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Biology subjects

Ebong, E. E.

Publications and source records attributed to Ebong, E. E..

2 recordsLinked to original sources

FRAGMENT MORPHOMETRY ANALYSIS AND SAME-COLOR-CHANNEL SEPARATION ENABLE OBJECTIVE QUANTIFICATION ACROSS BBB MODELS

Quantifying blood-brain barrier (BBB) integrity from fluorescence microscopy remains limited by subjective scoring and categorical classification methods that lack reproducibility. For objective and consistent BBB phenotyping, we present two semi-automated image-analysis pipelines that replace manual scoring with quantitative, continuous-variable measurements. Our in vitro pipeline, implemented in Python, quantifies the connectivity of tight junction structures by measuring discrete ZO-1 fragment objects within manually traced junction regions. It outputs continuous metrics including average fragment area, total junctional area, and a junctional fragmentation ratio that captures degree of ZO-1 continuity versus discontinuity. In human brain microvascular endothelial cells subjected to glycocalyx component knockdown, the pipeline detected significantly reduced fragment area (37% decrease for both CD44 and syndecan-1 (SDC1) knockdown, p = 0.0148 and 0.0084) and junctional fragmentation ratio (p = 0.0061 and 0.0137). Our in vivo pipeline integrates ilastik-based pixel classification with FIJI macro automation to quantify vascular marker colocalization and to separate vessel signal from microglial contamination within a single fluorescence channel, eliminating the need for dedicated counterstains. Applied across four mouse cohorts [young, aged, Alzheimers, traumatic brain injury (TBI)] and three brain regions [prefrontal cortex (PFC), hippocampus, midbrain], the pipeline revealed concurrent ZO-1 loss and ICAM-1 elevation in the PFC and hippocampus of aged and Alzheimers mice, with Alzheimers-specific doubling of eNOS occurring in the PFC (p = 0.0013). TBI mice showed persistent ZO-1 loss with transient ICAM-1 and eNOS changes. Both deterministic pipelines are available on GitHub and designed for adoption beyond the specific markers and systems analyzed here.

bioengineering↗

Co-Therapy with S1P and Heparan Sulfate Derivatives to Restore Endothelial Glycocalyx and Combat Pro-Atherosclerotic Endothelial Dysfunction

Endothelial cell (EC) glycocalyx (GCX) shedding due to disturbed blood flow and chemical factors leads to low-density lipoprotein infiltration and reduced nitric oxide synthesis, causing vascular dysfunction and atherosclerosis. This study evaluates a novel therapy combining sphingosine-1-phosphate (S1P) and heparin (heparan sulfate derivative). We hypothesized that heparin/S1P would repair mechanically damaged EC GCX in disturbed flow (DF) regions and restore anti-atherosclerotic mechanotransduction function, addressing cardiovascular disease. We used a parallel-plate flow chamber to simulate flow conditions in vitro and a partial carotid ligation mouse model to mimic DF in vivo. Heparin and albumin-bound S1P were administered to assess their reparative effects on the endothelial GCX. Immunocytochemistry, fluorescent staining, confocal microscopy, cellular alignment studies, and ultrasound were performed to evaluate EC function and endothelial-dependent vascular function. Barrier functionality was assessed via macrophage uptake. Heparin/S1P mechanism-of-action insights were gained through fluid dynamics simulations and staining of GCX synthesis enzyme as well as S1P receptor. Statistical analyses validated results. In vitro data showed that heparin/S1P therapy improves the function of DF-conditioned ECs by restoring EC GCX and promoting EC alignment and elevated vasodilator eNOS (endothelial-type nitric oxide synthase) expression. The in vivo studies confirmed GCX degradation, increased vessel inflammation and hyperpermeability, and vessel wall thickening in the partially ligated left carotid artery. Heparin/S1P treatment restored GCX in the left carotid artery, enhancing GCX thickness and coverage of the blood vessel wall. This work advances a new approach to regenerating the EC GCX and restoring its function in ECs under DF conditions.

bioengineering↗