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Different Microenvironments (different + microenvironment)
Selected AbstractsDistinct osteoblastic differentiation potential of murine fetal liver and bone marrow stroma-derived mesenchymal stem cellsJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 2 2008Olivia Fromigué Abstract Bone marrow-derived mesenchymal stem cells (MSC) are able to differentiate into osteoblasts under appropriate induction. Although MSC-derived osteoblasts are part of the hematopoietic niche, the nature of the stromal component in fetal liver remains elusive. Here, we determined the in vitro osteoblastic differentiation potential of murine clonal fetal liver-derived cells (AFT024, BFC012, 2012) in comparison with bone marrow-derived cell lines (BMC9, BMC10). Bone morphogenetic protein-2 (BMP2) increased alkaline phosphatase (ALP) activity, an early osteoblastic marker, in AFT024 and 2012 cells, whereas dexamethasone had little or no effect. BMP2, but not dexamethasone, increased ALP activity in BMC9 cells, and both inducers increased ALP activity in BMC10 cells. BMP2 increased ALP mRNA in AFT024, 2012 and BMC9 cells. By contrast, ALP was not detected in BMC10 and BFC012 cells. BMP2 and dexamethasone increased osteopontin and osteocalcin mRNA expression in 2012 cells. Furthermore, bone marrow-derived cells showed extensive matrix mineralization, whereas fetal liver-derived cell lines showed no or very limited matrix mineralization capacity. These results indicate that the osteoblast differentiation potential differs in bone marrow and fetal liver-derived cell lines, which may be due to a distinct developmental program or different microenvironment in the two hematopoietic sites. J. Cell. Biochem. 104: 620,628, 2008. © 2007 Wiley-Liss, Inc. [source] Effects of density and ontogeny on size and growth ranks of three competing tree speciesJOURNAL OF ECOLOGY, Issue 2 2009Suzanne B. Boyden Summary 1Rank reversals in species performance are theoretically important for structuring communities, maintaining diversity and determining the course of forest succession. Species growth ranks can change with ontogeny or in different microenvironments, but interactions between ontogeny and the environment are not well-understood because of the lack of long-term forest competition studies. While early differences in growth among species may reflect intrinsic differences in shade-tolerance and physiology, ontogenetic trends in growth and variation in neighbourhood density and composition may change or even reverse early patterns of growth rankings. 2We experimentally studied spatial and temporal patterns of species interactions and growth for three northern tree species: Larix laricina, Picea mariana and Pinus strobus. We compared species size and growth rankings over an 11-year period, for different species mixtures planted at four density levels in north-eastern Minnesota, USA. 3The benefits of different growth strategies changed with ontogeny and density leading to reversals in the size rank of competing species over time and space. High-density stands promoted dominance and resource pre-emption by L. laricina, whereas lower-density stands favoured gradual accumulation of biomass and eventual dominance by P. strobus. In the absence of strong neighbour competition, ontogenetic trends in growth had greater influence on growth patterns. 4Species interactions affected the productivity of mixed stands vs. monocultures. Species generally grew more in monoculture than when planted with P. strobus at low density, or with L. laricina at high density. Only L. laricina and P. mariana showed potential for greater overall productivity, or over-yielding, when planted together than alone, probably because of improved resource uptake by the highly stratified canopy. 5Synthesis. Density predictably determined whether size-asymmetric growth or ontogenetic growth trends would drive early establishment and growth patterns. Variation in vertical and horizontal structure that results from early competitive dynamics can influence the successional trajectory or character of the mature forest. This study extends previous efforts to identify the causes of rank reversals in communities and understand the importance of temporal changes beyond the early years of seedling establishment. [source] Bone resorption activity of osteolytic metastatic lung and breast cancersJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 6 2004Lih-Yuann Shih Abstract Production of bone resorption mediators and bone resorption activity were compared among osteolytic metastatic cancers, normal bone tissues, and soft tissue metastatic cancers to search for the possible factors leading to cancer-induced bone