Histamine activates an intracellular Ca signal in normal human lung fibroblast WI-38 cells.

Histamine is an inflammatory mediator that can be released from mast cells to induce airway remodeling and cause persistent airflow limitation in asthma. In addition to stimulating airway smooth muscle cell constriction and hyperplasia, histamine promotes pulmonary remodeling by inducing fibroblast proliferation, contraction, and migration. It has long been known that histamine receptor 1 (H1R) mediates the effects of histamine on human pulmonary fibroblasts through an increase in intracellular Ca concentration ([Ca]), but the underlying signaling mechanisms are still unknown.

ZO-2 favors Hippo signaling, and its re-expression in the steatotic liver by AMPK restores junctional sealing.

ZO-2 is a peripheral ight unction (TJ) protein whose silencing in renal epithelia induces cell hypertrophy. Here, we found that in ZO-2 KD MDCK cells, in compensatory renal hypertrophy triggered in rats by a unilateral nephrectomy and in liver steatosis of bese ucker (OZ) rats, ZO-2 silencing is accompanied by the diminished activity of LATS, a kinase of the Hippo pathway, and the nuclear concentration of YAP, the final effector of this signaling route. ZO-2 appears to function as a scaffold for the Hippo pathway as it associates to LATS1.

BASIC AND CLINICAL INSIGHTS IN CATECHOLAMINERGIC (FAMILIAL) POLYMORPHIC VENTRICULAR TACHYCARDIA.

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a potentially lethal disease, whose characteristic ventricular tachycardias are adrenergic-dependent. Although rare, CPVT should be considered in the differential diagnosis of young individuals with exercise-induced syncope. Mutations in five different genes (RYR2, CASQ2, CALM1, TRDN, and TECRL) are associated with the CPVT phenotype, although RYR2 missense mutations are implicated in up to 60 % of all CPVT cases.

Epidermal Growth Factor Potentiates Migration of MDA-MB 231 Breast Cancer Cells by Increasing NaV1.5 Channel Expression.

Introduction: Breast cancer is one of the leading causes of death worldwide and is the result of dysregulation of various signaling pathways in mammary epithelial cells. The mortality rate in patients suffering from breast cancer is high because the tumor cells have a prominent invasive capacity towards the surrounding tissues. Previous studies carried out in tumor cell models show that voltage-gated ion channels may be important molecular actors that contribute to the migratory and invasive capacity of the tumor cells.