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Marked Changes in Serum Amyloid A Distribution and High-Density Lipoprotein Structure during Acute Inflammation
Shitsuko Shimano1, Ryunosuke Ohkawa2, Mayu Nambu2
1Clinical Laboratory, Medical Hospital, Tokyo Medical and Dental University (TMDU), 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan.
Biomed Research International
|February 12, 2021
Summary
Acute inflammation rapidly alters high-density lipoprotein (HDL) structure and function, driven by serum amyloid A (SAA). These HDL changes may impact cardiovascular health and offer insights into qualitative HDL assessment.
Area of Science:
- Cardiovascular Research
- Lipoprotein Metabolism
- Inflammation Biology
Background:
- High-density lipoprotein (HDL) cholesterol is a key cardiovascular disease marker.
- HDL is heterogeneous and can become dysfunctional during inflammation.
- Understanding rapid HDL remodeling is crucial for assessing cardiovascular risk.
Purpose of the Study:
- To investigate rapid HDL remodeling during acute inflammation post-orthopedic surgery.
- To determine the role of serum amyloid A (SAA) in acute HDL changes.
- To assess the impact of these changes on HDL's atheroprotective functions.
Main Methods:
- Analysis of HDL from 13 orthopedic surgery patients (preoperative and POD 1-7).
- Quantification of SAA, apolipoprotein A-I (apoA-I), and apolipoprotein A-II (apoA-II).
- Assessment of HDL particle size, surface charge, and protein distribution using electrophoresis and chromatography.
Main Results:
- Plasma SAA peaked on postoperative day 3 (POD3).
- HDL showed a decreased apoA-I:apoA-II ratio and loss of small particles on POD3.
- HDL exhibited reduced negative surface charge, all SAA-dependent.
Conclusions:
- Orthopedic surgery-induced acute inflammation causes rapid, SAA-dependent HDL remodeling.
- Observed HDL changes (size, charge) may impair atheroprotective functions.
- SAA-driven HDL modifications provide a basis for qualitative HDL assessment in acute inflammatory states.
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