| Please add updates@feedmyinbox.com to your address book to make sure you receive these messages in the future. | |
| Nuclear morphology and deformation in engineered cardiac myocytes and tissues.
April 13, 2010 at 6:45 AM
|
| | Nuclear morphology and deformation in engineered cardiac myocytes and tissues. Biomaterials. 2010 Apr 9; Authors: Bray MA, Adams WJ, Geisse NA, Feinberg AW, Sheehy SP, Parker KK Cardiac tissue engineering requires finely-tuned manipulation of the extracellular matrix (ECM) microenvironment to optimize internal myocardial organization. The myocyte nucleus is mechanically connected to the cell membrane via cytoskeletal elements, making it a target for the cellular response to perturbation of the ECM. However, the role of ECM spatial configuration and myocyte shape on nuclear location and morphology is unknown. In this study, printed ECM proteins were used to configure the geometry of cultured neonatal rat ventricular myocytes. Engineered one- and two-dimensional tissue constructs and single myocyte islands were assayed using live fluorescence imaging to examine nuclear position, morphology and motion as a function of the imposed ECM geometry during diastolic relaxation and systolic contraction. Image analysis showed that anisotropic tissue constructs cultured on microfabricated ECM lines possessed a high degree of nuclear alignment similar ! to that found in vivo; nuclei in isotropic tissues were polymorphic in shape with an apparently random orientation. Nuclear eccentricity was also increased for the anisotropic tissues, suggesting that intracellular forces deform the nucleus as the cell is spatially confined. During systole, nuclei experienced increasing spatial confinement in magnitude and direction of displacement as tissue anisotropy increased, yielding anisotropic deformation. Thus, the nature of nuclear displacement and deformation during systole appears to rely on a combination of the passive myofibril spatial organization and the active stress fields induced by contraction. Such findings have implications in understanding the genomic consequences and functional response of cardiac myocytes to their ECM surroundings under conditions of disease. PMID: 20382423 [PubMed - as supplied by publisher] | | |
| Multimodal release of transforming growth factor-beta1 and the BB isoform of platelet derived growth factor from PEGylated fibrin gels.
April 13, 2010 at 6:45 AM
|
| | Multimodal release of transforming growth factor-beta1 and the BB isoform of platelet derived growth factor from PEGylated fibrin gels. J Control Release. 2010 Apr 7; Authors: Drinnan CT, Zhang G, Alexander MA, Pulido AS, Suggs LJ We designed a growth factor release system to potentially stabilize neovascularization in the treatment of ischemic tissue. In this study, the release of PDGF-BB and TGF-beta1 was controlled with distinct kinetics from injectable PEGylated fibrin gels. Growth factors can be loaded into PEGylated fibrin gels via 3 mechanisms: entrapment, conjugation through a homobifunctional amine reactive PEG linker, and physical affinity with the fibrin matrix. PDGF-BB was entrapped during thrombin-mediated crosslinking leading to a diffusion-controlled release over 2days. TGF-beta1 was both conjugated through the PEG linker and bound to the matrix via physical affinity, delaying the release rate of TGF-beta1 up to 10days. Further, the release rate was highly correlated to gel degradation rate indicating that TGF-beta1 release is degradation-controlled. Therefore, by modulating the molar ratio of PEG to fibrinogen, we were able to control the release rate of TGF-beta1 without al! tering the release kinetics of PDGF-BB. The bioactivity of loaded TGF-beta1 was maintained upon release as evidenced by the inhibition of cell proliferation. This system could be expanded to incorporate growth factors loaded via 3 schemes with differing release rates from an injectable system allowing for a high degree of flexibility in other combinational drug delivery and tissue engineering systems. PMID: 20381553 [PubMed - as supplied by publisher] | | |
| A nerve graft constructed with xenogeneic acellular nerve matrix and autologous adipose-derived mesenchymal stem cells.
