GO:0034358 plasma lipoprotein particle: Components, Assembly and Research Methods, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0034358 plasma lipoprotein particle describes a spherical particle with a hydrophobic core of triglycerides and/or cholesterol esters, surrounded by an amphipathic monolayer of phospholipids, cholesterol and apolipoproteins.
• These particles transport lipids, which are non-covalently associated with the particles, in the blood or lymph.
• Apolipoprotein B (apoB) is the major structural protein of atherogenic lipoprotein particles, including LDL and VLDL.
• Plasma lipoprotein particle size and concentration are modifiable by diet, such as sugar-sweetened beverage intake and algal docosahexaenoic acid supplementation.
• Nuclear magnetic resonance (NMR) spectroscopy is a key method for quantifying lipoprotein particle size and number.
• The plasma parameter log(TG/HDL-C) correlates with lipoprotein particle size and esterification rate, serving as an atherogenic index.
Description
Plasma lipoprotein particles are macromolecular assemblies that transport hydrophobic lipids through the aqueous environment of blood and lymph. They are composed of a hydrophobic core containing triglycerides and/or cholesterol esters, surrounded by a monolayer of phospholipids, free cholesterol, and apolipoproteins. This structural organization allows the solubilization and systemic distribution of lipids, which are otherwise insoluble in plasma. Researchers study plasma lipoprotein particles to understand lipid metabolism, cardiovascular disease risk, and the impact of dietary and pharmacological interventions. The GO term GO:0034358 provides a standardized annotation for these particles in cellular component ontologies, facilitating functional genomics and proteomics analyses. Given the strong association between apolipoprotein B-containing lipoproteins and atherogenesis, accurate characterization of particle size, number, and composition is critical for both basic and clinical research.
plasma lipoprotein particle At A Glance
| GO ID | GO:0034358 |
|---|---|
| GO term | plasma lipoprotein particle |
| Ontology | cellular_component |
| Synonym | none |
| Major function | Transport of non-covalently associated lipids in blood or lymph |
| Composition | Hydrophobic core of triglycerides and/or cholesterol esters; amphipathic monolayer of phospholipids, cholesterol, and apolipoproteins |
| Location | Extracellular space, blood, lymph |
| Related disease | Atherosclerosis, cardiovascular disease |
What Is GO:0034358?
According to the Gene Ontology, GO:0034358 plasma lipoprotein particle is defined as a spherical particle with a hydrophobic core of triglycerides and/or cholesterol esters, surrounded by an amphipathic monolayer of phospholipids, cholesterol and apolipoproteins. These particles transport lipids, which are non-covalently associated with the particles, in the blood or lymph. This definition captures the essential structural and functional features of lipoproteins, distinguishing them from other lipid-containing structures.
Why Is plasma lipoprotein particle Important in Cell Biology?
Plasma lipoprotein particles are central to lipid homeostasis and are directly implicated in the pathogenesis of atherosclerosis and cardiovascular disease. Elevated concentrations of apolipoprotein B-containing lipoproteins, such as LDL and VLDL, promote atherogenesis by depositing cholesterol in arterial walls. Moreover, lipoprotein particle size and number are independent risk factors for cardiovascular events, and they can be modified by lifestyle and dietary factors. Understanding the assembly, remodeling, and clearance of these particles is therefore essential for developing diagnostic and therapeutic strategies.
• Plasma lipoprotein particles transport triglycerides and cholesterol esters, which are non-covalently associated, through the bloodstream.
• Apolipoprotein B-containing lipoproteins are causal factors in atherogenesis and cardiovascular disease.
• Lipoprotein particle size and number are predictive of cardiovascular risk and correlate with the atherogenic index log(TG/HDL-C).
• Dietary interventions, such as sugar-sweetened beverage reduction or algal DHA supplementation, can alter lipoprotein particle size distribution.
• NMR spectroscopy enables precise quantification of lipoprotein particle subclasses, aiding clinical research.
