Try a new search

Format these results:

Searched for:



Total Results:


Contemporary Practice of Echocardiography in Transcatheter Aortic Valve Replacement [Editorial]

Pospishil, Liliya; Nampi, Robert G; Neuburger, Peter J
PMID: 34366216
ISSN: 1532-8422
CID: 5006092

Anesthetic Management of Conduction Disturbances Following Transcatheter Aortic Valve Replacement: A Review of the 2020 ACC Expert Consensus Decision Pathway [Editorial]

Neuburger, Peter J; Pospishil, Liliya; Ibrahim, Homam
PMID: 33441272
ISSN: 1532-8422
CID: 4746992

TAVR Versus SAVR for the Treatment of Aortic Stenosis: Do We Have a Clear Winner? [Editorial]

Nampi, Robert G; Pospishil, Liliya; Neuburger, Peter J
PMID: 32418828
ISSN: 1532-8422
CID: 4443692

In Pursuit of a Unicorn: Does the Ideal Parameter for Grading of Aortic Stenosis During Intraoperative Transesophageal Echocardiography Exist? [Editorial]

Pospishil, Liliya; Patel, Prakash A; Neuburger, Peter J
PMID: 31138469
ISSN: 1532-8422
CID: 3921462

Surgically Assisted Transcatheter Balloon-Expandable Valve in Inferior Vena Cava for Torrential Tricuspid Regurgitation

Mulaikal, Teresa A; Pospishil, Liliya; George, Isaac; Bapat, Vinayak N; Hahn, Rebecca T
PMID: 30370378
ISSN: 2468-6441
CID: 3399342

JS-K, a nitric oxide-releasing prodrug, modulates ß-catenin/TCF signaling in leukemic Jurkat cells: evidence of an S-nitrosylated mechanism

Nath, Niharika; Chattopadhyay, Mitali; Pospishil, Liliya; Cieciura, Lucyna Z; Goswami, Satindra; Kodela, Ravinder; Saavedra, Joseph E; Keefer, Larry K; Kashfi, Khosrow
β-Catenin is a central player of the Wnt signaling pathway that regulates cell-cell adhesion and may promote leukemia cell proliferation. We examined whether JS-K, an NO-donating prodrug, modulates the Wnt/β-catenin/TCF-4 signaling pathway in Jurkat T-Acute Lymphoblastic Leukemia cells. JS-K inhibited Jurkat T cell growth in a concentration and time-dependent manner. The IC(50)s for cell growth inhibition were 14±0.7 and 9±1.2μM at 24 and 48h, respectively. Treatment of the cells with JS-K for 24h, caused a dose-dependent increase in apoptosis from 16±3.3% at 10μM to 74.8±2% at 100μM and a decrease in proliferation. This growth inhibition was also due, in part, to alterations in the different phases of the cell cycle. JS-K exhibited a dose-dependent cytotoxicity as measured by LDH release at 24h. However, between 2 and 8h, LDH release was less than 20% for any indicated JS-K concentration. The β-catenin/TCF-4 transcriptional inhibitory activity was reduced by 32±8, 63±5, and 93±2% at 2, 10, and 25μM JS-K, respectively, based on luciferase reporter assays. JS-K reduced nuclear β-catenin and cyclin D1 protein levels, but cytosolic β-catenin expression did not change. Based on a time-course assay of S-nitrosylation of proteins by a biotin switch assay, S-nitrsolyation of nuclear β-catenin was determined to precede its degradation. A comparison of the S-nitrosylated nuclear β-catenin to the total nuclear β-catenin showed that β-catenin protein levels were degraded at 24h, while S-nitrosylation of β-catenin occurred earlier at 0-6h. The NO scavenger PTIO abrogated the JS-K mediated degradation of β-catenin demonstrating the need for NO.
PMID: 20797387
ISSN: 1873-2968
CID: 3242952