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Biorheology is an international interdisciplinary journal that publishes research on the deformation and flow properties of biological systems or materials. It is the aim of the editors and publishers of
Biorheology to bring together contributions from those working in various fields of biorheological research from all over the world. A diverse editorial board with broad international representation provides guidance and expertise in wide-ranging applications of rheological methods to biological systems and materials.
The aim of biorheological research is to determine and characterize the dynamics of physiological processes at all levels of organization. Manuscripts should report original theoretical and/or experimental research promoting the scientific and technological advances in a broad field that ranges from the rheology of macromolecules and macromolecular arrays to cell, tissue and organ rheology. In all these areas, the interrelationships of rheological properties of the systems or materials investigated and their structural and functional aspects are stressed.
The scope of papers solicited by
Biorheology extends to systems at different levels of organization that have never been studied before, or, if studied previously, have either never been analyzed in terms of their rheological properties or have not been studied from the point of view of the rheological matching between their structural and functional properties. This biorheological approach applies in particular to molecular studies where changes of physical properties and conformation are investigated without reference to how the process actually takes place, how the forces generated are matched to the properties of the structures and environment concerned, proper time scales, or what structures or strength of structures are required.
Biorheology invites papers in which such 'molecular biorheological' aspects, whether in animal or plant systems, are examined and discussed. While we emphasize the biorheology of physiological function in organs and systems, the biorheology of disease is of equal interest. Biorheological analyses of pathological processes and their clinical implications are encouraged, including basic clinical research on hemodynamics and hemorheology.
In keeping with the rapidly developing fields of mechanobiology and regenerative medicine,
Biorheology aims to include studies of the rheological aspects of these fields by focusing on the dynamics of mechanical stress formation and the response of biological materials at the molecular and cellular level resulting from fluid-solid interactions. With increasing focus on new applications of nanotechnology to biological systems, rheological studies of the behavior of biological materials in therapeutic or diagnostic medical devices operating at the micro and nano scales are most welcome.
Abstract: The cDNA microarray is an extremely beneficial tool for study of differential gene expression in the cardiovascular system. This technique is used in many different applications including drug discovery, environmental science, and the effects of mechanical forces on vascular cell phenotype. The paper reviews work by others, and describes our study on effects of shear stress on vascular endothelial cells. These microarray studies verified earlier findings using Northern and polymerase chain reaction (PCR) analyses in this area; and also found previously unidentified differentially expressed genes, leading to new hypotheses regarding how cells and tissues respond to biochemical and mechanical stimuli.
vol. 40, no. 1,2,3, pp. 5-11, 2003
Abstract: Ca2+ is an important intracellular second messenger in signal transduction of endothelial cells. It has long been recognized that a mechanosensitive Ca2+ ‐permeable channel is present in vascular endothelial cells. The activity of this channel may increase intracellular Ca2+ level in endothelial cells. A recent finding is that the activity of this channel may be regulated by cGMP through a protein kinase G‐dependent pathway. Inhibition of the channel by cGMP abolishes the Ca2+ influx elicited by flow. Several inhibitors of the cation channel including Gd3+ , Ni2+ , and SK&F‐96365 also inhibit the Ca2+ influx due…to flow stimulation. These data suggest that a mechanosensitive cation channel is the primary pathway mediating the flow‐induced Ca2+ entry in vascular endothelial cells. Another important finding is that the opening of this mechanosensitive channel by KT5823 leads to endothelium‐dependent vascular dilation. Therefore, it appears that this channel may play a crucial role in the regulation of vascular tone.
vol. 40, no. 1,2,3, pp. 23-30, 2003
Abstract: Caveolin‐1 is a principal component of caveolae and is involved in signaling transduction in a number of cells. A hypothesis was proposed in this work that mechanical forces due to flow induce caveolin‐1 translocation. So the changes of caveolin‐1 expression and distribution in cultured endothelial cells (HUVECs) exposed to a steady laminar flow were studied. For comparing with the influence of cytokine, caveolin‐1 in the cells stimulated by TNF‐α was also investigated. Indirect immunofluorescence and double fluorescence labeling showed that in control cells, caveolin‐1 was primarily localized on the cell surface, which corresponded to the peripheral distribution of F‐actin, and…presented some local concentrations. In the cells exposed to a laminar flow (1.0 Pa), caveolin‐1 distribution showed a time‐dependent variation. After 24 h of shear, the local concentration of caveolin‐1 was found, in the most cells, at upstream side of cell body. Also more caveolin‐1 molecules were observed in the cells. In contrast, TNF‐α induced a decrease of caveolin‐1 in cells. The redistribution of caveolin‐1 seems to be correlated to F‐actin organization.
