NDLI: Deficiency in $gp91^{Phox}$ (NOX2) Protects against Oxidative Stress and Cardiac Dysfunction in Iron Overloaded Mice

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Deficiency in $gp91^{Phox}$ (NOX2) Protects against Oxidative Stress and Cardiac Dysfunction in Iron Overloaded Mice

Content Provider	MDPI
Author	Mak, I. Tong Kramer, Jay H. Iantorno, Micaela Chmielinska, Joanna J. Weglicki, William B. Spurney, Christopher F.
Copyright Year	2020
Description	The role of NADPH oxidase subunit, gp91phox (NOX2) in development of oxidative stress and cardiac dysfunction due to iron (Fe)-overload was assessed. Control (C57BL/6J) and gp91phox knockout (KO) mice were treated for up to 8 weeks with Fe (2.5 mg/g/wk, i.p.) or Na-dextran; echocardiography, plasma 8-isoprostane (lipid peroxidation marker), cardiac Fe accumulation (Perl’s staining), and CD11b+ (WBCs) infiltrates were assessed. Fe caused no adverse effects on cardiac function at 3 weeks. At 6 weeks, significant declines in left ventricular (LV) ejection fraction (14.6% lower), and fractional shortening (19.6% lower) occurred in the Fe-treated control, but not in KO. Prolonging Fe treatment (8 weeks) maintained the depressed LV systolic function with a trend towards diastolic dysfunction (15.2% lower mitral valve E/A ratio) in controls but produced no impact on the KO. Fe-treatment (8 weeks) caused comparable cardiac Fe accumulation in both strains, but a 3.3-fold elevated plasma 8-isoprostane, and heightened CD11b+ staining in controls. In KO mice, lipid peroxidation and CD11b+ infiltration were 50% and 68% lower, respectively. Thus, gp91phox KO mice were significantly protected against oxidative stress, and systolic and diastolic dysfunction, supporting an important role of NOX2-mediated oxidative stress in causing cardiac dysfunction during Fe overload.
Ending Page	125
Page Count	9
Starting Page	117
e-ISSN	26733846
DOI	10.3390/hearts1020012
Journal	Hearts
Issue Number	2
Volume Number	1
Language	English
Publisher	MDPI
Publisher Date	2020-09-15
Access Restriction	Open
Subject Keyword	Hearts Peripheral Vascular Disease Nox2 Knockout Mice Iron Overload in Situ Cardiac Function Oxidative Stress Cardiac Iron Cardiac Inflammation
Content Type	Text
Resource Type	Article

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