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0Lipoproteins are carriers of insoluble lipids in the blood, and lipid-protein complexes are formed by combining insoluble lipids and proteins in the blood. The characteristics of lipoproteins are usually identified by their solubility characteristics, centrifugal sedimentation behavior, and chemical composition. Soluble lipoproteins, namely plasma lipoproteins, play an important role in the transport of lipids in animals. The lipids in lipoproteins can also exchange with components of cell membranes and participate in the regulation of cellular lipid metabolism. The main components of membranes (such as cell membranes, and organelle membranes). What are the types and metabolic pathways of lipoproteins? What are the commonly used lipoprotein reagents in scientific research?
1. What are the types of lipoproteins?
2. What is the lipoprotein metabolism pathway?
3. What are lipoprotein reagents commonly used in diagnostic reagents and scientific research?
4. What are the clinical indicators related to lipoproteins?
1. What are the types of lipoproteins?
Lipoprotein is a lipid-protein complex. There is no covalent bond between lipids and proteins in lipoproteins, most of which are bound by hydrophobic interaction between non-polar parts of lipids and protein components. Solubility, centrifugal sedimentation behavior, and chemical composition are commonly used to characterize lipoproteins.
The types of lipoproteins are chylomicron (CM), very low-density lipoprotein (VLDL), intermediate density lipoprotein (IDL), low-density lipoprotein (LDL), and high-density lipoprotein (HDL). increase sequentially, while particles decrease sequentially.
LDL is a cholesterol-rich lipoprotein, the main way is from the dissimilation and metabolism of VLDL, and the second way is directly secreted into the blood after liver synthesis. Each lipoprotein carries a certain amount of cholesterol, and the lipoprotein that carries the most cholesterol is LDL. The main function is to transport cholesterol to cells throughout the body and transport it to the liver to synthesize bile acid. It is one of the risk factors for atherosclerosis and is considered to be a pro-atherosclerotic factor.
HDL is a lipoprotein with the largest particle density and the smallest particle size in serum. It is rich in phospholipids and is the basic substance of blood lipid metabolism. And because HDL is small in size, it can penetrate the arterial intima, remove the cholesterol deposited inside, repair damaged cells in the vascular endothelium, and restore blood vessel elasticity. Therefore, it has the functions of removing excess blood fat in blood vessels, removing blood scale, and cleaning blood vessels. HDL is mainly synthesized by the liver and small intestine. The nascent HDL synthesized by the liver is mainly phospholipid and ApoAⅠ. Under the action of plasma lecithin cholesterol acyltransferase (LCAT), free cholesterol becomes cholesterol ester, and lipoprotein becomes mature spherical HDL3. It is then transformed into HDL2 by the action of LDL. HDL can combine free cholesterol accumulated in peripheral tissues with lipoproteins in the blood circulation or combine with certain macromolecules to deliver to tissue cells such as the liver, and carry cholesterol in surrounding tissues. It is then converted into bile acids or directly excreted from the intestine through bile. Arteriography proved that the content of high-density lipoprotein cholesterol (HDL-C) was significantly negatively correlated with the degree of arterial lumen stenosis. So HDL is an anti-atherosclerotic plasma lipoprotein and a protective factor for coronary heart disease.
2. What is the lipoprotein metabolism pathway?
The lipids and apolipoproteins in the plasma together form various lipoprotein particles, and the lipids and proteins in the particles are constantly exchanged and changed to complete the metabolism of lipoproteins. The lipoprotein metabolism pathway includes exogenous metabolism and endogenous metabolism. Exogenous metabolism is cholesterol and triglyceride ingested in the diet to synthesize CM and its metabolic process in the small intestine. The endogenous metabolic pathway is synthesized from the liver to VLDL and then converted into IDL and LDL, which are metabolized by the liver or other organs. Abnormal lipoprotein metabolism (usually accompanied by changes in lipid and protein components) is closely related to arteriosclerosis, diabetes, obesity, and tumorigenesis.
The mechanism of lipoprotein metabolism is closely related to HDL. HDL can drive reverse cholesterol transport, through which the excess cholesterol in blood and tissues is decomposed by the liver and then excreted from the body. And HDL can reverse endothelial dysfunction, inhibit endothelial cell apoptosis, stimulate the production of prostaglandins, reduce platelet aggregation, and lay a theoretical foundation for lipoprotein metabolism.
The metabolism of LDL in lipoproteins is complex, and 2/3 of LDL in the body is absorbed into the liver and extrahepatic tissues through the LDL receptor-mediated pathway and is cleared by metabolism. The remaining third is cleared through a "sweeper" pathway, which is taken up and dissimilated by surrounding tissues (including blood vessel walls). In this non-receptor pathway, macrophages bind to LDL and absorb cholesterol in LDL. Cholesterol remains inside the cells, becoming "foam" cells. The degradation of LDL is metabolized through the LDL receptor pathway. The covered lacuna on the surface of the cell membrane is the site where the LDL receptor exists, that is, ApoB100 in LDL is recognized by the receptor, and LDL is bound to the lacuna on the receptor. Membrane separation forms endocytic vesicles, which undergo the action of membrane H+-ATPase in the endocytic vesicles, and the pH decreases. LDL is separated from the receptor and fused with lysosomes, and then enzymatically hydrolyzed to generate cholesterol into the transport vesicles, or through cholesterol again Acyltransferase (ACAT) acts to re-esterify and accumulate. Therefore, LDL can enter the cells of the arterial wall and carry cholesterol with it. Excessive LDL levels can cause atherosclerosis, placing individuals at risk for coronary heart disease.
3. What are lipoprotein reagents commonly used in diagnostic reagents and scientific research?
YEASEN is committed to providing high-quality low-density lipoprotein (LDL) and high-density lipoprotein (HDL) for diagnostic reagent companies and scientific research users.
