Cancer cells cause vascular endothelial cell (vEC) retraction via 12(S)HETE secretion; the possible role of cancer cell derived microparticle.

Background: Cancer cell mediated vascular endothelial cell (vEC) retraction plays a pivotal role in cancer metastasis. The aim of this study is to clarify the biochemical character of vEC retraction factor derived from human breast cancer cell line, MCF-7.

Methods And Results: In order to estimate vEC retracting activity, transwell chamber assay system was employed.

Suppression of oxidative stress-induced hepatocyte injury by calpain antisense.

Background: Calpain, a cytosolic Ca(2+)-dependent proteinase, plays a pivotal role in cell injury. In this study, we investigated the effect of calpain-mu antisense oligonucleotide on oxidative stress induced-hepatocyte injury.

Materials And Methods: Hemagglutinating virus of Japan liposome complex with one of three types of antisense oligonucleotide (AS-1, AS-2, AS-3) or scramble oligonucleotide was added to the culture medium of HuH7 cells and incubated for 6 days.

Cancer cell contact causes oscillatory and polarized rise of cytoplasmic ionized calcium concentration in human umbilical vein endothelial cells.

The rise of cytoplasmic ionized Ca2+ concentration ([Ca2+]i) is an important factor in cellular signal transduction, which regulates a variety of cellular functions in vascular endothelial cells (vECs) such as morphological change, secretion of vaso-active molecules, or endothelial permeability. It is also known that the loss of vEC integrity plays pivotal roles in several physiological or pathological phenomena, such as inflammation or cancer metastasis. The aim of this study was to clarify the mode of cancer cell induced vEC retraction by cell to cell contact.

Ischemia-reperfusion injury of the liver with special reference to calcium-dependent mechanisms.

Ischemia-reperfusion (I/R) injury is a complex process involving numerous intracellular signaling pathways, mediators, cells, and pathophysiological disturbances; its prevention during liver surgery is of utmost importance. In this review, we divide hepatic I/R injury into two phases, intracellular and extracellular, for a better understanding of the processes involved. Ca2+ and Ca2+-dependent reactions play an important role as a trigger in the former phase, while the subsequent generation of bioactive substances plays a predominant role in the latter phase.