Elizabeth Susan O’Connor Butler

The Ohio State University

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Trends

Author Order

Document Type

Co-Authors

Narasimham L. Parinandi

The Ohio State University

Sainath R. Kotha

The Ohio State University Wexner Medical Center

Clay B. Marsh

The Ohio State University

Shariq I. Sherwani

The Ohio State University Wexner Medical Center

Sean M. Sliman

The Ohio State University Wexner Medical Center

Periannan Kuppusamy

Dartmouth College

Michelle A. Kline

The Ohio State University

Adam H Hinzey

The Ohio State University

Rao M. Uppu

Southern University and Agricultural and Mechanical College

M. Lakshmi Kuppusamy

Dartmouth College

Cooperative Institutions

The Ohio State University

The Ohio State University Wexner Medical Center

Lung Institute

Sutter Davis Hospital

American Association of Colleges of Pharmacy

Toxicologie, Pharmacologie et Signalisation Cellulaire

Johns Hopkins University

Hormel (United States)

University of Minnesota

University of Massachusetts Amherst

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Field

Lipoxygenase-Catalyzed Phospholipid Peroxidation: Preparation, Purification, and Characterization of Phosphatidylinositol Peroxides

Methods in molecular biology (2009)

Elizabeth Susan O’Connor Butler Jessica N. Mazerik Jason Cruff Shariq I. Sherwani Barbara K. Weis

10.1007/978-1-60327-029-8_23

Cite

Citations (6)

Calcium and Calmodulin Regulate Mercury-induced Phospholipase D Activation in Vascular Endothelial Cells

International Journal of Toxicology (2009)

Alon Peltz Shariq I. Sherwani Sainath R. Kotha Jessica N. Mazerik Elizabeth Susan O’Connor Butler

Earlier, we reported that mercury, the environmental risk factor for cardiovascular diseases, activates vascular endothelial cell (EC) phospholipase D (PLD). Here, we report the novel and significant finding that calcium and calmodulin regulated mercury-induced PLD activation in bovine pulmonary artery ECs (BPAECs). Mercury (mercury chloride, 25 μM; thimerosal, 25 μM; methylmercury, 10 μM) significantly activated PLD in BPAECs. Calcium chelating agents and calcium depletion of the medium completely attenuated the mercury-induced PLD activation in ECs. Calmodulin inhibitors significantly attenuated mercury-induced PLD activation in BPAECs. Despite the absence of L-type calcium channels in ECs, nifedipine, nimodipine, and diltiazem significantly attenuated mercury-induced PLD activation and cytotoxicity in BPAECs. This study demonstrated the importance of calcium and calmodulin in the regulation of mercury-induced PLD activation and the protective action of L-type calcium channel blockers against mercury cytotoxicity in vascular ECs, suggesting mechanisms of mercury vasculotoxicity and mercury-induced cardiovascular diseases.

Mercury

Calcium Signaling

10.1177/1091581809338077

Cite

Citations (24)

Hyperglycemic oxoaldehyde, glyoxal, causes barrier dysfunction, cytoskeletal alterations, and inhibition of angiogenesis in vascular endothelial cells: aminoguanidine protection

Molecular and Cellular Biochemistry (2009)

Sean M. Sliman Timothy D. Eubank Sainath R. Kotha M. Lakshmi Kuppusamy Shariq I. Sherwani

Glyoxal

Endothelial Dysfunction

Matrigel

10.1007/s11010-009-0199-x

Cite

Citations (42)

A Simple Method for Effective and Safe Removal of Membrane Cholesterol from Lipid Rafts in Vascular Endothelial Cells: Implications in Oxidant-Mediated Lipid Signaling

Methods in molecular biology (2009)

Michelle A. Kline Elizabeth Susan O’Connor Butler Adam H Hinzey Sean M. Sliman Sainath R. Kotha

Lipid raft

10.1007/978-1-60327-029-8_12

Cite

Citations (15)

Choice of cyclodextrin for cellular cholesterol depletion for vascular endothelial cell lipid raft studies: cell membrane alterations, cytoskeletal reorganization and cytotoxicity.

PubMed (2012)

Adam H Hinzey Michelle A. Kline Sainath R. Kotha Sean M. Sliman Elizabeth Susan O’Connor Butler

The use of cyclodextrins as tools to establish the role of cholesterol rafts in cellular functions has become a widely accepted procedure. However, the adverse effects of cyclodextrins as the cholesterol-depleting agents on cellular structure and functions are not reported in detail. Therefore, in the current study, we investigated the membrane-perturbing actions and cytotoxicity of the two widely used cellular cholesterol-depleting cyclodextrins methyl-beta-cyclodextrin (MbetaCD) and hydroxypropyl-beta-cyclodextrin (HPCD) in our well-established bovine pulmonary artery endothelial cell (BPAEC) in vitro model system. BPAECs treated with different concentrations of MbetaCD and HPCD (2% and 5%, wt/vol.) for 15-180 min showed significant loss of membrane cholesterol, cytotoxicity, cell morphology alterations, actin cytoskeletal reorganization, alterations in cellular proteins and membrane fatty acid composition, and decrease in trans-endothelial electrical resistance (TER). MbetaCD induced a marked loss of cellular proteins, as compared to that caused by HPCD under identical conditions. More noticeably, MbetaCD caused a drastic loss of membrane lipid fatty acids in BPAECs, as compared to HPCD which failed to cause such alteration. Removal of cholesterol by cyclodextrin (especially MbetaCD) treatment apparently caused loss of fluidity of the cell membrane and leakage of vital cellular molecules including proteins and fatty acids, and thus caused cytotoxicity and loss of cell morphology in BPAECs. Replenishment of cells with cholesterol following its depletion by MbetaCD treatment significantly attenuated the depletion of cellular cholesterol, cytotoxicity and morphological alterations in BPAECs, indicating the importance of membrane cholesterol in vascular EC integrity. Also, the current study offered a safer method of cholesterol removal from membranes and lipid rafts by HPCD, suggesting its use in studies to investigate the role of lipid raft-associated cholesterol in cellular functions.

Lipid raft

Beta-Cyclodextrins

Cell membrane

Membrane Lipids

Source

Cite

Citations (27)