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Increased Cell Size (increased + cell_size)
Selected AbstractsThe Role of Cardiac Tissue Alignment in Modulating Electrical FunctionJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 12 2007CHIUNG-YIN CHUNG M.S. Introduction:,Most cardiac arrhythmias are associated with pathology-triggered ion channel remodeling. However, multicellular effects, for example, exaggerated anisotropy and altered cell-to-cell coupling, can also indirectly affect action potential morphology and electrical stability via changed electrotonus. These changes are particularly relevant in structural heart disease, including hypertrophy and infarction. Recent computational studies showed that electrotonus factors into stability by altering dynamic properties (restitution). We experimentally address the question of how cell alignment and connectivity alter tissue function and whether these effects depend on the direction of wave propagation. Methods and Results:,We show that cardiac cell arrangement can alter electrical stability in an in vitro cardiac tissue model by mechanisms both dependent and independent of the direction of wave propagation, and local structural remodeling can be felt beyond a space constant. Notably, restitution of action potential duration (APD) and conduction velocity was significantly steepened in the direction of cell alignment. Furthermore, prolongation of APD and calcium transient duration was found in highly anisotropic cell networks, both for longitudinal and transverse propagation. This is in contrast to expected correlation between wave propagation direction and APD based on electrotonic effects only, but is consistent with our findings of increased cell size and secretion of atrial natriuretic factor, a hypertrophy marker, in the aligned structures. Conclusion:,Our results show that anisotropic structure is a potent modulator of electrical stability via electrotonus and molecular signaling. Tissue alignment must be taken into account in experimental and computational models of arrhythmia generation and in designing effective treatment therapies. [source] Retinoids directly activate the collagen X promoter in prehypertrophic chondrocytes through a distal retinoic acid response elementJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 1 2006Arthur J. Cohen Abstract Retinoids are essential for the terminal differentiation of chondrocytes during endochondral bone formation. This maturation process is characterized by increased cell size, expression of a unique extracellular matrix protein, collagen X, and eventually by mineralization of the matrix. Retinoids stimulate chondrocyte maturation in cultured cells and experimental animals, as well as in clinical studies of synthetic retinoids; furthermore, retinoid antagonists prevent chondrocyte maturation in vivo. However, the mechanisms by which retinoids regulate this process are poorly understood. We and others showed previously that retinoic acid (RA) stimulates expression of genes encoding bone morphogenetic proteins (BMPs), suggesting that retinoid effects on chondrocyte maturation may be indirect. However, we now show that RA also directly stimulates transcription of the collagen X gene promoter. We have identified three RA response element (RARE) half-sites in the promoter, located 2,600 nucleotides upstream from the transcription start site. These three half-sites function as two overlapping RAREs that share the middle half-site. Ablation of the middle half-site destroys both elements, abolishing RA receptor (RAR) binding and drastically decreasing RA stimulation of transcription. Ablation of each of the other two half-sites destroys only one RARE, resulting in an intermediate level of RAR binding and transcriptional stimulation. These results, together with our previously published data, indicate that retinoids stimulate collagen X transcription both directly, through activation of RARs, and indirectly, through increased BMP production. J. Cell. Biochem. © 2006 Wiley-Liss, Inc. [source] Quantitative nuclear proteomics reveals new phenotypes altered in lymphoblastoid cellsPROTEOMICS - CLINICAL APPLICATIONS, Issue 3 2009Paul Brennan Dr. Abstract B-lymphocytes are essential for the production of antibodies to fight pathogens and are the cells of origin in 95% of human lymphomas. During their activation, and immortalisation by Epstein,Barr virus (EBV) which contributes to human cancers, B-lymphocytes undergo dramatic changes in cell size and protein content. This study was initiated to compare the proteome of two B-cell lines, from the same individual, that reflect different patterns of activation, one is EBV negative and the other is EBV positive. Using isobaric tags, LC-MALDI TOF-TOF and subcellular fractionation, we quantified 499 proteins from B-cells. From a detergent lysed protein extract, we identified 34 proteins that were differentially expressed in EBV-immortalised B-cells. By analysing a nuclear extract, we identified a further 29 differentially expressed proteins with only four proteins shared between the two extracts, illustrating the benefit of subcellular fractionation. This analysis has identified proteins involved in the cytoskeletal phenotype of activated B-cells and the increased antigen recognition in EBV-immortalised cells. Importantly, we have also identified new regulators of transcription and changes in ribonuclear proteins that may contribute to the increased cell size and immortalisation of lymphoblastoid cells. [source] Ecological correlates of body size in relation to cell size and cell number: patterns in flies, fish, fruits and foliageBIOLOGICAL REVIEWS, Issue 2 2007Jeff Arendt Abstract Body size is important to most aspects of biology and is also one of the most labile traits. Despite its importance we know remarkably little about the proximate (developmental) factors that determine body size under different circumstances. Here, I review what is known about how cell size and number contribute to phenetic and genetic variation in body size in Drosophila melanogaster, several fish, and fruits and leaves of some angiosperms. Variation in resources influences size primarily through changes in cell number while temperature acts through cell size. The difference in cellular mechanism may also explain the differences in growth trajectories resulting from food and temperature manipulations. There is, however, a poorly recognized interaction between food and temperature effects that needs further study. In addition, flies show a sexual dimorphism in temperature effects with the larger sex responding by changes in cell size and the smaller sex showing changes in both cell size and number. Leaf size is more variable than other organs, but there appears to be a consistent difference between how shade-tolerant and shade-intolerant species respond to light level. The former have larger leaves via cell size under shade, the latter via cell number in light conditions. Genetic differences, primarily from comparisons of D. melanogaster, show similar variation. Direct selection on body size alters cell number only, while temperature selection results in increased cell size and decreased cell number. Population comparisons along latitudinal clines show that larger flies have both larger cells and more cells. Use of these proximate patterns can give clues as to how selection acts in the wild. For example, the latitudinal pattern in D. melanogaster is usually assumed to be due to temperature, but the cellular pattern does not match that seen in laboratory selection at different temperatures. [source] | ||||||||||