Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rat islets of Langerhans are organized as a core of B-cells surrounded by non-B-cells. It is believed that cell type segregation during histogenesis is the result of the differential expression of cell adhesion molecules (CAMs). Since we have previously shown that in contrast to non-B-cells, homotypic adhesion of pancreatic B-cells is dependent on the presence of Ca2+, the possibility exists that Ca(2+)-dependent CAMs (cadherins) might be in part responsible for islet topography. We now demonstrate that after selective removal of Ca(2+)-independent CAMs from the surface of islet cells by mild trypsin/Ca2+ digestion (TC-treatment), there is no significant difference in homotypic adhesion between sorted B- and non-B-cells in the presence of calcium, suggesting an identical deployment of cadherins. Flow cytometric analysis reveals high levels of uvomorulin on both B- and non-B-cells, without any difference between the two populations. On a "1 to 100" scale, B-cell aggregation in the presence of Ca2+ was decreased by anti-uvomorulin Fab fragments from 67 +/- 4 to 25 +/- 3 (mean +/- SEM, n = 4, P less than 0.01). This level is not different from the degree of B-cell aggregation seen in the presence of 0.5 mM EDTA (22 +/- 2). Aggregation of non-B-cells was only slightly decreased by anti-uvomorulin Fab fragments (from 69 +/- 3 to 52 +/- 4). However, after TC-treatment, homotypic cell aggregation of both B- and non-B-cells was completely inhibited by anti-uvomorulin Fab fragments. Thus, uvomorulin appears to be the only functional cadherin on islet cells, and cell type aggregation properties diverge only by virtue of higher levels of Ca(2+)-independent CAMs on non-B-cells. Fab fragments with the property of perturbing islet cell aggregation in the absence but not in the presence of calcium also prevented pseudoislet organization in vitro, suggesting that Ca(2+)-independent CAMs play the major role in islet cell type segregation. In conclusion, the results show that uvomorulin is responsible for the Ca(2+)-dependent aggregation of islet cells and suggest that the cellular organization within islets or pseudoislets results from the different level of Ca(2+)-independent CAMs on islet cell types.
 ...
PMID:Uvomorulin mediates calcium-dependent aggregation of islet cells, whereas calcium-independent cell adhesion molecules distinguish between islet cell types. 193 61

When groups of cells from the inner marginal zone (mesendoderm) of the early Xenopus gastrula are placed on a fibronectin-coated substratum, the explants of the dorsal region spread into monolayers whereas those from the ventral region, though they adhere to the substratum, do not show this spreading reaction. This different behaviour is not reflected in the in vitro behaviour of the respective cells kept in isolation. No difference between dorsal and ventral cells was observed, when they were tested for lamellipodia-driven spreading, movement over the substratum or properties of integrin- and cadherin-mediated adhesion. However, cell contacts between individual dorsal cells are significantly less stable than those between ventral cells. The higher flexibility of the cell-cell contacts seems to determine the spreading behaviour of the dorsal explants, which includes lamellipodia-driven outward movement of the peripheral cells, rearrangements of the cells, building up a horizontal tension within the aggregate and intercalation of cells from above into the bottom layer. Ventral explants lack these properties. Staining for F-actin revealed a decisive difference of the supracellular organisation of the cytoskeleton that underlies the morphology of the different types of explants. Evidence for a higher flexibility of cell-cell contacts in the dorsal mesendoderm was also obtained in SEM studies on gastrulating embryos. Dorsal mesendodermal cells show stronger protrusive activity as compared to ventral mesendodermal cells. The meaning of these observations for the mechanisms of morphogenetic movements during gastrulation is central to the discussion.
 ...
PMID:Dorsoventral differences in cell-cell interactions modulate the motile behaviour of cells from the Xenopus gastrula. 1178 71

