Barrier Structure and Function Studies

This study shows ischemic stroke causes long-term changes in brain stromal progenitor cells, leading to vascular dysfunction and potential recurrent stroke.

This study shows downstream capillary pericytes express -SMA and regulate blood flow through torsional contractions, challenging the view that capillaries are passive.

This study investigates how pericyte degeneration contributes to blood-brain barrier disruption in Alzheimer's disease by examining insulin signaling and MMP/TIMP imbalance in an in vitro model.

The paper characterizes primary cilia and centriole organization in mouse and human brain microvasculature, revealing interspecies differences and their potential role in sensing microenvironmental signals.

HaloTrace provides a spatiotemporal readout of BBB permeability in mice by using a fluorescent ligand that specifically accumulates in the brain at sites of BBB dysfunction.

The paper develops Brendo, a resource identifying BMEC-specific genes using bulk RNA-seq data and provides a web platform for exploring these genes.

This study identifies an inflammation-driven gene module in brain endothelial cells that compromises BBB integrity in Alzheimer's disease and shows that an NF-κB inhibitor can reverse these effects.

This paper develops a long-term in vitro model of human colonic epithelium that maintains barrier function for up to 30 days and responds to various challenges.

The paper develops a 3D Brain-Chip system using human iPSC-derived cells to model the BBB and study APOE4's role in Alzheimer's disease.

This study identifies endothelial type I interferon signaling as a regulator of vascular normalization after ischemic brain injury, showing it reduces BBB disruption and promotes junctional stability.

This study shows that tight junctions and cell-matrix adhesions in brain endothelial cells reciprocally control blood-brain barrier integrity through mechanical forces and protein expression changes.

This study classifies cell and brain penetrating peptides using machine learning, identifying key physicochemical features that distinguish brain-penetrating peptides from cell-penetrating peptides and non-BPP controls.

The paper develops a human neurovascular culture model to study TBI effects, finding incomplete vascular repair and glial-mediated signaling changes.

This study shows that deleting Hdac2 in adult CNS endothelial cells reactivates pro-angiogenic programs, promoting revascularization and neuronal regeneration after stroke.

This study identifies metabolic and lipidomic changes in mouse brain endothelial cells undergoing senescence in vitro, highlighting alterations in tight-junction proteins and key metabolic pathways.

This study investigates how NS1 proteins from high- and low-pathogenicity TBEV strains interact with BBB tight junction proteins, revealing strain-specific binding patterns that may explain differential neuropathogenicity.

The paper investigates how Angubindin-1 disrupts the blood-tumor barrier by targeting Angulin-1/LSR, enhancing drug permeability and reducing glioma progression.

This study shows that aging increases pulmonary microvascular endothelial cell permeability due to impaired cell-cell junctions and actin cytoskeleton changes, not inflammation.

This study develops humanized TfR1 and Tf gene-replacement rats to evaluate BBB transport of human-specific therapeutics, showing viability and partial functional compensation.

This study identifies isoDGR-induced endothelial cytoskeletal disruption as a key driver of age-related BBB breakdown and shows that targeting isoDGR preserves BBB integrity and reduces neuroinflammation.

This study identifies vascular luminal glycocalyx loss and complement activation as key drivers of BBB injury in hyperglycemic stroke, showing that targeting complement after reperfusion improves outcomes.

This study shows that blocking VCAM1 or VLA4 after stroke preserves vascular integrity and prevents cognitive decline by promoting blood vessel growth and restoring the blood-brain barrier.

The paper investigates how high-density lipoproteins (HDL) cross the blood-brain barrier, showing that LDLR and apoE composition determine HDL entry and brain localization.

This study shows that Epstein-Barr virus and Helicobacter pylori coinfection disrupts gut and brain barriers by altering junction proteins and inducing neuroinflammation.

This study identifies distinct Ca2+ signaling profiles in leptomeningeal fibroblast subgroups in awake mice under health and inflammation conditions.

This study investigates how murine cerebral capillary endothelial and pericyte cells respond to blood flow cessation, finding that pericytes mediate microvascular constriction via ET-1 and alter endothelial tight junctions.

The paper presents techniques to quantify the horizontal and vertical distribution of junctional proteins in fixed epithelial cells under different experimental conditions.

This study identifies vessel-type-specific vascular barrier dysfunction in Huntington's disease and shows partial rescue with an S1PR1 agonist.

This paper develops humanized TfR1-targeting nanobodies (NewroBus) that cross the BBB and deliver therapeutic payloads to the CNS.

This paper develops a 3D microfluidic chip model of the neurovascular unit that supports neural-vascular interactions and is used to study neuroinflammation and drug transcytosis.