• Quantitative assays of plasma apolipoproteins provide insights into lipoprotein metabolism and disease risk.
• Plasma lipoprotein particles are targets for therapeutic modulation in dyslipidemias.
• Characterization of surface charges on lipoproteins and extracellular vesicles can improve isolation methods.
• Lipoprotein particle analysis is used in large epidemiological studies to link diet and disease.
• The GO term GO:0034358 facilitates annotation of genes and proteins involved in lipoprotein biology.
Structure and Composition of plasma lipoprotein particle
Hydrophobic Core
In simple terms: The core is the oily center of the particle that carries fats.
The hydrophobic core of a plasma lipoprotein particle consists of triglycerides and/or cholesterol esters, which are nonpolar lipids sequestered away from the aqueous environment. This core is surrounded by an amphipathic monolayer that stabilizes the particle in plasma. The composition of the core varies among lipoprotein classes, influencing particle size and density.
Amphipathic Monolayer
In simple terms: The outer shell is made of molecules that have both water-loving and water-fearing parts.
The surface monolayer is composed of phospholipids, free cholesterol, and apolipoproteins. Phospholipids and cholesterol provide an amphipathic barrier, while apolipoproteins stabilize the particle and mediate interactions with enzymes and receptors. This monolayer also determines surface charge, which affects particle isolation and behavior.
Apolipoproteins
In simple terms: Apolipoproteins are proteins on the surface that act like address labels and structural supports.
Apolipoproteins are key protein components of plasma lipoprotein particles. Apolipoprotein B (apoB) is essential for the assembly and secretion of triglyceride-rich lipoproteins and is the primary structural protein of LDL and VLDL. Other apolipoproteins, such as apoA-I, apoE, and apoC-III, play roles in lipid transport, enzyme activation, and receptor binding. Quantitative assays of plasma apolipoproteins are important for research and clinical diagnostics.
Lipid Cargo
In simple terms: The fats carried inside the particle are its cargo.
Plasma lipoprotein particles transport lipids, which are non-covalently associated with the particles, in the blood or lymph. The lipid cargo includes triglycerides and cholesterol esters, and its composition determines the metabolic fate of the particle. The relative contribution of triglyceride-rich lipoprotein particle size and number to plasma triglyceride concentration has been documented.
Particle Heterogeneity
In simple terms: Lipoproteins come in different sizes and types.
Plasma lipoprotein particles are heterogeneous in size, density, and composition, leading to classifications such as HDL, LDL, VLDL, and chylomicrons. NMR spectroscopy can resolve these subclasses and quantify particle number and size. Dietary factors, such as sugar-sweetened beverage consumption, have been associated with changes in lipoprotein particle size and concentration.
Key Genes Involved in GO:0034358 plasma lipoprotein particle
The following genes and proteins are central to the structure, assembly, and metabolism of plasma lipoprotein particles.