April 13, 2010 at 6:45 AM
|
| | A nerve graft constructed with xenogeneic acellular nerve matrix and autologous adipose-derived mesenchymal stem cells. Biomaterials. 2010 Apr 7; Authors: Zhang Y, Luo H, Zhang Z, Lu Y, Huang X, Yang L, Xu J, Yang W, Fan X, Du B, Gao P, Hu G, Jin Y Since synthetic nerve conduits do not exhibit the characteristics of regeneration, they are generally inadequate substitutes for autologous nerve graft in the repair of long peripheral nerve defects. To resolve this problem, in this study, we constructed a nerve regeneration characteristics-containing nerve graft through integrating xenogeneic acellular nerve matrix (ANM) with autologous neural differentiated adipose-derived mesenchymal stem cells (ADSCs). Xenogeneic ANM was processed by a protocol removing cells and myelin sheath completely, meanwhile preserving growth factors and extracellular matrix (ECM) microstructure of natural nerve, such as porous and basal lamina tube. Cytocompatibility and immunocompatibility evaluation revealed that ANM could support cell attachment and proliferation, and did not stimulate vigorous host reject response. After inoculation of neural differentiated ADSCs onto ANM, differentiated cells were observed to align along longitudi! nal axis of ANM, resembling band of büngner, and persistently express NGF, GDNF, and BDNF. In vivo, neural differentiated ADSCs also presented glial cell characteristics and promote nerve regeneration 7 days post transplantation. We repaired 1cm Sprague Dawley rat sciatic nerve defects using this nerve graft construction and nerve gap regeneration was indicated by electrophysiology, retrograde labeling and histology analysis. Therefore, we conclude that constructed nerve graft, offering nerve regeneration characteristics, hold great promise to replace autologous in repair peripheral nerve defect. PMID: 20381139 [PubMed - as supplied by publisher] | | |
| Bioengineered skin in diabetic foot ulcers.
April 13, 2010 at 6:45 AM
|
| | Bioengineered skin in diabetic foot ulcers. Diabetes Obes Metab. 2010 Apr;12(4):307-15 Authors: Teng YJ, Li YP, Wang JW, Yang KH, Zhang YC, Wang YJ, Tian JH, Ma B, Wang JM, Yan X OBJECTIVE: Bioengineered skin (BS) has been shown to play an important role in the treatment of diabetic foot ulcers (DFUs). Whether BS in the therapy of DFU can improve the outcomes still remains uncertain. We performed a quantitative meta-analysis of available randomized controlled trials to determine the effectiveness and safety of BS in the treatment of patients with DFUs. DESIGN AND METHODS: Comprehensive search strategies of various electronic databases were used for this study to evaluate the effectiveness and safety between BS and conventional treatment (CT) in patients with DFU, and only randomized controlled trials were adopted in our review. Search terms included 'bioengineered skin', 'tissue-engineering skin', 'human-tissue graft', 'human-skin device', 'living-skin equivalent' and 'diabetic foot', 'diabetic ulcer', 'diabetic wound'. Analysis outcomes included complete wound closure, complications, ulcer recurrence and adverse severe events (ASEs). RESU! LTS: Seven randomized controlled trials on BS vs. CT were included, and 880 participants met inclusion criteria. Pooled analysis showed a significant effectiveness and safety advantages for BS treatment compared to CT for patients with DFUs. In analysis of complications, only statistically significant difference of infection was noted. And no included trials reported ASEs related to these treatments. CONCLUSIONS: Based on the meta-analysis, patients with DFUs may benefit from the BS because of its high effectiveness and safety and reduced risk for infections in comparison to CT. PMID: 20380651 [PubMed - in process] | | |
| Yield and characterization of subcutaneous human adipose-derived stem cells by flow cytometric and adipogenic mRNA analyzes.
