P2X7 receptor-dependent blebbing and the activation of Rho-effector kinases, caspases, and IL-1 beta release.

P2X7 Receptor-Dependent Blebbing and the Activation of Rho-Effector Kinases, Caspases, and IL-1 Release

P 107: P2x7 Receptors: as a Novel Targets for the Treatment of Neuroinflammation

P2x7 receptors are Purineric receptors that are extracellular ATP-gated ion channel. These receptors require high dose or prolonged exposure to ATP for initial activation. The Activation of these receptors facilitates the formation of inflammasome which activates caspase 1. The P20 and P10 subunits of caspase 1 form active enzyme that then releases active interleukin (IL)-1 β and IL-18, tu...

Temporal Interleukin-1β Secretion from Primary Human Peripheral Blood Monocytes by P2X7-independent and P2X7-dependent Mechanisms*

The processing and regulated secretion of IL-1beta are critical points of control of the biological activity of this important pro-inflammatory cytokine. IL-1beta is produced by both monocytes and macrophages, but the rate and mechanism of release differ according to the differentiation status and the origin of these cells. We aimed to study the control of processing and release in human blood ...

Purinergic Modulation of Interleukin-1β Release from Microglial Cells Stimulated with Bacterial Endotoxin

Microglial cells express a peculiar plasma membrane receptor for extracellular ATP, named P2Z/P2X7 purinergic receptor, that triggers massive transmembrane ion fluxes and a reversible permeabilization of the plasma membrane to hydrophylic molecules of up to 900 dalton molecule weight and eventual cell death (Di Virgilio, F. 1995. Immunol. Today, 16:524-528). The physiological role of this newly...

The angiotensin II type 1 receptor induces membrane blebbing by coupling to Rho A, Rho kinase, and myosin light chain kinase.

The angiotensin II type 1 receptor (AT(1)R) is a G alpha(q/11)-coupled G protein-coupled receptor that is widely expressed in multiple tissues, including vascular smooth muscle cells, brain, and kidney. Activation of the AT(1)R in vascular smooth muscle cells leads to alterations in actin-based membrane protrusions such as lamellipodia, filopodia, and membrane blebs that ultimately lead to cell...