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Calcium ions play essential roles in most cellular activities, including fertilization, cell division, motility and contraction, excitability and secretion. Moreover, altered Ca2+ regulation and signaling play central roles in many pathological conditions. My current research concerns the regulation of the intracellular Ca2+ concentration and its role in normal and pathological cell signaling in vascular smooth muscle, with a focus on the pathogenesis of salt-dependent hypertension.
The sarcoplasmic/endoplasmic reticulum (S/ER) accumulates and stores Ca2+ for subsequent release as "signal Ca2+". We identified a "signaling complex" region, termed the "PlasmERosome", that regulates Ca2+ storage and signaling. The PLasmERosome consists of three main elements: certain plasma membrane (PM) microdomains, the adjacent "junctional" S/ER (jS/ER), and the tiny pocket of cytosol between the PM and jS/ER. Ca2+ is regulated within this cytosolic region by specific ion channels, transporter isoforms and receptors contained in the PM microdomains. This, in turn, regulates Ca2+ storage and Ca2+ release (i.e., the Ca2+ signals) from the S/ER. We are identifying the component transporters within these complexes and determining how the complexes are organized and how they influence local and global Ca2+ concentrations and signaling. We employ a variety of molecular and cellular biological methods, including digital imaging. Several transgenic mouse lines are used to study cardiovascular parameters in intact animals, and the properties of isolated small arteries, individual myocytes, and cultured myocytes. Our findings are unraveling the molecular links between salt and hypertension.
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American journal of physiology. Cell physiology (2024)
Science Signalingno. 788 (2023)
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