Amyloid P component, serum cerebral a...

Amyloid P component, serum cerebral artery atherosclerotic stenosis

Posted in the Molecular Biology Forum

Since: May 12

Fremont, CA

#1 May 24, 2012
Amyloid P component, serum (APCS) exists in the body of mammals and birds, the synthesis of the site is mainly in the liver, composed of the same cluster of genes encoding a group of pleomorphic protein. S from the apolipoprotein family includes different forms of expression, acute phase protein A (Amyloid P component, serum, APCS) and structural type of the APCS (constitutive Amyloid P component, serum, C-APCS). Normal serum APCS value of 0-0.78mg / L When the body by a variety of inflammatory response factors to stimulate the serum level of APCS increased rapidly in the 5-6h of about 1000 times, 8 ~ 12h within the APCS can reach peak increased amplitude of up to 2000 times the normal value. The half-life is also very short, only 50min. Therefore, when control of the body's inflammatory response can be rapidly reduced to normal levels. This feature allows APCS to become the most sensitive one of the inflammatory response markers.APCS can induce the synthesis of collagenase and inhibition of interleukin-1 (interleukin-1, IL-1), IL-5, IL-6 or tumor necrosis factor (tumor necrosis factor, TNF) caused by fever; inhibit platelet 5-HT release and platelet aggregation. With this protein functions, one by one was found, APCS has gradually become the people to overcome artery atherosclerosis (athero-sclerosis, AS) research focus, but also by the expert attention of cardiovascular and cerebrovascular diseases.
APCS is considered to be a multifunctional protein, play an important role in the inflammatory reaction, regulate cholesterol metabolism and transporter. APCS is mainly present in the composition of serum high density lipoprotein (> 90%) of the old J. This part of the APCS with the reverse cholesterol transport. Found j of ApoA I) and a small amount of APCS phospholipid particles increased by apolipoprotein Al (apolipoprotein A-I, lecithin cholesterol acyltransferase (1ecithincholesterol acyltransferase, LCAT) activity; but this is rich in APCS particles, but lower the function of LCAT. LCAT cholesterol into cholesteryl ester. Of ApoA. I is one of the enzyme activator of LCAT activation play an important role in reverse cholesterol transport, and therefore prove that APCS involved in the process of reverse cholesterol transport. Exist to reduce the affinity of HDL on the normal liver cells 2 times the contrary, the affinity of macrophages increased by 3-4 times; inflammatory response of macrophages, HDL / APCS (containing HDL) affinity of APCS and the sites on liver cells is reduced, the net effect of HDL cholesterol transport capacity significantly towards the macrophages. APCS can enhance the absorption capacity of the HDL / APCS by macrophages, and promote rapid outflow of cholesterol in the cholesterol-load macrophages.In the tissue injury area, macrophages are loaded with cholesterol, this is because theysuck the cholesterol-rich membrane fragments. HDL / APCS to promote cholesterol effluxcapacity in the APCS, rather than the other HDL apolipoprotein feeding roar. HDL / APCScan also serve as extracellular receptors of macrophage cholesterol. Acyl-coenzyme Acholesterol acyltransferase (acyl coenzyme A-cholesterol acyltransferase, ACAT) andesterified cholesterol as storage, neutral cholesteryl ester hydrolase (neutralcholesterol ester hydrolase, nCEH) esterification of cholesterol lead to the outflow. APCS can inhibitthe ACAT, can improve nCEH activity, it can be to adjust the balance through the storage and transfer of free cholesterol. Although a large number of experiments proved that the APCS can be elevated oxidized cholesterol levels, and thus increased free cholesterol efflux from macrophages, but in cells that role directly through the APCS or indirectlythrough the APCS increased oxidation of cholesterol levels, elevated macrophage cellular transport of cholesterol efflux, is not yet clear.

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