April 13, 2010 at 6:45 AM
|
| | Yield and characterization of subcutaneous human adipose-derived stem cells by flow cytometric and adipogenic mRNA analyzes. Cytotherapy. 2010 Apr 9; Authors: Yu G, Wu X, Dietrich MA, Polk P, Scott LK, Ptitsyn AA, Gimble JM Abstract Background aims. Adipose-derived stromal/stem cells (ASC) capable of multipotential differentiation can be isolated with high yields from human subcutaneous lipoaspirates. This study reports our recent experience of isolating and immunophenotypically characterizing ASC from >60 human patients with a mean age of 43.6 and body mass index (BMI) of 27. Methods. We examined the ASC yield per unit volume of lipoaspirate tissue, the surface antigen profile based on flow cytometry, histochemical differentiation potential along the adipogenic and osteogenic pathways, and expression of adipogenic mRNA by transcriptomic microarray and reverse transcription (RT)-polymerase chain reaction (PCR). Results. The population (n = 64) of predominantly Caucasian (84.3%) female (90.6%) donors had a mean age of 43.6 +/- 11.1 years and a mean BMI of 27.0 +/- 3.8. A yield of 375 +/- 142 x 10(3) ASC was obtained per milliliter of lipoaspirate within a 4.1 +/- 0.7-day culture pe! riod (n = 62). The ASC population was uniformly CD29(+) CD34(+) CD44(lo) CD45(lo) CD73(+) CD90(+) CD105(+) and capable of undergoing both adipogenesis and osteogenesis in vitro based on Oil Red O and Alizarin Red staining, respectively. Adipogenic differentiation was associated with a significant induction of multiple mRNA associated with lipid storage and synthesis based on microarray analysis of n = 3 donors. During an adipogenic differentiation time-course, representative mRNA (adiponectin, C/EBPalpha, leptin and LPL) displayed increases of several orders of magnitude. Conclusions. These findings demonstrate the reproducibility of subcutaneous lipoaspirates as a consistent and abundant source of functional ASC from donors across a spectrum of ages and BMI. These results have relevance for regenerative medical applications exploiting autologous and allogeneic ASC for soft and hard tissue engineering. PMID: 20380539 [PubMed - as supplied by publisher] | | |
| Vascularization shaping the heart.
April 13, 2010 at 6:45 AM
|
| | Vascularization shaping the heart. Ann N Y Acad Sci. 2010 Feb;1188:46-51 Authors: Lesman A, Gepstein L, Levenberg S Myocardial infarction can lead to irreversible heart failure. In an attempt to restore function in the failing heart, tissue-engineered cardiac constructs can be applied to repopulate scar tissue with a new pool of contractile cells. Effective engineering of viable thick complex tissue-constructs requires intense vascularization. Furthermore, endothelial-cardiomyocyte crosstalk plays a key role in mutually enhancing tissue functionality, which can further improve construct survival. The ability to generate an engineered, vascularized muscle tissue was demonstrated by us using the skeletal and the cardiac muscle models. In the skeletal model, we showed that prevascularization of the construct promoted perfusion of the graft. More recently, we successfully generated a beating human cardiac muscle-construct, containing an endothelial network, by co-culturing human embryonic stem cell-derived-cardiomyocytes, fibroblasts, and endothelial cells within biodegradable scaf! folds. Such muscle-constructs could contribute significantly to the emerging discipline of cardiovascular regenerative medicine as well as to the study of the important role of tissue vascularization. PMID: 20201885 [PubMed - indexed for MEDLINE] | | |
| Cartilage engineering using cell-derived extracellular matrix scaffold in vitro.
