficits in vivo. Our data identify JNK3 as a common and critical mediator of dopaminergic neuron death induced by paraquat and rotenone, suggesting that it is a potential drug target for Parkinson disease treatment. PMID: 20418776 [PubMed - indexed for MEDLINE] | | |
| Beta-catenin signaling increases in proliferating NG2+ progenitors and astrocytes during post-traumatic gliogenesis in the adult brain.
May 15, 2010 at 6:09 AM
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| | Beta-catenin signaling increases in proliferating NG2+ progenitors and astrocytes during post-traumatic gliogenesis in the adult brain. Stem Cells. 2010 Feb;28(2):297-307 Authors: White BD, Nathe RJ, Maris DO, Nguyen NK, Goodson JM, Moon RT, Horner PJ Wnt/beta-catenin signaling can influence the proliferation and differentiation of progenitor populations in the hippocampus and subventricular zone, known germinal centers in the adult mouse brain. It is not known whether beta-catenin signaling occurs in quiescent glial progenitors in cortex or spinal cord, nor is it known whether beta-catenin is involved in the activation of glial progenitor populations after injury. Using a beta-catenin reporter mouse (BATGAL mouse), we show that beta-catenin signaling occurs in NG2 chondroitin sulfate proteoglycan+ (NG2) progenitors in the cortex, in subcallosal zone (SCZ) progenitors, and in subependymal cells surrounding the central canal. Interestingly, cells with beta-catenin signaling increased in the cortex and SCZ following traumatic brain injury (TBI) but did not following spinal cord injury. Initially after TBI, beta-catenin signaling was predominantly increased in a subset of NG2+ progenitors in the cortex. One week f! ollowing injury, the majority of beta-catenin signaling appeared in reactive astrocytes but not oligodendrocytes. Bromodeoxyuridine (BrdU) paradigms and Ki-67 staining showed that the increase in beta-catenin signaling occurred in newly born cells and was sustained after cell division. Dividing cells with beta-catenin signaling were initially NG2+; however, by four days after a single injection of BrdU, they were predominantly astrocytes. Infusing animals with the mitotic inhibitor cytosine arabinoside prevented the increase of beta-catenin signaling in the cortex, confirming that the majority of beta-catenin signaling after TBI occurs in newly born cells. These data argue for manipulating the Wnt/beta-catenin pathway after TBI as a way to modify post-traumatic gliogenesis. PMID: 19960516 [PubMed - indexed for MEDLINE] | | | | 
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