Abstract

High-density lipoprotein- (HDL-) cholesterol measurements are generally used in the diagnosis of cardiovascular diseases. However, HDL is a complicated heterogeneous lipoprotein, and furthermore, it can be converted into dysfunctional forms during pathological conditions including inflammation. Therefore, qualitative analysis of pathophysiologically diversified HDL forms is important. A recent study demonstrated that serum amyloid A (SAA) can remodel HDL and induce atherosclerosis not only over long periods of time, such as during chronic inflammation, but also over shorter periods. However, few studies have investigated rapid HDL remodeling. In this study, we analyzed HDL samples from patients undergoing orthopedic surgery inducing acute inflammation. We enrolled 13 otherwise healthy patients who underwent orthopedic surgery. Plasma samples were obtained on preoperative day and postoperative days (POD) 1-7. SAA, apolipoprotein A-I (apoA-I), and apolipoprotein A-II (apoA-II) levels in the isolated HDL were determined. HDL particle size, surface charge, and SAA and apoA-I distributions were also analyzed. In every patient, plasma SAA levels peaked on POD3. Consistently, the HDL apoA-I : apoA-II ratio markedly decreased at this timepoint. Native-polyacrylamide gel electrophoresis and high-performance liquid chromatography revealed the loss of small HDL particles during acute inflammation. Furthermore, HDL had a decreased negative surface charge on POD3 compared to the other timepoints. All changes observed were SAA-dependent. SAA-dependent rapid changes in HDL size and surface charge were observed after orthopedic surgery. These changes might affect the atheroprotective functions of HDL, and its analysis can be available for the qualitative HDL assessment.

Highlights

  • High-density lipoprotein (HDL) is a well-known, multifunctional particle that has been shown to suppress the progression of atherosclerosis by numerous epidemiological and experimental studies [1,2,3,4]

  • Plasma serum amyloid A (SAA) peaked on POD3; the extent of the increase varied

  • Plasma High-density lipoprotein- (HDL-)C and albumin levels were measured and displayed similar trends, decreasing by 34 ± 14% for HDL-C and 28 ± 12% for albumin POST compared to PRE, remaining largely unchanged through POD3

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Summary

Introduction

High-density lipoprotein (HDL) is a well-known, multifunctional particle that has been shown to suppress the progression of atherosclerosis by numerous epidemiological and experimental studies [1,2,3,4]. HDL is a complicated and heterogeneous lipoprotein, and it can be converted into dysfunctional forms during pathological conditions like diabetes [11, 12], oxidative stress [13, 14], and inflammation. Levels of small HDL particles were low in patients with rheumatoid arthritis, who had elevated coronary calcification [17]. Patients infected with human immunodeficiency virus display increased large HDL particles and decreased small HDL particles [18]

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