| Gene | Major Role | Research Relevance |
|---|---|---|
| APOB | Structural apolipoprotein of LDL and VLDL; essential for assembly and secretion | Target for knockout and knock-in models to study atherogenesis |
| APOA1 | Major apolipoprotein of HDL; activates LCAT | Studied for HDL function and reverse cholesterol transport |
| APOE | Ligand for LDL receptor and LRP; involved in lipoprotein clearance | Knockout mice are models for atherosclerosis and Alzheimer's disease |
| APOC3 | Inhibits lipoprotein lipase and hepatic lipase | Target for antisense and CRISPR knockout to lower triglycerides |
| LDLR | Receptor mediating uptake of LDL particles | Mutations cause familial hypercholesterolemia; knockout models widely used |
| MTTP | Microsomal triglyceride transfer protein; required for apoB lipidation | Knockout causes abetalipoproteinemia; studied for drug targets |
| PCSK9 | Regulates LDL receptor degradation | Target for monoclonal antibodies and CRISPR base editing |
| CETP | Cholesteryl ester transfer protein; transfers lipids between lipoproteins | Inhibitors tested for cardiovascular risk; knockout models available |
| LPL | Lipoprotein lipase; hydrolyzes triglycerides in chylomicrons and VLDL | Deficiency causes hypertriglyceridemia; knockout models exist |
| HL | Hepatic lipase; hydrolyzes triglycerides and phospholipids in HDL and LDL | Studied for HDL remodeling and atherosclerosis |
| LCAT | Lecithin-cholesterol acyltransferase; esterifies cholesterol on HDL | Deficiency causes fish-eye disease; knockout models |
| PLTP | Phospholipid transfer protein; transfers phospholipids between lipoproteins | Knockout mice show altered HDL levels |
| ABCG1 | Cholesterol efflux transporter to HDL | Knockout models show impaired reverse cholesterol transport |
| ABCA1 | Cholesterol efflux transporter to apoA-I | Mutations cause Tangier disease; knockout models |
| SCARB1 | Scavenger receptor class B type I; mediates HDL cholesterol uptake | Knockout models show altered steroidogenesis |
| SORT1 | Sortilin; regulates VLDL secretion | Genome-wide association studies link to LDL-C; knockout models |
| ANGPTL3 | Inhibits lipoprotein lipase and endothelial lipase | Target for CRISPR knockout to reduce triglycerides |
| APOA5 | Activates lipoprotein lipase | Polymorphisms associated with hypertriglyceridemia |
How Is plasma lipoprotein particle Regulated?
Plasma lipoprotein particle metabolism is regulated at multiple levels, including transcriptional control of apolipoprotein genes, post-translational modification of enzymes, and hormonal signals. For example, insulin promotes lipoprotein lipase activity, while inflammatory cytokines can suppress it. Dietary factors, such as sugar-sweetened beverage intake, have been shown to modulate plasma lipoprotein cholesterol and particle size concentrations. Algal docosahexaenoic acid supplementation also affects lipoprotein particle size distribution in overweight and obese adults. The atherogenic index log(TG/HDL-C) correlates with lipoprotein particle size and esterification rate, reflecting integrated regulation.
plasma lipoprotein particle and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| APOB | Atherosclerosis, familial hypercholesterolemia | Knockout and knock-in mouse models |
| LDLR | Familial hypercholesterolemia | LDLR knockout mice and CRISPR-corrected iPSCs |
| PCSK9 | Hypercholesterolemia | Knockout and base-edited models |
| MTTP | Abetalipoproteinemia | Liver-specific knockout mice |
| APOC3 | Hypertriglyceridemia | Knockout mice and CRISPR-edited hepatocytes |
Atherosclerosis and Cardiovascular Disease
Apolipoprotein B-containing lipoproteins, including LDL and VLDL, are directly involved in atherogenesis. Elevated plasma concentrations of these particles lead to cholesterol deposition in arterial walls, plaque formation, and cardiovascular events. The atherogenic index log(TG/HDL-C) is correlated with lipoprotein particle size and esterification rate, providing a practical marker for risk assessment.
Metabolic Syndrome and Dyslipidemia
Alterations in plasma lipoprotein particle size and number are hallmarks of metabolic syndrome and dyslipidemia. Sugar-sweetened beverage consumption has been associated with unfavorable changes in lipoprotein particle concentrations and apolipoprotein levels. Dietary interventions, such as algal DHA supplementation, can modulate particle size distribution in overweight and obese individuals.
Genetic Disorders of Lipoprotein Metabolism
Mutations in genes encoding apolipoproteins, receptors, and enzymes cause monogenic disorders such as familial hypercholesterolemia (LDLR, APOB, PCSK9), abetalipoproteinemia (MTTP), and Tangier disease (ABCA1). These conditions underscore the critical roles of specific proteins in lipoprotein particle assembly and clearance.