April 13, 2010 at 6:45 AM
|
| | Cartilage engineering using cell-derived extracellular matrix scaffold in vitro. J Biomed Mater Res A. 2010 Mar 15;92(4):1567-77 Authors: Jin CZ, Choi BH, Park SR, Min BH A cell-derived extracellular matrix (ECM) scaffold was constructed using cultured porcine chondrocytes via a freeze-drying method, and its ability to promote cartilage formation was evaluated in vitro. Scanning electron microscope (SEM) revealed that the scaffold had highly uniform porous microstructure. Then, rabbit chondrocytes were seeded dynamically on ECM scaffold and cultured for 2 days, 1, 2, and 4 weeks in vitro for analysis. Polyglycolic acid (PGA) scaffold was used as a control. On gross observation of neocartilage tissue, a silvery white cartilage-like tissue was observed after 1 week of culture in ECM scaffold, while similar morphology was seen only after 4 weeks in PGA scaffold. The volume of neocartilage-like tissue was significantly increased in both ECM and PGA groups. The compressive strength was gradually increased with time in ECM group, while gradually decreased in PGA group. DNA, glycosaminoglycan (GAG) and collagen contents also increased gra! dually with time in both groups, but showed more significant increase in ECM group. Histological staining for GAG (Safranin O staining) and type II collagen (immunohistochemistry) showed sustained accumulation of ECM molecules with time, which gradually and uniformly filled porous space in ECM scaffold. On the contrary, they accumulated only at the peripheral area of PGA scaffold. These results suggest that a novel cell-derived ECM scaffold can provide a promising environment for generating a high quality cartilage in vitro. PMID: 19437434 [PubMed - indexed for MEDLINE] | | |
| Dendritic cell responses to self-assembled monolayers of defined chemistries.
April 13, 2010 at 6:45 AM
|
| | Dendritic cell responses to self-assembled monolayers of defined chemistries. J Biomed Mater Res A. 2010 Mar 15;92(4):1487-99 Authors: Shankar SP, Petrie TA, García AJ, Babensee JE Biomaterial contact triggers dendritic cell (DC) maturation, to an extent depending on the biomaterial, ultimately enhancing an immune response toward associated antigens, implying a role for biomaterials as adjuvants. Self-assembled monolayers (SAM) of alkanethiols on titanium/gold-coated surfaces presenting different chemistries were used to study effects of biomaterial surface chemistry on DC maturation. Although DCs treated with OH, COOH, or NH(2) SAMs showed modest maturation, those treated with CH(3) SAMs were least mature, all based on cytospins, allostimulatory capacity, or maturation marker expression. Surprisingly, DCs treated with CH(3) SAMs secreted highest levels of proinflammatory tumor necrosis factor-alpha (TNF-alpha) or interleukin-6 (IL-6) but were least mature. Secretion of anti-inflammatory mediators by DCs treated with CH(3) SAMs was not responsible for mitigating DC maturation under these conditions. Interestingly, elevated levels of apoptoti! c markers were measured associated with DCs and T cells upon CH(3) SAMs contact. Since phagocytosis of apoptotic DCs has strong immunosuppressive effects on DCs, more apoptotic DCs on CH(3) SAMs may account for lower DC maturation. Finally, higher expression of cytotoxic T lymphocyte associated antigen receptor-4 (CTLA-4) on T cells may imply a mechanism of T cell inhibition on CH(3) SAMs. PMID: 19425048 [PubMed - indexed for MEDLINE] | | |
| SDF-1alpha inhibits hypoxia and serum deprivation-induced apoptosis in mesenchymal stem cells through PI3K/Akt and ERK1/2 signaling pathways.
April 13, 2010 at 6:45 AM
|
| | SDF-1alpha inhibits hypoxia and serum deprivation-induced apoptosis in mesenchymal stem cells through PI3K/Akt and ERK1/2 signaling pathways. Mol Biol Rep. 2010 Apr 10; Authors: Yin Q, Jin P, Liu X, Wei H, Lin X, Chi C, Liu Y, Sun C, Wei Y Bone marrow-derived mesenchymal stem cells (BMSCs) have been demonstrated to be a promising cell sources for cardiac regeneration. Poor survival rate of transplanted BMSCs in infarcted myocardium attenuated its clinical application. It's reported that stromal-derived factor-1 (SDF-1) could protect progenitor cells including endothelial progenitor cells and embryonic stem cells from apoptosis. But little is known whether SDF-1alpha protein has the same protective effects on BMSCs under conditions of hypoxia and serum deprivation (hypoxia/SD). In present study, we verified that SDF-1alpha (0.50-2.0 mug/ml) inhibited hypoxia/SD induced apoptosis of BMSCs through mitochondrial pathway. After administration of SDF-1alpha, the loss of mitochondrial membrane potential and cytochrome c released from mitochondria to cytosol were significantly inhibited, and caspase 3 activity also declined. Furthermore, the effect of SDF-1alpha on mitochondrial pathway was neutralized by u! sing PI3K inhibitor (Wortmannin) and ERK1/2 inhibitor (U0126). Our observations suggested that SDF-1alpha inhibits hypoxia/SD induced BMSCs apoptosis through PI3K/Akt and ERK1/2 signaling pathways. These data also imply that the anti-apoptotic effect mediated by SDF-1alpha may enhance cell survival after cell transplantation. PMID: 20383584 [PubMed - as supplied by publisher] | | |
| Activation of the imprinted Dlk1-Dio3 region correlates with pluripotency levels of mouse stem cells.
