Publications by authors named "T Chernichovski"
Acute kidney injury (AKI) is characterized by cell death and inflammation. CD24 is a protein induced during tissue damage and is not expressed in mature renal tissue. We explored the role of CD24 in the pathogenesis of folic acid-induced AKI (FA-AKI) in mice.
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- Endothelial dysfunction and nitric oxide inactivation may contribute to preeclampsia, with maternal L-arginine deficiency playing a significant role in its development.
- Adopting an adenovirus approach to overexpress sFlt-1 in mice resulted in symptoms similar to preeclampsia, including hypertension and albuminuria; L-arginine helped mitigate these symptoms in pregnant mice but not in non-pregnant ones.
- The study indicates that during pregnancy, the transport of L-arginine is affected, leading to decreased nitric oxide generation in the kidneys, which can be improved with L-arginine treatment, thus highlighting potential intervention strategies for preeclampsia.
Blockade of the mineralocorticoid receptor (MCR) has been shown to improve endothelial function far beyond blood pressure control. In the current studies we have looked at the effect of MCR antagonists on cationic amino acid transporter-1 (CAT-1), a major modulator of endothelial nitric oxide (NO) generation. Using radio-labeled arginine, {[H] l-arginine} uptake was determined in human umbilical vein endothelial cells (HUVEC) following incubation with either spironolactone or eplerenone with or without silencing of MCR.
View Article and Find Full Text PDFBackground/aims: Vascular endothelial growth factor (VEGF) is an endothelium-specific peptide that stimulates angiogenesis via two receptor tyrosine kinases, Flt-1 and KDR. Endothelial nitric oxide synthase (eNOS) plays a major role in VEGF signaling. Delivery of arginine to membrane bound eNOS by the cationic amino acid transporter-1 (CAT-1) has been shown to modulate eNOS activity.
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- Dimethyl sulfoxide (DMSO) is a solvent used in medicine, but its effects on endothelial function and nitric oxide (NO) production are unclear.
- The study investigates how DMSO affects arginine transport, NO generation, and the protein expressions of key transporters in human umbilical vein endothelial cells (HUVECs), finding that DMSO reduces arginine transport and NO production.
- Results show that DMSO alters protein expressions related to arginine transport and induces structural changes in HUVECs, ultimately concluding that DMSO inhibits NO generation in endothelial cells by affecting CAT-1 activity.