From plasma lipoprotein particle-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does APOB loss affect lipoprotein particle assembly? | APOB knockout hepatocytes or mice |
| Can a point mutation in LDLR alter LDL uptake? | LDLR point-mutation knock-in mice |
| Does overexpression of APOA1 increase HDL particle number? | APOA1 transgenic mice or overexpression cell lines |
| What is the effect of PCSK9 knockout on LDL cholesterol? | PCSK9 knockout mice or CRISPR-edited cells |
| How does APOC3 knockdown affect triglyceride-rich lipoproteins? | APOC3 knockout or knockdown models |
| Can a tagged APOB be used to track lipoprotein secretion? | APOB knock-in with fluorescent tag |
How to Study the plasma lipoprotein particle Process
| Method | What It Measures | Typical Application |
|---|---|---|
| NMR spectroscopy | Lipoprotein particle size and number | Clinical and epidemiological studies |
| Immunoassays | Apolipoprotein concentrations | Diagnostics and research |
| Gradient gel electrophoresis | Particle size distribution | Lipoprotein subclass analysis |
| Mass spectrometry | Apolipoprotein quantification and modifications | Proteomics and biomarker discovery |
| Dynamic light scattering | Particle size | Quality control of lipoprotein preparations |
| Surface charge modulation | Zeta potential and isolation efficiency | Extracellular vesicle and lipoprotein isolation |
| Lipidomic profiling | Lipid composition of particles | Metabolic studies |
| CRISPR screening | Gene function in lipoprotein metabolism | Target discovery |
Nuclear Magnetic Resonance (NMR) Spectroscopy
NMR spectroscopy is a powerful method for quantifying lipoprotein particle size and number. It can resolve subclasses such as HDL, LDL, and VLDL and is used in large epidemiological studies to link lipoprotein profiles with disease risk.
Quantitative Assays of Plasma Apolipoproteins
Immunoassays and mass spectrometry-based methods allow quantification of apolipoproteins such as apoB, apoA-I, and apoE. These assays are essential for characterizing lipoprotein particles and assessing cardiovascular risk.
Lipoprotein Particle Size Analysis
Techniques such as gradient gel electrophoresis and dynamic light scattering measure lipoprotein particle size distribution. The relative contribution of triglyceride-rich lipoprotein particle size and number to plasma triglyceride concentration has been studied using these methods.
Surface Charge Characterization
Surface charge properties of plasma lipoproteins and extracellular vesicles can be modulated to enhance isolation and analysis. This is particularly useful for separating particle subpopulations and improving downstream assays.
How CRISPR Can Be Used to Study GO:0034358 plasma lipoprotein particle
Knockout
CRISPR knockout of genes such as APOB, APOC3, or PCSK9 in cell lines or animal models can elucidate their roles in lipoprotein particle assembly and clearance. For example, APOC3 knockout reduces triglyceride-rich lipoprotein levels.
Point Mutation
Introducing point mutations in genes like LDLR or APOB using CRISPR base editing or homology-directed repair can model familial hypercholesterolemia and assess functional consequences on lipoprotein particle metabolism.
Knock-in
Knock-in of tagged versions of APOB or APOA1 allows real-time tracking of lipoprotein particle secretion and trafficking in cells. This approach is valuable for studying particle assembly and secretion dynamics.
Overexpression
Overexpression of APOA1 or other apolipoproteins using CRISPR activation or lentiviral vectors can increase specific lipoprotein particle populations, enabling studies of HDL function and reverse cholesterol transport.
How EDITGENE Supports plasma lipoprotein particle Research
Researchers studying plasma lipoprotein particle-related genes often need to determine whether a candidate gene is causally involved in particle assembly, remodeling, or clearance. EDITGENE provides comprehensive CRISPR-based services to generate precisely engineered cell and animal models, accelerating functional validation and therapeutic target discovery.
Contact EDITGENE today to design your custom CRISPR model for plasma lipoprotein particle research.
