Description

Product Description

LVGRQLEEFL (mouse) (CAS 608513-82-2) is a synthetic peptide fragment derived from amino acids 113–122 of apolipoprotein J (apoJ), also known as clusterin. ApoJ is a multifunctional glycoprotein involved in lipid transport, complement regulation, apoptosis modulation, and cellular stress response. Within apoJ, the LVGRQLEEFL sequence represents a highly conserved motif responsible for several of its anti-inflammatory and anti-atherogenic effects.

Origin and Structural Context

The LVGRQLEEFL sequence is positioned within the α-helical domain of apoJ that mediates interactions with lipid surfaces and other apolipoproteins. In the mouse apoJ structure, this peptide corresponds to residues 113 through 122, forming part of a lipid-binding amphipathic helix. This region is essential for the formation of HDL-like particles, lipid solubilization, and cell membrane stabilization.

The sequence LVGRQLEEFL has been isolated, synthesized, and studied as a functional peptide, often referred to as the G* peptide. It exhibits properties reminiscent of native apoJ, including anti-inflammatory, antioxidant, and anti-atherogenic actions.

Biological and Functional Role

ApoJ (clusterin) is an apolipoprotein expressed in nearly all tissues and body fluids. It plays a crucial protective role in lipoprotein metabolism, inflammation control, and tissue injury responses. The G* peptide (LVGRQLEEFL) recapitulates several of these beneficial properties by mimicking apoJ’s amphipathic helix, which interacts with lipid membranes and scavenges oxidized molecules.

Functional Highlights:

• Anti-inflammatory activity: Suppresses macrophage activation and cytokine release.

• Anti-atherogenic activity: Reduces lipid accumulation and oxidative stress in vascular walls.

• Cytoprotective effect: Prevents oxidant-induced apoptosis in endothelial and retinal pigment epithelial (RPE) cells.

• Lipid modulation: Enhances HDL-like particle formation and cholesterol efflux capacity.

These effects make LVGRQLEEFL a versatile research peptide in the study of atherosclerosis, inflammation, and oxidative stress-related diseases.

Integration into HM-10/10 Peptide

LVGRQLEEFL can be incorporated into HM-10/10, a synthetic chimeric HDL mimetic peptide designed to emulate both apoA-I and apoJ functions. HM-10/10 contains domains from apoA-I (responsible for cholesterol efflux and lipid binding) and apoJ (providing anti-inflammatory and antioxidative protection).

This hybrid structure enhances lipid binding, antioxidant capacity, and protective effects against oxidative damage in vascular and retinal tissues. HM-10/10 has demonstrated efficacy in preventing:

• Retinal pigment epithelium (RPE) cell death

• Photoreceptor degeneration

• Endothelial injury

• Inflammatory cytokine accumulation

The apoJ-derived LVGRQLEEFL domain plays a critical role in the anti-inflammatory and cytoprotective profile of HM-10/10, making it a valuable tool for mechanistic and therapeutic studies.

Research Relevance in Atherosclerosis

In cardiovascular research, LVGRQLEEFL (mouse) is used to explore HDL functionality, lipid oxidation, and macrophage-mediated inflammation. ApoJ and its mimetic peptides are known to stabilize lipid rafts and prevent oxidation of low-density lipoproteins (LDL), a key step in atherogenesis.

Studies indicate that apoJ-derived peptides reduce the expression of adhesion molecules (e.g., VCAM-1, ICAM-1) and inhibit foam cell formation in vascular endothelium. LVGRQLEEFL contributes to these effects by modulating NF-κB signaling, leading to reduced vascular inflammation and improved endothelial health.

Role in Retinal and Neuroprotective Research

LVGRQLEEFL’s incorporation into HM-10/10 confers neuroprotective effects, particularly against oxidative stress in retinal cells. Oxidative stress is a major contributor to retinal degenerative diseases such as age-related macular degeneration (AMD). HM-10/10 peptides containing the LVGRQLEEFL motif protect RPE and photoreceptors by:

• Neutralizing reactive oxygen species (ROS)

• Reducing lipid peroxidation

• Preserving mitochondrial integrity

• Inhibiting apoptotic pathways

These effects establish LVGRQLEEFL as a key sequence for developing apoJ-derived therapeutic mimetics targeting retinal degeneration and vascular oxidative injury.

