Modulation of the mitochondrial Ca uniporter complex subunit expression by different shear stress patterns in vascular endothelial cells.

Mitochondrial calcium ( Ca ) uptake occurs via the Mitochondrial Ca Uniporter (MCU) complex and plays a critical role in mitochondrial dynamics, mitophagy, and apoptosis. MCU complex activity is in part modulated by the expression of its regulatory subunits. Cardiovascular disease models demonstrated altered gene/protein expression of one or multiple subunits in different cells, including vascular endothelial cells (ECs).

The mitochondrial Ca uniporter channel synergizes with fluid shear stress to induce mitochondrial Ca oscillations.

The mitochondrial calcium (Ca) uniporter (MCU) channel is responsible for mitochondrial Ca influx. Its expression was found to be upregulated in endothelial cells (ECs) under cardiovascular disease conditions. Since the role of MCU in regulating cytosolic Ca homeostasis in ECs exposed to shear stress (SS) is unknown, we studied mitochondrial Ca dynamics (that is known to decode cytosolic Ca signaling) in sheared ECs.

Molecular nature and physiological role of the mitochondrial calcium uniporter channel.

Calcium (Ca) signaling is critical for cell function and cell survival. Mitochondria play a major role in regulating the intracellular Ca concentration ([Ca]). Mitochondrial Ca uptake is an important determinant of cell fate and governs respiration, mitophagy/autophagy, and the mitochondrial pathway of apoptosis.

Monocyte recruitment and fate specification after myocardial infarction.

Monocytes are critical mediators of the inflammatory response following myocardial infarction (MI) and ischemia-reperfusion injury. They are involved in both initiation and resolution of inflammation and play an integral role in cardiac repair. The antagonistic nature of their function is dependent on their subset heterogeneity and biphasic response following injury.

Modeling the role of endoplasmic reticulum-mitochondria microdomains in calcium dynamics.

Upon inositol trisphosphate (IP) stimulation of non-excitable cells, including vascular endothelial cells, calcium (Ca) shuttling between the endoplasmic reticulum (ER) and mitochondria, facilitated by complexes called Mitochondria-Associated ER Membranes (MAMs), is known to play an important role in the occurrence of cytosolic Ca concentration ([Ca]) oscillations. A mathematical compartmental closed-cell model of Ca dynamics was developed that accounts for ER-mitochondria Ca microdomains as the µd compartment (besides the cytosol, ER and mitochondria), Ca influx to/efflux from each compartment and Ca buffering. Varying the distribution of functional receptors in MAMs vs.