Inductive heating kills cells that contribute to plaque: a proof-of-concept.
Bottom Line: Two days of subsequent observation demonstrated that inductive heating led to a significant reduction in cell number.After 48 h we observed a 95% reduction in cell growth for both spherical and iron particles.These results demonstrate the feasibility of targeting cells involved in atherosclerosis and warrant further research into potential clinical applications.
Affiliation: Kytaro Inc. , Miami, FL , USA.
Inducing cell death by heating targeted particles shows promise in cancer treatment. Here, we aim to demonstrate the feasibility of extending the use of this technique to treat and remove vascular deposits and thrombosis. We used induction heating of macrophages, which are key contributors to atherosclerosis and have demonstrated clear feasibility for heating and destroying these cells using ferromagnetic and pure iron particles. Specifically, iron particles achieved maximum temperatures of 51 ± 0.5 °C and spherical particles achieved a maximum temperature of 43.9 ± 0.2 °C (N = 6) after 30 min of inductive heating. Two days of subsequent observation demonstrated that inductive heating led to a significant reduction in cell number. Prior to induction heating, cell density was 105,000 ± 20,820 cells/ml (N = 3). This number was reduced to 6,666 ± 4,410 cells/ml for the spherical particles and 16,666 ± 9,280 cells/ml for the iron particles 24 h after inductive heating. Though cell density increased on the second day following inductive heating, the growth was minimal. Cells grew to 26,667 ± 6,670 cells/ml and 30,000 ± 15,280 cells/ml respectively. Compared to cell cultures with iron and spherical particles that were not subjected to induction heating, we observed a 97% reduction in cell count for the spherical particles and a 91% reduction for the iron particles after the first 24 h. After 48 h we observed a 95% reduction in cell growth for both spherical and iron particles. Induction heating of microparticles was thus highly effective in reducing the macrophage population and preventing their growth. These results demonstrate the feasibility of targeting cells involved in atherosclerosis and warrant further research into potential clinical applications.
No MeSH data available.
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Mentions: We investigated the differences in cell number across groups as a way to determine the actual impact of inductive heating on cell death. Significant reduction in cell survival was observed in inductively heated cells, compared to the controls, as shown in Fig. 3. While the initial number of cells was 105,000 ± 20,820 cells/ml, 24 h after induction heating the cell count was reduced to 6,666 ± 4,410 cells/ml for the spherical particles and to 16,666 ± 9,280 cells/ml for the iron particles (N = 3). After an additional 24 h, the cell count was 26,667 ± 6,670 cells/ml for the spherical particles and 30,000 ± 15,280 cells/ml for the iron particles respectively (N = 3). In contrast, the cells that with no particles grew to 226,670 ± 23,330 cells/ml after 24 h and to 921,670 ± 78,550 cells/ml after 48 h. Further, the cells with spherical particles that were not subjected to heating grew to 216,660 ± 42,262 cells/ml after 24 h and 516,660 ± 76,720 cells/ml after 48 h. Cells with iron particles that were not heated grew to 188,333 ± 4,409 cells/ml after 24 h and to 648,333 ± 151,116 cells/ml after 48 h. (P < 0.002 of controls vs. ferromag. day 1 and iron day 1, t-test. P < 0.001 of controls vs. ferromag. day 2 and iron day 2, t-test.)
No MeSH data available.