Anti-Inflammatory Mechanisms

LVGRQLEEFL reduces the release of TNF-α, IL-1β, and IL-6 from activated macrophages and microglia. It interferes with TLR and NF-κB signaling, suppressing inflammatory cascades while enhancing cell survival pathways such as PI3K/Akt and Nrf2. This dual regulation of oxidative and inflammatory stress makes it a promising peptide for investigating chronic inflammatory pathologies.

Experimental Evidence

Experimental data suggest that G* peptide analogs such as LVGRQLEEFL:

• Decrease oxidized lipid accumulation in aortic tissues.

• Improve HDL functionality in murine atherosclerosis models.

• Protect retinal cells from H₂O₂-induced apoptosis.

• Restore mitochondrial function under oxidative stress.

These findings underscore the translational potential of LVGRQLEEFL-based peptides for metabolic, vascular, and ocular research.

Product Specifications

Synonyms

• G* peptide

• ApoJ fragment (113–122)

• Clusterin-derived peptide

• HM-10/10 component

• Apolipoprotein J mimetic sequence

Mechanism of Action

LVGRQLEEFL (mouse) acts as a bioactive mimetic fragment of apolipoprotein J (apoJ). Its amphipathic α-helical structure enables it to interact with lipid bilayers and apolipoprotein complexes, replicating apoJ’s lipid transport and anti-inflammatory functions.

1. Lipid Interaction and HDL Formation
   The peptide’s hydrophobic and hydrophilic residues allow integration into phospholipid monolayers, promoting HDL-like nanoparticle assembly. This structural mimicry improves cholesterol efflux and enhances reverse cholesterol transport.

2. Antioxidant Protection
   LVGRQLEEFL neutralizes reactive oxygen species (ROS) and inhibits lipid peroxidation. By scavenging oxidized phospholipids, it prevents the formation of oxidized LDL (oxLDL), a central mediator of atherosclerosis.

3. Inflammation Suppression
   The peptide inhibits activation of NF-κB and MAPK pathways, reducing expression of inflammatory cytokines and adhesion molecules. It interferes with macrophage activation and vascular endothelial inflammation, mitigating plaque development.

4. Cytoprotection in Retinal Cells
   In RPE and photoreceptor cells, LVGRQLEEFL-containing mimetics like HM-10/10 protect against oxidative apoptosis by stabilizing mitochondrial membranes and upregulating antioxidant enzymes (SOD2, HO-1, catalase).

5. Vascular Health and Atheroprotection
   LVGRQLEEFL enhances endothelial nitric oxide synthase (eNOS) activity, improving vascular relaxation and endothelial barrier integrity. This contributes to anti-atherogenic and anti-inflammatory vascular profiles.

   

Side Effects / Safety Notes

 is for research use only and not approved for clinical applications. It has low cytotoxicity in in vitro studies and is considered biologically safe when handled under standard laboratory conditions.

Avoid direct skin or eye contact, inhalation, or ingestion. Use gloves and protective eyewear. Dispose of peptide solutions according to institutional biosafety regulations.

Disclaimer

All information provided about LVGRQLEEFL (mouse) is for scientific research and educational purposes only. The product is not intended for human or veterinary use. It must not be administered to animals or humans. End users are responsible for ensuring proper handling and compliance with biosafety protocols.

Keywords

LVGRQLEEFL peptide, apoJ fragment, clusterin-derived peptide, G* peptide, HM-10/10 peptide, HDL mimetic, anti-inflammatory peptide, anti-atherogenic peptide, oxidative stress modulator, retinal protection peptide, apolipoprotein J mimetic, lipid metabolism regulator, vascular research peptide

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