|Compton, David - Dave|
Submitted to: Biochimica et Biophysica Acta
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/16/2013
Publication Date: 1/1/2014
Citation: Evans, K.O., Laszlo, J.A., Compton, D.L. 2014. Carboxyl-terminated PAMAM dendrimer interaction with 1-palmitoyl-2-oleoyl phosphocholine bilayers. Biochimica et Biophysica Acta. 1838(1,Pt.B):445-455.
Interpretive Summary: This work explores and details the basic interactions between two environmentally friendly delivery systems of active agents, liposomes, and dendrimers. Our objective is to develop novel types of nano-structured platforms for timed-release of beneficial active agents for use in human skin care, veterinary medicine, and agriculture. Our current research demonstrates that dendrimers functionalized with a carboxyl endgroup have a size-dependent interaction with liposomes. Our results demonstrate that a larger dendrimer interacted most favorably to form a combined delivery system with liposomes. This work will benefit fellow scientists exploring designs for nano-structured delivery systems.
Technical Abstract: Polycationic polymers and liposomes have a great potential use as individual drug delivery systems and greater potential as a combined drug delivery system. Thus, it is important to better understand the interactions of polymers with phospholipid bilayers. A mechanistic study of carboxyl-terminated poly(amindoamine) (PAMAM) dendrimers interaction with 1-palmitoyl-2-oleoyl-phosphatidylcholine (POPC) bilayer using fluorescence leakage and quartz crystal microbalance with dissipation monitoring (QCMD) was conducted. Fluorescence leakage experiments demonstrated that carboxyl-terminated generation 2 (G2) dendrimers caused increased vesicle leakage with increasing dendrimer concentration over a 0 to 20 micro range. Generation 5 (G5), on the other hand, reduced leakage over the same concentration range, presumably by increasing lipid packing. QCMD measurements demonstrated that G2 weakly and reversibly (dynamically) bound to supported bilayers, resulting in minor lipid loss. In contrast, G5 binding was strong and permanent (static) with no bilayer mass loss.