April 13, 2010 at 6:45 AM
|
| | Activation of the imprinted Dlk1-Dio3 region correlates with pluripotency levels of mouse stem cells. J Biol Chem. 2010 Apr 9; Authors: Liu L, Luo GZ, Yang W, Zhao X, Zheng Q, Lv Z, Li W, Wu HJ, Wang L, Wang XJ, Zhou Q Low reprogramming efficiency and reduced pluripotency have been the two major obstacles in induced pluripotent stem (iPS) cell research. An effective and quick method to assess the pluripotency levels of iPS cells at early stages would significantly increase the success rate of iPS cell generation and promote its applications. We have identified a conserved imprinted region of the mouse genome, the Dlk1-Dio3 region, which was activated in fully pluripotent mouse stem cells but repressed in partially pluripotent cells. The degree of activation of this region was positively correlated with the pluripotency level of stem cells. A mammalian conserved cluster of miRNAs encoded by this region exhibited significant expression differences between full- and partial-pluripotent stem cells. Several miRNAs from this cluster potentially target the PRC2 silencing complex, and may form a feed-forward regulatory loop resulting in the expression of all genes and non-coding RNAs en! coded by this region in full-pluripotent stem cells. No other genomic regions were found to exhibit such clear expression changes between cell lines with different pluripotency levels, therefore the Dlk1-Dio3 region may serve as a marker to identify fully pluripotent iPS or ES cells. These findings also provide a step forward toward understanding the operating mechanisms during reprogramming to produce iPS cells, and can potentially promote the application of iPS cells in regenerative medicine and cancer therapy. The putative synergetic effects of several miRNAs also furthered the understanding of the coordinative functions of miRNAs in regulating complex biological processes. PMID: 20382743 [PubMed - as supplied by publisher] | | |
| Enhancement of bone formation ex vivo and in vivo by a helioxanthin-derivative.
April 13, 2010 at 6:45 AM
|
| | Enhancement of bone formation ex vivo and in vivo by a helioxanthin-derivative. Biochem Biophys Res Commun. 2010 Apr 8; Authors: Nakajima K, Komiyama Y, Hojo H, Ohba S, Yano F, Nishikawa N, Aburatani H, Takato T, Chung UI To effectively treat serious bone defects using bone-regenerative medicine, a small chemical compound that potently induces bone formation must be developed. We previously reported on the osteogenic effect of 4-(4-methoxyphenyl)pyrido[40,30:4,5]thieno[2,3-b]pyridine-2-carboxamide (TH), a helioxanthin-derivative, in vitro. Here, we report on TH's osteogenic effects ex vivo and in vivo. TH induced new bone formation in both calvarial and metatarsal organ cultures. A novel monitoring system of osteoblastic differentiation using MC3T3-E1 cells revealed that TH was released from alpha-TCP bone cement and this release continued for more than one month. Lastly, the implantation of the alpha-TCP carrier containing TH into defects in mouse skull resulted in increased new bone areas within the defects after 4 weeks. A TH-containing scaffold may help establish a more efficient bone regeneration system. PMID: 20382113 [PubMed - as supplied by publisher] | | |
| Calcification after myocardial infarction is independent of amniotic fluid stem cell injection.
