Mechanically Activated Calcium Channel PIEZO1 Modulates Radiation-Induced Epithelial-Mesenchymal Transition by Forming a Positive Feedback With TGF-β1.

TGF-β-centered epithelial-mesenchymal transition (EMT) is a key process involved in radiation-induced pulmonary injury (RIPI) and pulmonary fibrosis. PIEZO1, a mechanosensitive calcium channel, is expressed in myeloid cell and has been found to play an important role in bleomycin-induced pulmonary fibrosis. Whether PIEZO1 is related with radiation-induced EMT remains elusive.

PIEZO1 Ion Channel Mediates Ionizing Radiation-Induced Pulmonary Endothelial Cell Ferroptosis Ca/Calpain/VE-Cadherin Signaling.

Pulmonary endothelial cell dysfunction plays an important role in ionizing radiation (IR)-induced lung injury. Whether pulmonary endothelial cell ferroptosis occurs after IR and what are the underlying mechanisms remain elusive. Here, we demonstrate that 15-Gy IR induced ferroptosis characterized by lethal accumulation of reactive oxygen species (ROS), lipid peroxidation, mitochondria shrinkage, and decreased glutathione peroxidase 4 (GPX4) and SLC7A11 expression in pulmonary endothelial cells.

PIEZO1 might be involved in cerebral ischemia-reperfusion injury through ferroptosis regulation: a hypothesis.

Stroke is associated with high mortality and extremely high disability rate. Regulating ferroptosis seems to be a promising way to treat ischemic stroke. After stroke, vasogenic edema exerts a mechanical force on surrounding structures, which could activate the mechanosensitive PIEZO1 channel.

Comparative effects of mesenchymal progenitor cells, endothelial progenitor cells, or their combination on myocardial infarct regeneration and cardiac function.

Objective: Recent evidence suggests that the effects of mesenchymal progenitor cell transplantation into the infarcted myocardium might be mediated by local paracrine angiogenesis. We compared the effects of mesenchymal progenitor cell transplantation versus those of a primarily angiogenic cell, the endothelial progenitor cell, in a rat model of myocardial infarction.

Methods: Twenty-one days after left anterior descending artery ligation, rats were injected in their infarcted anterior myocardium with 1 x 10(6) mesenchymal progenitor cells, 1 x 10(6) endothelial progenitor cells, 5 x 10(5) mesenchymal progenitor cells plus 5 x 10(5) endothelial progenitor cells, or phosphate-buffered saline (n = 6-8 per group).

[Effect of neuropeptide Y and neurotensin on diurnal rhythm of blood pressure and target organ damage for essential hypertension].

Objective: To investigate the effect of plasma neuropeptide Y (NPY), neurotensin (NT) and their relationships on the diurnal rhythm of BP and target organ damage for essential hypertension.

Methods: Ambulatory BP monitoring (ABPM) for 24 hours was performed in ninety patients with essential hypertension and thirty healthy subjects. The patients were divided into two groups: 55 dippers and 35 non-dippers according to the ABPM results.

Homocysteine alters monocyte-endothelial interaction in vitro.

Objective: To determine whether homocysteine induced endothelial damage through monocyte-endothelial interaction and to characterize both cell types in vitro.

Methods: Radiomethods were performed on monocyte adhesion to/through endothelium and endothelial damage experiments.

Results: Homocysteine-treated endothelial cells increased monocyte adhesion and transmigration.