resorption. Twenty-five patients with untreated osteolytic metastatic breast or non-small cell lung cancers consisted of the study group. Normal bone tissues obtained from the same patient were used as internal controls; and tumor tissues from patients with soft tissue metastasis were used as external controls. Serum and urinary bone turnover markers were measured. Tissues harvested during surgery were subjected to tissue culture. The levels of prostaglandin E2 (PGE2), tumor necrosis factor-, (TNF-,), and interleukin-6 (IL-6) in the supernatant after 72 h of culture were measured. Bone resorption activity was measured by calcium release from cultured calvarias, and bone volume as well as osteoclast number in bone sections. Patients with osteolytic metastatic cancers showed significantly decreased serum osteocalcin, increased serum alkaline phosphatase, and urinary deoxypyridinoline levels. Osteolytic metastatic cancers produced significantly more PGE2 than both controls. Conditioned medium from osteolytic metastatic tumors showed significantly enhanced bone resorption activity, and indomethacin significantly reduced this activity. Levels of PGE2, and bone resorption activity increased in osteolytic tumor tissues than soft tissue metastatic tissues in the same patient indicated that the same tumor cells might respond differently to different microenvironments. Our observation showed that PGE2 was produced by osteolytic metastatic cancers and stimulated bone resorption in mice calvarias. PGE2 inhibitor may be applicable in reducing bone resorption by osteolytic metastatic cancers. © 2004 Orthopaedic Research Society. Published by Elsevier Ltd. All rights reserved. [source] Metastasis-associated gene expression profile of liver and subcutaneous lesions derived from mouse pheochromocytoma cellsMOLECULAR CARCINOGENESIS, Issue 4 2008Shoichiro Ohta Abstract The development of metastatic cancer is associated with overexpression or downregulation of specific genes and cell regulatory pathways. Some of these genes and pathways may be involved in invasion and dissemination of tumor cells, while others may promote seeding, survival or growth of cells at specific distant sites. In this investigation, gene expression profiles of nonmetastasizing tumors generated by injecting mouse pheochromocytoma cells (MPCs) subcutaneously were compared to those of liver tumors generated by injecting the cells intravenously. Both were compared to the cultured parental cell line. Tumors in the liver have a route of spread, anatomical distribution, and growth environment similar to naturally metastasizing pheochromocytomas, while intravenous injection of cells bypasses the initial steps of metastasis occurring spontaneously from a primary tumor. Eight genes were upregulated in liver tumors, 15 in subcutaneous tumors and seven in both compared to the cultured cells. Using quantitative real-time PCR, expression of five genes (Metap2, Reck, S100a4, Timp2, and Timp3) was verified as significantly lower in liver tumors than in subcutaneous tumors. Downregulation of these genes has been previously been associated with malignancy of pheochromocytomas. These findings indicate that different microenvironments can differentially affect the expression of metastasis-related genes in pheochromocytomas, and that overexpression or underexpression of these genes need not be present when the tumor cells are initially disseminated. The hepatic localization of tumors formed by intravenously injected MPC cells and the tumors' gene expression profile resembling that of naturally occurring pheochromocytoma metastases support the use of this model to study pheochromocytoma metastasis. © 2007 Wiley-Liss, Inc. [source] Water diffusion in the different microenvironments of breast cancerNMR IN BIOMEDICINE, Issue 4 2004Yael Paran Abstract The parameters that characterize the intricate water diffusion in tumors may serve to reveal their distinct pathology. Specifically, the application of diffusion magnetic resonance imaging (MRI) can aid in characterizing breast cancer, as well as monitoring response to therapy. We present here a non-invasive, quantitative MRI investigation, at high spatial resolution, of water diffusion in hormonal dependent MCF7 breast tumors implanted orthotopically in immunodeficient mice. Distinctive MRI protocols were designed in this study, utilizing a broad range of diffusion times and diffusion gradient strengths. Application of these protocols allowed water diffusion in the tissue extracellular and intracellular compartments to be distinguished, and the effect of restricted diffusion and water exchange on the water diffusion in these compartments to be evaluated. Pixel-by-pixel analysis yielded parametric