During the process of bone formation, titanium (Ti) surface is an important factor in the modulation of osteoblastic function. This study was conducted in order to determine the effects of different Ti surfaces on the biological responses of a human osteoblast-like cell line (MG63). MG63 cells were cultured on smooth (S), sandblasted large-grit and acid etching (SLA), hydroxyapatite (HA), hydroxyfluoride (HF), titanium nitrate (TIN), and diamond-like carbon (DLC) Ti. The morphology of these cells were assessed by SEM. The cDNAs prepared from the total RNAs of the MG63 were hybridized into a human cDNA microarray (1152 elements). The appearances of the surfaces observed by SEM were different on each of the six dental substrate types. The SLA and HA surfaces were determined to be rougher than the others. MG63 cells cultured on SLA and HA exhibited cell-matrix interactions. In the expression of genes involved in osseointegration, several genes, including bone morphogenetic protein, cadherin, integrin, and insulin-like growth factors, were upregulated on the different surfaces. Several genes, including fibroblast growth factor receptor 4, Bcl 2-related protein, and collagen, were downregulated on the different surfaces. The attachment and expression of key osteogenic regulatory genes were enhanced by the surface roughness of the dental materials used.
 ...
PMID:Effect of various implant coatings on biological responses in MG63 using cDNA microarray. 1662 96

Endothelial-like progenitor cells circulate in the peripheral blood (PB) and can be enumerated using cell culture-based progenitor assays. These circulating vascular progenitor cells (VPCs) are implicated in new vessel formation and regenerative potential in several animal and human models of tissue injury. Given the emerging role of VPCs in regenerative processes and the limited information on the availability of such progenitor cells, we sought to determine baseline circulating VPC levels in healthy allogeneic donors and autologous hematopoietic transplant patients. VPC numbers were also measured in peripheral blood stem cell (PBSC) grafts from both graft types. Immunohistochemistry revealed that VPC clusters obtained under our culture conditions were CD45(+) and acquired endothelial features (CD31 and vascular endothelial-cadherin) in vitro upon angiogenic stimulation and gradually lost monocytic surface markers (CD14). Before PBSC mobilization, VPCs levels varied substantially in healthy donors and were markedly lower in patients with hematologic malignancies compared with healthy allogeneic donors with 27 +/- 15 versus 99 +/- 21 VPCs/mL (mean +/- SEM), respectively (P = .001). In patients undergoing stem cell mobilization, VPCs in the PB increased from 7 +/- 2 on day 0 to 51 +/- 9 by day 7 of mobilization (P = .05), representing a median fold increase of 8.9 (range, 3.0-29.8). Although autologous transplant patients underwent more intensive mobilization, VPCs were higher in allogeneic (7.2 +/- 1.4 x 10(3)/kg) than in autologous (2.6 +/- 1.5 x 10(3)/kg) mobilized PB grafts (P = .045). To identify predictors of VPC content, graft VPCs were compared with levels of CD34(+) cells, total colony forming unit (CFU), or granulocyte-macrophage colony forming unit (GM-CFU). None of these hematopoietic progenitors correlated with VPC numbers in PBSC grafts (P = NS). However, PB monocyte levels were highly correlated with circulating VPC levels (r = 0.71, P < .0001). Thus, our analysis identified significant variability in VPCs at baseline and in PBSC grafts from healthy donors. Nevertheless, these donors remain a better source of VPCs than do autologous transplant patients. Importantly, VPC mobilization occurs independently of hematopoietic mobilization. In view of the potential role of VPCs in recovery from transplant-related tissue injury, angiogenic mobilization strategies that complement hematopoietic mobilization will need to be specifically designed.
 ...
PMID:Endothelial-like vascular progenitor cells (VPCs) from allogeneic and autologous donors: mobilization features distinct from hematopoietic progenitors. 1738 49

Extracellular matrix (ECM) plays a fundamental role in regulating cell attachment, proliferation, migration and differentiation. Both synthetic and biologically derived materials have been explored as an ECM in regenerative medicine and tissue engineering. To biomimick the extracellular matrix, we combined the advantages of the biological properties of nanofibrous scaffolds and the fusion protein to apply for the culture of human mesenchymal stem cells in vitro. In this study, we fabricated well random-oriented/aligned nanofibrous scaffolds with PCL, modified with hE-cadherin-Fc fusion protein and studied the synergistic effect of the scaffolds. The random-oriented/aligned architecture was observed in the nanofibrous scaffolds by SEM. XPS and WCA measurements evidenced that hE-cadherin-Fc was successfully modified on the PCL nanofibrous scaffolds and hydrophilicity of the scaffolds was well improved after fusion protein coating. The hE-cadherin-Fc modified markedly promoted the adhesion and proliferation of hMSCs and guided hMSCs to a spindlier morphology compared with unmodified nanofibrous scaffolds. Furthermore, hMSCs on the hE-cadherin-Fc-coated nanofibrous scaffolds also had differentiation potential. These results suggested that the combination of PCL nanofibrous scaffolds and hE-cadherin-Fc fusion protein may be a promising artificial ECM for the behavior of hMSCs in vitro.
 ...
PMID:Artificial biomimicking matrix modifications of nanofibrous scaffolds by hE-cadherin-Fc fusion protein to promote human mesenchymal stem cells adhesion and proliferation. 2473 44