Keywords: Caveolin‐1, shear stress, endothelial cell, TNF‐α, F‐actin, signal transduction
vol. 40, no. 1,2,3, pp. 31-39, 2003
Abstract: The adhesion of breast adenocarcinoma cells (MDA‐MB‐231) to human umbilical vein endothelial cells (HUVEC) was studied in whole blood and under varying flow conditions. This study was done on HUVEC either kept under static conditions or pre‐conditioned in flow for 2 hours at a shear stress of 5 or 13 dyn/cm2 . Coverslips coated by HUVEC were placed in a parallel plate perfusion chamber and perfused at a shear rate of 300 or 1500 sec−1 with heparin‐anticoagulated blood containing 111 In labelled MDA‐MB‐231 cells. We report here the optimal conditions for studying the adhesion of MDA‐MB‐231 to endothelial cells…under shear constraints corresponding to those observed into small and medium sized arteries.
vol. 40, no. 1,2,3, pp. 41-45, 2003
Abstract: Integrins may serve as mechanosensors in endothelial cells (ECs): shear stress causes integrin–Shc association, assembly of the signaling complex and then leads to JNK activation. Flow also mediates selective and cell‐specific alterations in vascular cell G‐protein expression that correlate with changes in cell‐signalling, G‐protein functionality and modulate Ca2+ concentration. In this study, we explored the cross‐talks between EC membrane mechanosensors, such as integrins, ion channels, and G‐proteins in shear stress‐induced signal transduction by their specific inhibition. Confluent monolayer of bovine aortic endothelial cells (BAECs) were incubated with or without specific inhibitors prior to shearing experiments. Our results showed an…attenuation of integrin–Shc association under shear stress with RGD, and with PTX, but not with BAPTA/AM. The inhibitions of shear‐activated JNK are similar for RGD and PTX. However, unlike for integrin association, the chelation of calcium reduced JNK activation. These results provide several lines of evidence of the interactions between different mechanosensors in ECs. First, integrin–Shc association required cell attachment and G‐protein activity, but not intracellular calcium. Second, shear‐induced JNK activation is regulated by multiple mechano‐sensing mechanisms such as integrin, G‐protein and calcium concentration.
Abstract: In order to demonstrate that IL‐8 mRNA expression in endothelial cells is not only regulated by chemical factors, but also by mechanical factors, in this article, after pretreating cultured human umbilical vein endothelial cells (HUVECs) with shear stress for different time, we employed both RT‐PCR to assay IL‐8 mRNA expression and immunocytochemical staining to detect NF‐κB activation in HUVECs. We found that: (i) IL‐8 mRNA expressed little in HUVECs untreated or pretreated with low laminar shear stress for 0.5 hour; IL‐8 mRNA expression was increased when HUVECs were pretreated with low laminar shear stress for 1 hour, and increased further…when pretreated for 2 hours; (ii) the immunoreactivity of NF‐κB p65 in the nuclei of HUVECs untreated or pretreated with low laminar shear stress for 0.5 hour was negative, while it became weak positive in the nuclei of HUVECs pretreated with shear stress for 1 hour and positive in the nuclei of HUVECs pretreated for 2 hours. The results imply that low laminar shear stress was capable of inducing IL‐8 gene expression and activating NF‐κB, which were both time‐dependent. The induction of IL‐8 gene expression by laminar shear stress is probably due to the activation of NF‐κB. We suggest that IL‐8 mRNA expression in endothelial cells induced by low shear stress may play a key role in the pathogenesis and development of both inflammation and arterioatherosclerosis.