Aim: Haptoglobin (Hpt) was previously found to inhibit reverse cholesterol transport (RCT), as binding ApoA-I and preventing its stimulation of both cholesterol (C) efflux and Lecithin-Cholesterol Acyl-Transferase (LCAT). This study aimed to find out whether Hpt influences RCT from macrophages differentiated from primary culture of human monocytes. Methods: Monocytes were isolated from human buffy coats, and kept for 6 days in culture for differentiation into macrophages. After treatment with ³H-C for 24 h, the cells were incubated with ApoA-I (0.04 mg/mL), or ApoA-I plus increasing Hpt amounts (0.1-0.75 mg/mL). After 16 h of incubation, homologous plasma was added as LCAT source. After further incubation for 16 h, supernatants were aliquoted from culture medium to measure their radioactivity content, representing the released C. Supernatant lipids were extracted and separated by TLC to measure the LCAT activity as conversion of unesterified ³H-C into C esters. Results: Addition of Hpt increasing amounts to macrophages significantly inhibited both ApoA-I dependent stimulation of C efflux (down to 27% of the control value) and LCAT activity (down to 50% of the control value). The changes were significant (P<0.01). Conclusion: Macrophages play a key role in atherosclerosis onset and progression as they differentiate to foam cell, triggering the formation of the atheromatous plaque, when RCT is defective. Increase of Hpt concentration, as it occurs during inflammatory process, might impair the efficiency of cholesterol efflux from these cells and LCAT activity in the medium. Therefore high levels of Hpt might contribute to adverse cardiovascular events.

Haptoglobin influences both cholesterol efflux from macrophages and Lecithin-Cholesterol Acyl-Transferase activity / C. R., Pugliese; Cigliano, Luisa; P., Saporito; A., Carlucci; A., Salvatore; Abrescia, Paolo. - STAMPA. - 191:(2007), pp. 108-109. (Intervento presentato al convegno 58th Congress of the Italian Physiological Society tenutosi a Lecce - Italy nel 19-21 September 2007).

Haptoglobin influences both cholesterol efflux from macrophages and Lecithin-Cholesterol Acyl-Transferase activity.

CIGLIANO, LUISA;ABRESCIA, PAOLO
2007

Abstract

Aim: Haptoglobin (Hpt) was previously found to inhibit reverse cholesterol transport (RCT), as binding ApoA-I and preventing its stimulation of both cholesterol (C) efflux and Lecithin-Cholesterol Acyl-Transferase (LCAT). This study aimed to find out whether Hpt influences RCT from macrophages differentiated from primary culture of human monocytes. Methods: Monocytes were isolated from human buffy coats, and kept for 6 days in culture for differentiation into macrophages. After treatment with ³H-C for 24 h, the cells were incubated with ApoA-I (0.04 mg/mL), or ApoA-I plus increasing Hpt amounts (0.1-0.75 mg/mL). After 16 h of incubation, homologous plasma was added as LCAT source. After further incubation for 16 h, supernatants were aliquoted from culture medium to measure their radioactivity content, representing the released C. Supernatant lipids were extracted and separated by TLC to measure the LCAT activity as conversion of unesterified ³H-C into C esters. Results: Addition of Hpt increasing amounts to macrophages significantly inhibited both ApoA-I dependent stimulation of C efflux (down to 27% of the control value) and LCAT activity (down to 50% of the control value). The changes were significant (P<0.01). Conclusion: Macrophages play a key role in atherosclerosis onset and progression as they differentiate to foam cell, triggering the formation of the atheromatous plaque, when RCT is defective. Increase of Hpt concentration, as it occurs during inflammatory process, might impair the efficiency of cholesterol efflux from these cells and LCAT activity in the medium. Therefore high levels of Hpt might contribute to adverse cardiovascular events.
2007
Haptoglobin influences both cholesterol efflux from macrophages and Lecithin-Cholesterol Acyl-Transferase activity / C. R., Pugliese; Cigliano, Luisa; P., Saporito; A., Carlucci; A., Salvatore; Abrescia, Paolo. - STAMPA. - 191:(2007), pp. 108-109. (Intervento presentato al convegno 58th Congress of the Italian Physiological Society tenutosi a Lecce - Italy nel 19-21 September 2007).
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11588/368162
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