April 13, 2010 at 6:45 AM
|
| | Calcification after myocardial infarction is independent of amniotic fluid stem cell injection. Cardiovasc Pathol. 2010 Apr 8; Authors: Delo DM, Guan X, Wang Z, Groban L, Callahan M, Smith T, Sane DC, Payne RM, Atala A, Soker S Ischemic heart disease remains one of the most common causes of mortality in developed countries. Recently, stem cell therapy is being considered for treating ischemic heart diseases. On the other hand, there has been evidence of chondro-osteogenic mass formation after stem cell injection in the heart. In a recent publication, Chiavegato et al. (J Mol Cell Cardiol. 42 (2007) 746-759) has suggested that amniotic fluid-derived stem (AFS) cells cause chondro-osteogenic masses in the infarcted heart. The goal of the current study was to further examine the formation of such masses, specifically, the role of AFS cells in this process. Our results confirm the presence of similar bone-like masses in the left ventricular wall of infarcted rats; however, this phenomenon occurred independent of AFS cell injection into the myocardium. Moreover, AFS cell injection did not increase the presence of chondro-osteogenic masses. Echocardiographic analysis of large infarctions in ra! ts frequently revealed the presence of echogenic structures in the left ventricular wall. We further demonstrated a significant relationship between the infarction size and chondro-osteogenic formation and subsequent decrease in cardiac function. Collectively, our study indicates that chondro-osteogenic differentiation can take place in infarcted rat heart independent of cell injection. These results have significant implications for future design and testing of stem cell therapy for treatment of cardiac muscle diseases. PMID: 20382039 [PubMed - as supplied by publisher] | | |
| Apical conicity ratio: A new index on left ventricular apical geometry after myocardial infarction.
April 13, 2010 at 6:45 AM
|
| | Apical conicity ratio: A new index on left ventricular apical geometry after myocardial infarction. J Thorac Cardiovasc Surg. 2010 Apr 7; Authors: Fan H, Zheng Z, Feng W, Zhang Y, Jin L, Li P, Hu S OBJECTIVE: Our objective was to introduce a new index to evaluate left ventricular aneurysm by quantitative analysis of left ventricular apical geometry. METHODS: A total of 116 selected subjects underwent magnetic resonance imaging, 28 healthy volunteers, 29 patients with dilated cardiomyopathy, and 59 patients with ischemic heart disease (26 with left ventricular aneurysm; 33 with no aneurysm). The apical conicity ratio was calculated as the ratio of left ventricular apical area over apical triangle. RESULTS: Diastolic apical conicity ratio of patients with left ventricular aneurysm was 1.62 +/- 0.20 and systolic apical conicity ratio was 1.78 +/- 0.43. After left ventricular reconstruction, the diastolic apical conicity ratio decreased to 1.47 +/- 0.23 and the systolic ratio to 1.51 +/- 0.21, which came close to the normal level, whereas other global indices remained. In patients with dilated cardiomyopathy, sphericity index and eccentricity index increased sig! nificantly without changes in the apical conicity ratio. Among patients with ischemic heart disease, the apical conicity ratio of the group with left ventricular aneurysm was significantly higher than that of the group without an aneurysm when the other indices between the 2 groups showed no statistically difference. Receiver operating characteristic curves showed only apical conicity ratio had high power of discriminating left ventricular aneurysm from no aneurysm. CONCLUSIONS: The new index, apical conicity ratio, can be used to quantify the regional left ventricular deformation, especially in patients with left ventricular aneurysm resulting from myocardial infarction. PMID: 20381083 [PubMed - as supplied by publisher] | | |
| Long non-coding RNAs in nervous system function and disease.