maps of the estimated volume fraction and apparent diffusion coefficient of each compartment. The diffusion of the water in the extracellular microenvironment was approximately two fold slower than that of free water, and in the intracellular compartment was about one order of magnitude slower than that of free water and demonstrated restriction of water diffusion at long diffusion times. Mapping of the water fraction in each compartment was further employed to monitor changes during tumor progression and to assess tumor response to hormonal manipulation with a new antiestrogenic drug, tamoxifen methiodide (TMI). It was found that, in parallel to the growth arrest by this drug, the volume fraction of the slowly diffusing water increased, suggesting a TMI-induced cell swelling. This study can serve as a basis for extending diffusion breast MRI in the clinical setting. Copyright © 2004 John Wiley & Sons, Ltd. [source] Structural properties of trimers and tetramers of ribonuclease APROTEIN SCIENCE, Issue 10 2001Arianna Nenci Abstract Ribonuclease A aggregates (dimers, trimers, tetramers, pentamers) can be obtained by lyophilization from 40% acetic acid solutions. Each aggregate forms two conformational isomers distinguishable by different basic net charge. The crystal structure of the two dimers has recently been determined; the structure of the higher oligomers is unknown. The results of the study of the two trimeric and tetrameric conformers can be summarized as follows: (1) RNase A trimers and tetramers form by a 3D domain-swapping mechanism. N-terminal and C-terminal types of domain swapping could coexist; (2) the secondary structures of the trimeric and tetrameric conformers do not show significant differences if compared with the secondary structure of monomeric RNase A or its two dimers; (3) a different exposure of tyrosine residues indicates that in the aggregates they have different microenvironments; (4) the two trimeric and tetrameric conformers show different susceptibility to digestion by subtilisin; (5) dimers, trimers, and tetramers of RNase A show unwinding activity on double-helical poly(dA-dT) , poly(dA-dT), that increases as a function of the size of the oligomers; (6) the less basic conformers are more stable than the more basic ones, and a low concentration in solution of trimers and tetramers favors their stability, which is definitely increased by the interaction of the aggregates with poly(dA-dT) , poly(dA-dT); (7) the products of thermal dissociation of the two trimers indicate that their structures co ld be remarkably different. The dissociation products of the two tetramers allow the proposal of two models for their putative structures. [source] The prostatic environment suppresses growth of androgen-independent prostate cancer xenografts: An effect influenced by testosteroneTHE PROSTATE, Issue 11 2009Karin Jennbacken Abstract BACKGROUND Interactions between prostate cancer cells and their surrounding stroma play an important role in the growth and maintenance of prostate tumors. To elucidate this further, we investigated how growth of androgen-dependent (AD) LNCaP and androgen-independent (AI) LNCaP-19 prostate tumors was affected by different microenvironments and androgen levels. METHODS Tumor cells were implanted subcutaneously and orthotopically in intact and castrated immunodeficient mice. Orthotopic tumor growth was followed by magnetic resonance imaging (MRI). Gene expression in the tumors was evaluated by means of microarray analysis and microvessel density (MVD) was analyzed using immunohistochemistry. RESULTS The results showed that LNCaP-19 tumors grew more rapidly at the subcutaneous site than in the prostate, where tumors were obviously inhibited. Castration of the mice did not affect ectopic tumors but did result in increased tumor growth in the prostatic environment. This effect was reversed by testosterone treatment. In contrast to LNCaP-19, the LNCaP cells grew rapidly in the prostate and castration reduced tumor development. Gene expression analysis of LNCaP-19 tumors revealed an upregulation of genes, inhibiting tumor growth (including ADAMTS1, RGS2 and protocadherin 20) and a downregulation of genes, promoting cell adhesion and metastasis (including N-cadherin and NRCAM) in the slow-growing orthotopic tumors from intact mice. CONCLUSIONS The results show that the prostatic environment has a varying impact on AD and AI tumor xenografts. Data indicate that the androgen-stimulated prostatic environment limits growth of orthotopic AI tumors through induction of genes that inhibit tumor growth and suppression of genes that promote cell adhesion and metastasis. Prostate 69:1164,1175, 2009. © 2009 Wiley-Liss, Inc. [source] | |||||||||||||