Investigation of the assembly mechanism and molecularlevel structure of β-hairpin peptide hydrogelators

Date
2015
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University of Delaware
Abstract
Designed and naturally derived self-assembling peptides have utility as building blocks in the fabrication of hydrogels as tissue engineering platforms and drug delivery depots. Additionally, designed peptides and those derived from amyloidogenic proteins can serve as tools to understand the biophysical principles that guide amyloid-like fibril formation and define the molecular-level interactions that constitutes the assembled state. Similarly to amyloid-derived self-assemblers, many designed material-forming peptides also assemble to form -sheet rich fibrils. To date, however, mechanistic and structural determination of biomaterial-based peptide assemblies significantly lags behind efforts to define assemblies of disease-associated amyloid fibrils. To this end, the mechanism of assembly and final solid state structure of the self-assembling hydrogelator MAX1 has been investigated in this dissertation. MAX1 is a 20-amino acid peptide designed de novo to form a facially amphiphilic - hairpin. The peptide is composed of two strands of alternating hydrophobic valine and hydrophilic lysine residues that flank a four residue turn-promoting sequence (- VDPLPT-). Under aqueous, low ionic strength conditions, the peptide adopts an ensemble of random coil conformations due to electrostatic repulsion between lysine side chains. Upon addition of a high pH or high ionic strength solution, the lysine borne charge is attenuated and the peptide assembles to form a -sheet rich network of fibrils that constitute a self-supporting hydrogel. The objective of this work is to identify the mode of assembly and the final molecular-level structure of the MAX1 peptide alone and in the presence of its enantiomer DMAX1. For pure solutions of MAX1, it was found that random coil, monomeric peptide undergo hydrophobic collapse to form unstructured oligomers that precede the formation of -sheet structure. The data strongly argue against an initial unimolecular folding event that subsequently leads to fibril formation. The early time assembly events are defined by a multi-component solution of peptide composed of both unstructured oligomers and monomeric peptide. Overtime, these species become competent for the formation of the -sheet rich fibrils that define the final assembled state. The molecular-level structure of MAX1 within these peptide fibrils are further investigated by solid state NMR. It is shown that MAX1 forms the designed -hairpin secondary structure with a type II’ -turn. Within fibrils, hairpins are arranged in a Syn/Anti configuration where turns are aligned along a given -sheet monolayer but do not directly oppose each other across the fibril bilayer. This arrangement leads to the formation of critical hydrophobic and van der Waals interactions that are not accessible in completing arrangements and, thus, leads to the formation of highly monomorphic fibrils within a kinetically trapped network. In separate work, the molecular-level interactions between peptide enantiomers MAX1 and DMAX1 in coassembled fibrils are investigated. Hydrogels formed from enantiomeric mixtures of MAX1 and DMAX1 are significantly more rigid than hydrogels produced from either peptide alone, with the racemic mixture exhibiting a four-fold increase in mechanical rigidity. Using an arsenal of rheological, spectroscopic, scattering, and microscopic techniques it was determined that the peptide enantiomers co-assemble to form fibrils that are more stiff than those formed by either pure MAX1 or DMAX1. The fibril stiffness stems from key nested hydrophobic interactions between laterally associated enantiomers that cannot be accessed within pure enantiomeric assemblies and is the ultimate reason for the enhanced mechanical rigidity of the racemic hydrogel. Finally, in a separate project, hydrogels formed from negatively charged -hairpins are explored as drug delivery vehicles. Here, the effect of network electrostatics on the release of a series of model proteins is investigated. The data show that attractive electrostatic interactions play a large role in the retention of proteins within the hydrogel network and open the door to the further optimization of this new class of gels. Overall, this thesis demonstrates how knowledge of the assembly mechanism and final molecular structure of naturally-occurring and disease-related self-assembled peptides can be applied to material formation peptides and further lead to the rational optimization of peptide assembly and ultimate biomaterial mechanical behavior.
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