TY  - JOUR
A1  - Prüfer, Nicole
A1  - Kleuser, Burkhard
A1  - van der Giet, Markus
T1  - The role of serum amyloid A and sphingosine-1-phosphate on high-density lipoprotein functionality
JF  - Biological chemistry
N2  - The high-density lipoprotein (HDL) is one of the most important endogenous cardiovascular protective markers. HDL is an attractive target in the search for new pharmaceutical therapies and in the prevention of cardiovascular events. Some of HDL's anti-atherogenic properties are related to the signaling molecule sphingosine-1-phosphate (S1P), which plays an important role in vascular homeostasis. However, for different patient populations it seems more complicated. Significant changes in HDL's protective potency are reduced under pathologic conditions and HDL might even serve as a proatherogenic particle. Under uremic conditions especially there is a change in the compounds associated with HDL. S1P is reduced and acute phase proteins such as serum amyloid A (SAA) are found to be elevated in HDL. The conversion of HDL in inflammation changes the functional properties of HDL. High amounts of SAA are associated with the occurrence of cardiovascular diseases such as atherosclerosis. SAA has potent pro-atherogenic properties, which may have impact on HDL's biological functions, including cholesterol efflux capacity, antioxidative and anti-inflammatory activities. This review focuses on two molecules that affect the functionality of HDL. The balance between functional and dysfunctional HDL is disturbed after the loss of the protective sphingolipid molecule S1P and the accumulation of the acute-phase protein SAA. This review also summarizes the biological activities of lipid-free and lipid-bound SAA and its impact on HDL function.
KW  - atherosclerosis
KW  - high-density lipoprotein (HDL)
KW  - inflammation
KW  - serum amyloid A (SAA)
KW  - sphingosine-1-phosphate (S1P)
Y1  - 2015
U6  - https://doi.org/10.1515/hsz-2014-0192
SN  - 1431-6730
SN  - 1437-4315
VL  - 396
IS  - 6-7
SP  - 573
EP  - 583
PB  - De Gruyter
CY  - Berlin
ER  - 
TY  - JOUR
A1  - Chaykovska, Lyubov
A1  - Zientara, Alicja
A1  - Reser, Diana
A1  - Weise, Alexander
A1  - Reichert, Wolfgang
A1  - Hocher, Berthold
T1  - Development and validation of a macroarray system - MutaCHIP (R) ARTERO - for the detection of genetic variants involved in the pathogenesis of atherosclerosis
JF  - Clinical laboratory : the peer reviewed journal for clinical laboratories and laboratories related to blood transfusion
N2  - Background: Cardiovascular diseases are the leading cause of death in developed countries. The underlying mechanism is often atherosclerotic remodeling of blood vessels in organs such as heart, kidney, brain, and large arteries in case of peripheral arterial disease. Beside environmental and behavioral factors such as smoking or lack of physical activity, genetic variants in genes involved in lipid metabolism, blood pressure regulation, oxidative stress, and coagulation play a prominent role in the pathogenesis of atherosclerosis.
 Methods: Thus, we developed and validated for clinical use and research a macroarray system for the simultaneous detection of key genetic variants in genes involved in lipid metabolism, blood pressure regulation, oxidative stress, and coagulation.
 Results: When compared with standard PCR technologies to determine all these genetic variants in parallel, the macroarray system (MutaCHIP (R) ARTERO) was as accurate but faster, cheaper, and easier to handle compared to classical real time PCR based technologies.
 Conclusions: MutaCHIP (R) ARTERO is a gene chip for diagnostics of a complex genetic panel involved in the pathogenesis of atherosclerosis. This method is as sensitive and precise as real time PCR and is able to replicate real time PCR data previously validated in evaluation studies.
KW  - cardiovascular disease
KW  - atherosclerosis
KW  - genes
KW  - rapid detection method
KW  - macroarray
Y1  - 2014
U6  - https://doi.org/10.7754/Clin.Lab.2014.140104
SN  - 1433-6510
VL  - 60
IS  - 5
SP  - 873
EP  - 878
PB  - Clin Lab Publ., Verl. Klinisches Labor
CY  - Heidelberg
ER  -