Kalen Biomedical's Research Corner
At Kalen Biomedical we pride ourselves on providing high quality lipoproteins to researchers producing high quality research. Look at the interactive infographic below to get a glimpse at some of the exciting research happening with the use of our products!
Alzheimer’s disease is a debilitating neural affliction that affects memory and cognition. A study showed that when endolysosomes (parts of cells that take in matter from the outside microenvironment and degrade it) in primary-cultured neurons are exposed to ApoB-containing LDL, the endolysosomes accumulate cholesterol and become enlarged. This alters the structure and function of the endolysosomes and also contributes to an increase in production of Amyloid Beta. Amyloid Beta peptides can aggregate and become misfolded leading to the formation of Amyloid plaques. These plaques are toxic to the surrounding neurons and are a major part of the pathology of Alzheimer’s Disease.
Products Used: Native LDL
Preeclampsia is a pregnancy complication characterized by high blood pressure and organ damage. It can lead to Eclampsia which involves women experiencing seizures that threaten the health of the mother and child. Improper placentation causes oxidative stress, thus inducing the release of oxidized lipids into the maternal blood stream. The increase in Oxidized LDL circulation leads to an increase in OxLDL binding to LOX-1 receptors that produce a blood-brain-barrier (BBB) damaging chemical called peroxynitrite. The damaged BBB becomes more permeable to free radicals and produces an immune response that can cause seizures.
Schreurs, M. P., Hubel, C. A., Bernstein, I. M., Jeyabalan, A., & Cipolla, M. J. (2013). Increased oxidized low-density lipoprotein causes blood-brain barrier disruption in early-onset preeclampsia through LOX-1. The FASEB Journal, 27(3), 1254-1263.
Products Used: High Oxidized LDL
Chronic Kidney Disease is associated with atherosclerosis and increased oxidative stress. The primary function of HDL is to take excess plaque-causing cholesterol to the liver to be broken down. A study found, however, in patients with End Stage Renal Disease, there are fewer available components that form HDL, such as Apolipoprotein A1, thus less HDL. In addition to there being less overall HDL, the antioxidant properties of HDL are impaired and consequentially this HDL isn’t as efficient in reducing the amount of oxidized lipoproteins. Without HDL transporting cholesterol and to the liver and reducing Oxidized LDL, the patients are more at risk for heart attack causing plaques.
Products Used: Oxidized LDL
Bones are constantly in a state of being formed and reabsorbed. Osteoclasts help maintain the balance by reabsorbing bone tissue. Mouse cells growing in media devoid of LDL show a reduction of RANKL- induced (a membrane protein belonging to Tumor Necrosis Factor superfamily) osteoclast generation. Similarly, mice without LDL receptors showed osteoclast cell formation was delayed and produced smaller, less functional cells than normal and other proteins that help with the creation of osteoclasts were also reduced. This suggest a correlation between LDL receptors and cell-to-cell fusion. In vivo, the mice showed decreased bone reabsorption and increased bone mass, but no changes in bone formation. LDL may aid in maintaining the balance of bone tissue synthesis.
Okayasu, M., Nakayachi, M., Hayashida, C., Ito, J., Kaneda, T., Masuhara, M., ... & Hakeda, Y. (2012). Low-density lipoprotein receptor deficiency causes impaired osteoclastogenesis and increased bone mass in mice because of defect in osteoclastic cell-cell fusion. Journal of Biological Chemistry, 287(23), 19229-19241.
*This study was done using mouse models