Sitong Zhou¹, Jiandi Wan^1,*

Molecular & Cellular Biomechanics, Vol.16, Suppl.2, pp. 70-70, 2019, DOI:10.32604/mcb.2019.06978

Abstract Piezo proteins (Piezo1 and Piezo2) are recently identified mechanically activated cation channels in eukaryotic cells and associated with physiological responses to touch, pressure, and stretch. In particular, human RBCs express Piezo1 on their membranes, and mutations of Piezo1 have been linked to hereditary xerocytosis. To date, however, physiological functions of Piezo1 on normal RBCs remain poorly understood. Here, we show that Piezo1 regulates mechanotransductive release of ATP from human RBCs by controlling the shear-induced Ca2+ influx [1]. We find that, in human RBCs treated with Piezo1 inhibitors or having mutant Piezo1 channels, the amounts of More >

Ken-ichi Tsubota^1,2,*, Yuya Kodama¹, Hiroyoshi Aoki², Yutaka Yamagata²

Molecular & Cellular Biomechanics, Vol.16, Suppl.2, pp. 38-39, 2019, DOI:10.32604/mcb.2019.07285

Abstract We measured a blood flow in a polydimethysiloxane micro channel to reflect the complex geometry of a microvascular network. A flow rate was compared between two working fluids: water and blood. The measured flow rate reflected the bifurcation effects on the apparent viscosity determined by hematocrit, as well as the effects of the surrounding flow channels as bypasses. More >

Muyi Guo¹, Yan Cai¹, Zhiyong Li^1,2,*

Molecular & Cellular Biomechanics, Vol.16, Suppl.1, pp. 49-49, 2019, DOI:10.32604/mcb.2019.05727

Abstract Observational studies have identified angiogenesis from the adventitial vasa vasorum and intraplaque hemorrhage (IPH) as critical factors in atherosclerotic plaque progression and destabilization. Here we propose a mathematical model incorporating intraplaque neovascularization and hemodynamic calculation for the quantitative evaluation of atherosclerotic plaque hemorrhage. An angiogenic microvasculature based on histology of a patient’s carotid plaque is generated by two-dimensional nine-point model of endothelial cell migration. Three key cells (endothelial cells, smooth muscle cells and macrophages) and three key chemicals (vascular endothelial growth factors, extracellular matrix and matrix metalloproteinase) are involved in the intraplaque angiogenesis model, and… More >

Pablo Marino^1,2, Gabriella de Oliveira Lopes^1,3, Juliana Pereira Borges³, Maria Carolina Terra Cola¹, Daniel Arkader Kopiler¹, Eduardo Tibirica¹

Congenital Heart Disease, Vol.13, No.6, pp. 978-987, 2018, DOI:10.1111/chd.12660

Abstract Objective: Adults with congenital heart disease share some features with those with chronic heart failure. Although microvascular endothelial dysfunction has been de‐ scribed in chronic heart failure, evaluation of the microcirculation in adults with con‐ genital heart disease is lacking. The present study aimed to investigate systemic microvascular reactivity in adults with congenital heart disease.
Interventions: The patients initially underwent cardiopulmonary exercise testing. Then, the cutaneous microvascular reactivity was evaluated in these patients using a laser speckle contrast imaging system coupled with skin iontophoresis of endothelial‐de‐ pendent (acetylcholine) or ‐independent (sodium nitroprusside) vasodilators and pos‐ tocclusive reactive… More >

Shile Liang^†, Meghan Hoskins^†, Cheng Dong^‡

Molecular & Cellular Biomechanics, Vol.7, No.2, pp. 77-91, 2010, DOI:10.3970/mcb.2010.007.077

Abstract To complete the metastatic journey, cancer cells have to disseminate through the circulation and extravasate to distal organs. However, the extravasation process, by which tumor cells leave a blood vessel and invade the surrounding tissue from the microcirculation, remains poorly understood at the molecular level. In this study, tumor cell adhesion to the endothelium (EC) and subsequent extravasation were investigated under various flow conditions. Results have shown polymorphonuclear neutrophils (PMNs) facilitate melanoma cell adhesion to the EC and subsequent extravasation by a shear-rate dependent mechanism. Melanoma cell-PMN interactions are mediated by the binding between intercellular More >