Frequently Asked Questions About plasma lipoprotein particle
What is GO:0034358 plasma lipoprotein particle?
GO:0034358 is a Gene Ontology cellular component term describing a spherical particle with a hydrophobic core of triglycerides and/or cholesterol esters, surrounded by an amphipathic monolayer of phospholipids, cholesterol and apolipoproteins, which transports lipids in blood or lymph.
What genes are involved in plasma lipoprotein particle metabolism?
Key genes include APOB, APOA1, APOE, APOC3, LDLR, PCSK9, MTTP, and LPL, among others.
How are plasma lipoprotein particles measured?
They are commonly measured by NMR spectroscopy, immunoassays for apolipoproteins, and gradient gel electrophoresis for particle size.
What is the role of apolipoprotein B in lipoprotein particles?
Apolipoprotein B is the major structural protein of LDL and VLDL and is essential for the assembly and secretion of triglyceride-rich lipoproteins.
Can diet affect plasma lipoprotein particle size?
Yes, sugar-sweetened beverage consumption and algal DHA supplementation have been shown to alter lipoprotein particle size and concentrations.
What diseases are associated with plasma lipoprotein particles?
Atherosclerosis, cardiovascular disease, familial hypercholesterolemia, and hypertriglyceridemia are linked to abnormalities in lipoprotein particles.
What is the atherogenic index log(TG/HDL-C)?
It is a plasma parameter that correlates with lipoprotein particle size and esterification rate, serving as a marker of atherogenic risk.
How can CRISPR be used to study lipoprotein particles?
CRISPR knockout, point mutation, knock-in, and overexpression models can be used to dissect gene function in lipoprotein assembly, secretion, and clearance.
What is the difference between LDL and VLDL particles?
LDL and VLDL are both apoB-containing lipoproteins, but VLDL is larger and triglyceride-rich, while LDL is smaller and cholesterol-rich.
Why is NMR spectroscopy used for lipoprotein analysis?
NMR spectroscopy can simultaneously quantify particle size and number across multiple lipoprotein subclasses, providing detailed profiles for clinical research.
Conclusion
Plasma lipoprotein particles are essential for lipid transport and are deeply implicated in cardiovascular and metabolic diseases. The GO term GO:0034358 provides a standardized definition that encompasses their unique structure and function. Advances in CRISPR gene editing and analytical methods such as NMR spectroscopy continue to unravel the genetic and environmental factors that regulate these particles, offering new avenues for therapeutic intervention.
References
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- 2. Borén J et al.. 2025. Apolipoprotein B-containing lipoproteins in atherogenesis.. Nat Rev Cardiol 22(6):399-413 PMID: 39743565
- 3. Woo HK et al.. 2022. Characterization and modulation of surface charges to enhance extracellular vesicle isolation in plasma.. Theranostics 12(5):1988-1998 PMID: 35265194
- 4. Haslam DE et al.. 2022. Sugar-Sweetened Beverage Consumption and Plasma Lipoprotein Cholesterol, Apolipoprotein, and Lipoprotein Particle Size Concentrations in US Adults.. J Nutr 152(11):2534-2545 PMID: 36774119
- 5. Poljak A et al.. 2020. Quantitative Assays of Plasma Apolipoproteins.. Methods Mol Biol 2138:49-81 PMID: 32219740
- 6. Jeyarajah EJ et al.. 2006. Lipoprotein particle analysis by nuclear magnetic resonance spectroscopy.. Clin Lab Med 26(4):847-70 PMID: 17110242
- 7. Poapst M et al.. 1985. Relative contribution of triglyceride-rich lipoprotein particle size and number to plasma triglyceride concentration.. Arteriosclerosis 5(4):381-90 PMID: 4015510
- 8. Neff LM et al.. 2011. Algal docosahexaenoic acid affects plasma lipoprotein particle size distribution in overweight and obese adults.. J Nutr 141(2):207-13 PMID: 21178084
