Acute aerobic exercise regulation of myocardial calcium homeostasis involves CASQ1, CASQ2, and TRDN.

Exercise maintains cardiac calcium homeostasis and promotes cardiovascular health. This study explored temporal changes of calcium-related myocardial transcriptome changes during the recovery phase following a single bout of moderate-intensity aerobic exercise. Healthy male Sprague-Dawley rats were anesthetized with sodium pentobarbital after moderate-intensity aerobic exercise at four time points (0, 12, 24, and 72 h postexercise). The hearts were removed and RNA-seq and bioinformatics analyses were used to examine temporal transcriptional changes in the myocardium. Casq1, Casq2, and Trdn were identified as key genes in the regulation of calcium homeostasis during myocardial recovery. The highest expression of Casq1, Casq2, and Trdn genes and the proteins they encode occurred 24 h after exercise. An in vitro calcium overload heart model using the Langendorff heart perfusion method was used to examine myocardial calcium buffering capacity. Calcium overload caused the least changes in left ventricular developed pressure, infarct area, Lactate dehydrogenase release, and extent of morphological damage to myocardial cells, with the highest protein expressions of CASQ1, CASQ2, and TRDN at 24 h after acute exercise. This study indicates that maximal myocardial Ca2+ buffering capacity occurs 24 h postexercise in rats. Our study provides insights into exercise-mediated improvements in cardiovascular function and exercise preconditioning.NEW & NOTEWORTHY Acute aerobic exercise upregulates myocardial Casq1, Casq2, and Trdn genes and the proteins they encode in rats. Higher protein levels of CASQ1, CASQ2, and TRDN conferred an improved ability of the myocardium to resist calcium overload. Furthermore, 24 h postexercise is the time point with optimal myocardial calcium buffer capacity.

A novel therapeutic system for malignant glioma: nanoformulation, pharmacokinetic, and anticancer properties of cell-nano-drug delivery.

Macrophage carriage, release, and antitumor activities of polymeric nanoformulated paclitaxel (PTX) were developed as a novel delivery system for malignant glioma. To achieve this goal, the authors synthesized PTX-loaded nanoformulations (nano-PTX), then investigated their uptake, release, and toxicological properties. Chemosensitivity was significant in U87 cells (P < 0.05) at concentrations from 10(-4) to 10(-8) M following 72 hours' exposure to bone-marrow-derived macrophages (BMM)-nano-PTX in comparison with treatment with nano-PTX alone. The most significant reductions in U87 cell viability (P < 0.05) were observed in the transwell cocultures containing BMM-nano-PTX. Limited toxicity to BMM was observed at the same concentrations. BMM functions were tested by analysis of microtubules and actin filaments, as the cytoarchitecture, demonstrating a similar cytoskeleton pattern before and after nano-PTX was loaded into cells. This data indicate that nanoformulations of PTX facilitate cell uptake, delay toxicity, and show improved therapeutic efficacy by BMM-nano-PTX delivery. FROM THE CLINICAL EDITOR: In this study the delivery, release, and antitumor activity of polymeric nanoformulated paclitaxel carried by macrophages are described as a novel and efficient system for treatment of resistant malignant glioma.

WITHDRAWN: A novel therapeutic system for malignant glioma: nanoformulation, pharmacokinetic, and anticancer properties of cell-nano-drug delivery.

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