April 13, 2010 at 6:45 AM
|
| | Long non-coding RNAs in nervous system function and disease. Brain Res. 2010 Apr 6; Authors: Qureshi IA, Mattick JS, Mehler MF Central nervous system (CNS) development, homeostasis, stress responses, and plasticity are all mediated by epigenetic mechanisms that modulate gene expression and promote selective deployment of functional gene networks in response to complex profiles of interoceptive and environmental signals. Thus, not surprisingly, disruptions of these epigenetic processes are implicated in the pathogenesis of a spectrum of neurological and psychiatric diseases. Epigenetic mechanisms involve chromatin remodeling by relatively generic complexes that catalyze DNA methylation and various types of histone modifications. There is increasing evidence that these complexes are directed to their sites of action by long non-protein-coding RNAs (lncRNAs), of which there are tens if not hundreds of thousands specified in the genome. LncRNAs are transcribed in complex intergenic, overlapping and antisense patterns relative to adjacent protein-coding genes, suggesting that many lncRNAs regu! late the expression of these genes. LncRNAs also participate in a wide array of subcellular processes, including the formation and function of cellular organelles. Most lncRNAs are transcribed in a developmentally regulated and cell-type specific manner, particularly in the CNS, wherein over half of all lncRNAs are expressed. While the numerous biological functions of lncRNAs are yet to be characterized fully, a number of recent studies suggest that lnRNAs are important for mediating cell identity. This function seems to be especially important for generating the enormous array of regional neuronal and glial cell subtypes that are present in the CNS. Further studies have also begun to elucidate additional roles played by lncRNAs in CNS processes, including homeostasis, stress responses and plasticity. Herein, we review emerging evidence that highlights the expression and function of lncRNAs in the CNS and suggests that lncRNA deregulation is an important factor in various C! NS pathologies including neurodevelopmental, neurodegenerative! and neu roimmunological disorders, primary brain tumors, and psychiatric diseases. PMID: 20380817 [PubMed - as supplied by publisher] | | |
| Gene therapy: back on track?
April 13, 2010 at 6:45 AM
|
| | Gene therapy: back on track? EMBO Rep. 2010 Feb;11(2):75 Authors: Mavilio F PMID: 20118988 [PubMed - indexed for MEDLINE] | | |
| Kruppel-like factor 4 (Klf4) prevents embryonic stem (ES) cell differentiation by regulating Nanog gene expression.
April 13, 2010 at 6:45 AM
|
| | Kruppel-like factor 4 (Klf4) prevents embryonic stem (ES) cell differentiation by regulating Nanog gene expression. J Biol Chem. 2010 Mar 19;285(12):9180-9 Authors: Zhang P, Andrianakos R, Yang Y, Liu C, Lu W Transcription factor Kruppel-like factor 4 (Klf4) is essential for somatic cell reprogramming. In addition, Klf4 seems to play a redundant role along with other Klf family proteins in embryonic stem (ES) cell self-renewal. However, how Klf4 regulates ES cell self-renewal and somatic cell reprogramming is still poorly understood. Here we report that Klf4 is required for both ES cell self-renewal and maintenance of pluripotency and that the expression of Klf4 prevents ES cell differentiation in response to withdrawal of leukemia inhibitory factor (LIF) or bone morphogenetic protein 4 (BMP4). In addition, Klf4 directly binds to the promoter region of Nanog and regulates its expression. Expression of Nanog prevents ES cell differentiation even when Klf4 gene expression is knocked down. On the other hand, knockdown of Nanog expression induces differentiation of ES cells that overexpress Klf4. Taken together, these results demonstrate that Klf4 functions upstream of Nan! og in ES cell self-renewal and in preventing ES cell differentiation. PMID: 20071344 [PubMed - indexed for MEDLINE] | | |
| Yield and characterization of subcutaneous human adipose-derived stem cells by flow cytometric and adipogenic mRNA analyzes.
