Controlled Blood-Brain Barrier Modulation by a High-Affinity Claudin-5 Peptide Binder
Listed in
This article is not in any list yet, why not save it to one of your lists.Abstract
The blood-brain barrier (BBB) is a specialized interface that tightly regulates the exchange of molecules between the bloodstream and the brain. Its barrier function relies on a monolayer of brain endothelial cells sealed by tight junctions (TJs) that restrict paracellular flux through claudin-5 (CLDN5) multimeric complexes. To improve the delivery of nutrients and drugs to the brain, CLDN5-competitive peptides are promising carriers for creating size-controlled, temporary openings in the paracellular pathway. Here, we combine generative protein design and atomistic simulations to design ST9, a peptide with high nanomolar affinity for CLDN5. Compared with f1-C5C2, a CLDN5-binding peptide that we previously reported, ST9 induces a rapid, transient, size-controlled, and fully reversible increase in paracellular permeability, without altering CLDN5 expression or the proteomic profile of brain endothelial cells, indicating distinct mechanisms of TJ destabilization. This work provides a promising approach for developing next-generation BBB-opening agents to effectively treat neurological diseases.
Highlights
-
A new peptide design strategy, using generative modeling based on RFdiffusion, identified de novo a lead CLDN5-binding peptide;
-
The new ST9 peptide displayed a high-nanomolar affinity for CLDN5, high solubility, and absent toxicity;
-
ST9 induces a rapid, transient, size-controlled, and fully reversible increase in paracellular permeability;
-
ST9-induced paracellular permeabilization was not associated with CLDN5 degradation, altered proteomic profile, or endothelial apoptosis.