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Hancco Zirena, I.

Publications and source records attributed to Hancco Zirena, I..

2 recordsLinked to original sources

Molecular insights into protein disulfide isomerase antagonism by punicalagin

Punicalagin, an ellagic acid polyphenol from pomegranate, has been proposed as an antagonist of protein disulfide isomerase (PDI) and endoplasmic reticulum resident protein 57 (ERp57), thiol oxidoreductases that regulate protein folding and extracellular thrombotic signaling. Here, biochemical oxidase and reductase assays on PDI show that punicalagin inhibits both activities with micromolar potency, thereby extending earlier work that described only disulfide reductase inhibition. In parallel, thiol labeling of catalytic cysteines revealed no change in the redox state, supporting a noncovalent, allosteric of inhibition. Molecular docking and molecular dynamics simulations showed that punicalagin binds stably and preferentially to defined sites on the Nterminal domains of PDI through extensive hydrogen bonding and van der Waals contacts, which is an alternative binding mode to previously reported C-terminal binding. Finally, artificial intelligence-driven network analysis identified PDI as a high-confidence target of punicalagin and related galloylated polyphenols, alongside additional signaling proteins. Together, these findings provide further mechanistic framework for punicalagin-mediated antagonism of PDI and highlight galloylated polyphenols as promising scaffolds for protein disulfide isomerase-targeted therapeutics. HighlightsO_LIPunicalagin, a galloylated polyphenol, antagonizes not only the reductase activity but also the oxidase activity of protein disulfide isomerase C_LIO_LIProtein disulfide isomerase inhibition by punicalagin is through N-terminal binding C_LIO_LIPunicalagin inhibits conformationally rather than catalytic cysteine modification C_LIO_LIArtificial intelligence network analysis reveals pathway inhibition by punicalagin C_LI

biochemistry↗

Isoquercetin treatment of mouse sickled red blood cells shows a discernible deformability and sickling phenotype

IntroductionSickle cell disease is an inherited hemoglobinopathy with defective red cell deformability. The defective deformability promotes microvascular occlusion and subsequent vaso-occlusion in sickle cell disease patients. Previous studies have demonstrated that thiol isomerases, an endoplasmic reticulum-resident oxidoreductase that is released from vascular cells into the bloodstream, are present on red cell membrane and contribute to cellular dehydration and sickling. However, the role of membrane-bound thiol isomerases on sickled red blood cells is unclear. MethodsUsing red blood cells from Townes humanized sickle cell or non-sickled mice, we performed ektacytometry assay under shear using laser assisted optical rotational cell analyzer (LORRCA) to assess the effects of antagonizing thiol isomerases with isoquercetin and a functional blocking monoclonal antibody. The densitometric properties of sickled red blood cells in the presence of isoquercetin was also tested using magnetic levitation. ResultsThiol isomerase antagonism increased sickled red cell elongation, cellular dehydration and the diamagnetic signature compared to control treatment. ConclusionThiol isomerases may be involved in regulating sickled red blood cells mechanical properties through mechanisms that require further investigation.

pharmacology and toxicology↗