April 13, 2010 at 6:37 AM
|
| | Yield and characterization of subcutaneous human adipose-derived stem cells by flow cytometric and adipogenic mRNA analyzes. Cytotherapy. 2010 Apr 9; Authors: Yu G, Wu X, Dietrich MA, Polk P, Scott LK, Ptitsyn AA, Gimble JM Abstract Background aims. Adipose-derived stromal/stem cells (ASC) capable of multipotential differentiation can be isolated with high yields from human subcutaneous lipoaspirates. This study reports our recent experience of isolating and immunophenotypically characterizing ASC from >60 human patients with a mean age of 43.6 and body mass index (BMI) of 27. Methods. We examined the ASC yield per unit volume of lipoaspirate tissue, the surface antigen profile based on flow cytometry, histochemical differentiation potential along the adipogenic and osteogenic pathways, and expression of adipogenic mRNA by transcriptomic microarray and reverse transcription (RT)-polymerase chain reaction (PCR). Results. The population (n = 64) of predominantly Caucasian (84.3%) female (90.6%) donors had a mean age of 43.6 +/- 11.1 years and a mean BMI of 27.0 +/- 3.8. A yield of 375 +/- 142 x 10(3) ASC was obtained per milliliter of lipoaspirate within a 4.1 +/- 0.7-day culture pe! riod (n = 62). The ASC population was uniformly CD29(+) CD34(+) CD44(lo) CD45(lo) CD73(+) CD90(+) CD105(+) and capable of undergoing both adipogenesis and osteogenesis in vitro based on Oil Red O and Alizarin Red staining, respectively. Adipogenic differentiation was associated with a significant induction of multiple mRNA associated with lipid storage and synthesis based on microarray analysis of n = 3 donors. During an adipogenic differentiation time-course, representative mRNA (adiponectin, C/EBPalpha, leptin and LPL) displayed increases of several orders of magnitude. Conclusions. These findings demonstrate the reproducibility of subcutaneous lipoaspirates as a consistent and abundant source of functional ASC from donors across a spectrum of ages and BMI. These results have relevance for regenerative medical applications exploiting autologous and allogeneic ASC for soft and hard tissue engineering. PMID: 20380539 [PubMed - as supplied by publisher] | | |
| Calcification after myocardial infarction is independent of amniotic fluid stem cell injection.
April 13, 2010 at 6:02 AM
|
| | Calcification after myocardial infarction is independent of amniotic fluid stem cell injection. Cardiovasc Pathol. 2010 Apr 8; Authors: Delo DM, Guan X, Wang Z, Groban L, Callahan M, Smith T, Sane DC, Payne RM, Atala A, Soker S Ischemic heart disease remains one of the most common causes of mortality in developed countries. Recently, stem cell therapy is being considered for treating ischemic heart diseases. On the other hand, there has been evidence of chondro-osteogenic mass formation after stem cell injection in the heart. In a recent publication, Chiavegato et al. (J Mol Cell Cardiol. 42 (2007) 746-759) has suggested that amniotic fluid-derived stem (AFS) cells cause chondro-osteogenic masses in the infarcted heart. The goal of the current study was to further examine the formation of such masses, specifically, the role of AFS cells in this process. Our results confirm the presence of similar bone-like masses in the left ventricular wall of infarcted rats; however, this phenomenon occurred independent of AFS cell injection into the myocardium. Moreover, AFS cell injection did not increase the presence of chondro-osteogenic masses. Echocardiographic analysis of large infarctions in ra! ts frequently revealed the presence of echogenic structures in the left ventricular wall. We further demonstrated a significant relationship between the infarction size and chondro-osteogenic formation and subsequent decrease in cardiac function. Collectively, our study indicates that chondro-osteogenic differentiation can take place in infarcted rat heart independent of cell injection. These results have significant implications for future design and testing of stem cell therapy for treatment of cardiac muscle diseases. PMID: 20382039 [PubMed - as supplied by publisher] | | | | 
| This email was sent to regenmd@gmail.com. Account Login
Don't want to receive this feed any longer? Unsubscribe here
This email was carefully delivered by Feed My Inbox. 230 Franklin Road Suite 814 Franklin, TN 37064 | |
No comments:
Post a Comment