3.1 Product Application
& Application of conventional lipoprotein
Figure 1. Application of conventional lipoprotein
& Application of acetyl lipoprotein
Figure 2. Application of acetyl lipoprotein
& Application of oxidizing lipoprotein
Figure 3. Application of oxidizing lipoprotein
3.2 LDL Related Products
LDL is converted from Very Low-Density Lipoprotein (VLDL). Its main function is to transport cholesterol to cells throughout the body. Cholesterol is transported to the liver for the synthesis of cholic acid. It can be used to study receptor - mediated endocytosis. Plasma derived LDL can be used to study the oxidative role of LDL in function and metabolism, especially in diseases such as atherosclerosis.
Table 1. Related Products
|
Product Name |
Cat# |
Size |
|
20604ES05 |
2 mg |
|
|
20604ES10 |
5×2 mg |
|
|
20606ES75 |
500 μg |
|
|
20608ES05 |
2 mg |
|
|
20609ES75 |
500 μg |
|
|
20613ES05 |
2 mg |
|
|
20614ES75 |
500 μg |
|
|
20617ES05 |
2 mg |
3.3 High Density Lipoprotein
HDL unlike other large lipoproteins, which primarily transport lipids to the cell, HDL carries lipids out of the cell. Therefore, High-density lipoprotein can remove excess blood lipids, remove blood scale, clean blood vessels, and maintain the relative balance of cholesterol in cells, to limit the occurrence and development of atherosclerosis and play an anti-atherosclerosis role.
Table 2. HDL Related Products
|
Product Name |
Cat# |
Size |
|
20610ES05 |
2 mg |
|
|
20615ES05 |
2 mg |
4. What are the clinical indicators related to lipoproteins?
The clinical indicators related to lipoprotein mainly include lipoprotein (a) [LP (a)], low-density lipoprotein cholesterol (LDL-C), HDL-C, total cholesterol (TCH), TG, etc., all of which are related to atherosclerosis. It has a certain reference role in the clinical diagnosis and treatment of cardiovascular diseases.
LDL-C is a heterogeneous lipoprotein particle. As the main lipoprotein in fasting plasma, it is about 2/3 of plasma lipoprotein. It is converted from VLDL in plasma. The synthesis site is blood vessels, and the degradation site is the liver. LDL-C can transport cholesterol to extrahepatic tissues, act on the arterial intima to form atherosclerotic plaques, and is closely related to coronary heart disease and related mortality. Elevated LDL-C concentrations predict high risk even when total cholesterol is in the normal range, with elevated levels in patients with hypothyroidism, nephrotic syndrome, chronic renal failure, liver disease, diabetes, anorexia nervosa, etc. The reasons for the increase include non-pathological factors and pathological factors, among which non-pathological factors are an unbalanced diet, excessive intake of fat, smoking, drinking, etc. Pathological factors include abnormal liver function, atherosclerosis, hypertension, cardiac vascular disease, etc. LDL-C levels are reduced in patients with malnutrition, chronic anemia, intestinal malabsorption, liver disease, and acute myocardial infarction.
HDL-C is a common cholesterol that can transport blood lipids in blood vessels to the liver for processing, and transfer the foam cells of atherosclerotic plaques to the liver for excretion. HDL protects against heart disease and other cardiovascular diseases and is anti-atherosclerotic cholesterol. The level is reduced in people with cerebrovascular disease, coronary heart disease, hypertriglyceridemia, liver damage, diabetes, and lack of exercise. It can be used as a risk indicator for coronary heart disease. The more serious the degree of metabolic disorder, the risk of cardiovascular and cerebrovascular events bigger. For every 0.026mmol/L increase in blood HDL-C level, the risk of coronary heart disease decreased by 2% to 3%, and for every 0.13mmol/L decrease, the risk increased by 14%. HDL-C greater than 1.56mmol/L can transform excess cholesterol produced by the liver, inhibit lipoprotein oxidation, hinder the formation of atherosclerosis, and protect blood vessels. The influencing factors of HDL-C can be divided into two categories, genetic factors, and environmental factors. Epidemiological studies have shown that environmental factors such as gender, age, smoking, drinking, diet, exercise, drugs, and other metabolic abnormalities can affect HDL-C levels, while genetic factors are more complex and may be monogenic or polygenic The combined effect is the decisive factor for the level of HDL-C.
References
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[2] Augmenting ATG14 alleviates atherosclerosis and inhibits inflammation via promotion of autophagosome-lysosome fusion in macrophages. Autophagy. 2021 Dec;17(12):4218-4230. DOI: 10.1080/15548627.2021.1909833. Epub 2021 May 4. （IF:16.016)
[3] Lysosomal integral membrane protein-2 (LIMP-2/SCARB2) is involved in lysosomal cholesterol export. Nat Commun. 2019 Aug 6;10(1):3521. DOI: 10.1038/s41467-019-11425-0.（IF:11.878)
[4] An atherosclerotic plaque-targeted single-chain antibody for MR/NIR-II imaging of atherosclerosis and anti-atherosclerosis therapy. J Nanobiotechnology. 2021 Sep 28;19(1):296. DOI: 10.1186/s12951-021-01047-4.（IF:10.435)
[5] Efficient endothelial and smooth muscle cell differentiation from human pluripotent stem cells through a simplified insulin-free culture system. Biomaterials. 2021 Apr;271:120713. DOI: 10.1016/j.biomaterials.2021.120713.（IF:12.479)
[6] Inhibition of ASGR1 decreases lipid levels by promoting cholesterol excretion. Nature. 2022 Aug;608(7922):413-420. DOI: 10.1038/s41586-022-05006-3. （IF:69.504）