The role of biomaterials surface in controlling the interfacial biological events leading to implant integration is of key importance. In this study, the effects of NiTi surfaces treated by plasma electrolytic oxidation (PEO) on human umbilical vein endothelial cells (HUVECs) have been investigated. The changes in NiTi surface morphology and chemistry were assessed by SEM, XPS and cross-section TEM/EDX analyzes whereas the effects of the resultant surfaces on in vitro endothelialization and cell junction proteins have been evaluated by life/dead staining, SEM, cells counting, qPCR and immunofluorescence. The findings indicated that the PEO-treated NiTi, with a microporous morphology and oxide dominated surface chemistry, supports viability and proliferation of HUVECs. Numerous thin filopodia probing the microporous surface assisted cells attachment. In addition, claudin-5 and occludin have been upregulated and expression of vascular endothelial-cadherin was not suppressed on PEO-treated NiTi relative to the reference electropolished surfaces. The results of this study suggest that novel NiTi surfaces may be developed using the PEO process, which can be of benefit to atherosclerosis treatment.
...
PMID:The effects of plasma electrolytically oxidized NiTi on in vitro endothelialization. 2687 87

Macular corneal dystrophy (MCD) is characterized by multiple punctate gray-white opacities in the corneal stromal region, due to the accumulation of abnormally sulfated keratan sulfates. We attempted to develop an in vitro model of MCD by simulating the sulfation inhibition using sodium chlorate, a chemical inhibitor of 3'-phosphoadenosine-5'-phosphosulfate (PAPs). The SEM and micro-Raman spectroscopy results showed the hallmark feature of MCD. Further the gene expression studies elucidated the direct effect of sulfation inhibition on the WNT pathway, that in turn downregulated production of matrix metalloproteinases (MMPs), which causes abnormal matrix deposits leading to loss of transparency in vivo. It also resulted in downregulation of integrin and cadherin complexation that leads to disruption of the epithelial layer in the MCD affected corneas. This study offers a promising initial step toward establishing a relevant in vitro MCD disease model, to assess signaling transduction pathways and devise potential treatment strategies based on MMP administration to the MCD affected corneas.
 ...
PMID:Establishment of an in vitro monolayer model of macular corneal dystrophy. 2774 34

Breast cancer (BC) represents the most incident cancer case in women (29%), with high mortality rate. Bone metastasis occurs in 20-50% cases and, despite advances in BC research, the interactions between tumor cells and the metastatic microenvironment are still poorly understood. In vitro 3D models gained great interest in cancer research, thanks to the reproducibility, the 3D spatial cues and associated low costs, compared to in vivo and 2D in vitro models. In this study, we investigated the suitability of a poly-ether-urethane (PU) foam as 3D in vitro model to study the interactions between BC tumor-initiating cells and the bone microenvironment. PU foam open porosity (>70%) appeared suitable to mimic trabecular bone structure. The PU foam showed good mechanical properties under cyclic compression (E=69-109kPa), even if lower than human trabecular bone. The scaffold supported osteoblast SAOS-2 cell line proliferation, with no cytotoxic effects. Human adipose derived stem cells (ADSC) were cultured and differentiated into osteoblast lineage on the PU foam, as shown by alizarin red staining and RT-PCR, thus offering a bone biomimetic microenvironment to the further co-culture with BC derived tumor-initiating cells (MCFS). Tumor aggregates were observed after three weeks of co-culture by e-cadherin staining and SEM; modification in CaP distribution was identified by SEM-EDX and associated to the presence of tumor cells. In conclusion, we demonstrated the suitability of the PU foam to reproduce a bone biomimetic microenvironment, useful for the co-culture of human osteoblasts/BC tumor-initiating cells and to investigate their interaction.
 ...
PMID:Polyurethane foam scaffold as in vitro model for breast cancer bone metastasis. 2892 31