17-β-Estradiol decreases p38 MAPK-mediated myocardial inflammation and dysfunction following acute ischemia

Wang, Meijing; Tsai, Ben M.; Reiger, Karen M; Brown, John W.; Meldrum, Daniel R.

doi:10.1016/j.yjmcc.2005.06.019

Cited by 90 publications

(88 citation statements)

References 38 publications

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“…These targets include tissues of the reproductive system, such as the mammary gland and uterus, cells in the hypothalamus and pituitary, bone, and liver, as well as the cardiovascular system, where estrogens exert cardioprotective effects [35]. In addition to stimulating normal mammary gland growth and duct development, pathological levels of estrogens increase proliferation and metastatic activity of breast cancer cells and stimulate proliferation of uterine cells [36,37].…”

Section: Discussionmentioning

confidence: 99%

Redox regulation of human estrogen sulfotransferase (hSULT1E1)

Maiti¹,

Zhang²,

Chen³

2007

Biochemical Pharmacology

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Sulfotransferases (SULTs) are enzymes that catalyze the sulfation of hydroxyl-containing compounds. Sulfation regulates hormone activities and detoxifies xenobiotics. Human estrogen sulfotransferase (hSULT1E1) catalyzes the sulfation of estrogens and regulates estrogen bioactivities. Oxidative regulation provides a biological mechanism for regulating enzyme activities in vivo. The oxidative regulation of human SULTs has not been reported. In this study, we used amino acid modification, manipulation of intracellular redox state, and site-directed mutagenesis to study the redox regulation of human SULTs and specifically the mechanism of hSULT1E1 inhibitory regulation by oxidized glutathione (GSSG). Of the four major human SULTs, hSULT1A1, hSULT1A3, and hSULT2A1 do not undergo redox regulation; hSULT1E1, on the other hand, can be redox regulated. GSSG inactivated hSULT1E1 activity in an efficient, time-and concentrationdependant manner. The co-enzyme adenosine 3′-phosphate 5′-phosphosulfate protected hSULT1E1 from GSSG-associated inactivation. A reduced glutathione (GSH) inducer (N-acetyl cysteine) significantly increased while a GSH depletor (buthionine sulfoxamine) significantly decreased hSULT1E1 activity, but both failed to affect the amount of hSULT1E1 protein in human hepatocyte carcinoma Hep G2 cells. Crystal structure suggested that no Cys residues exist near the active sites of hSULT1A1, hSULT1A3, and hSULT2A1, but Cys residues do exist within the active site of hSULT1E1. Site-directed mutagenesis demonstrated that Cys83 is critical for the redox regulation of hSULT1E1. This first report on the redox regulation of human SULTs suggests that the redox regulation of hSULT1E1 may interrupt the regulation and function of estrogens under various physiological and pathological conditions.

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Section: Discussionmentioning

confidence: 99%

Redox regulation of human estrogen sulfotransferase (hSULT1E1)

Maiti¹,

Zhang²,

Chen³

2007

Biochemical Pharmacology

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“…Castration and ovarectomy were performed 4-6 weeks prior to experimentation. This time frame has been shown to adequately deplete endogenous sex hormones [19,26].…”

Section: Animalsmentioning

confidence: 99%

The Effects of Endogenous Sex Hormones and Acute Hypoxia on Vasoconstriction in Isolated Rat Pulmonary Artery Rings

Patel

Lahm

Crisostomo

et al. 2008

Journal of Surgical Research

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“…Clinically, men have higher overall incidence of heart failure, more progression to heart failure, worse age-matched cardiac contractility than women, and worse preservation of myocardial mass as they age 17 . Experimentally, animal studies have indicated that male hearts are more sensitive to acute I/R injury as exhibited by worse myocardial functional recovery, higher proinflammatory cytokine production and increased apoptotic signaling following I/R 3,4 . Although overwhelming data have established the protective effects of estrogen in females, testosterone is also an important sex hormone, which may lead to deleterious effects seen in the male heart subjected to acute injury.…”

Section: Discussionmentioning

confidence: 99%

“…Understanding the detailed cellular and molecular events that modulate the severity of myocardial ischemia will potentially allow us to develop novel techniques for the treatment of myocardial infarction. We have reported gender-specific differences in hearts subjected to acute I/R 3,4 . Specifically, male hearts exhibit decreased functional recovery, elevated myocardial inflammation and increased cardiomyocyte apoptosis in response to I/R 3,4 .…”

Section: Introductionmentioning

confidence: 95%

“…We have reported gender-specific differences in hearts subjected to acute I/R 3,4 . Specifically, male hearts exhibit decreased functional recovery, elevated myocardial inflammation and increased cardiomyocyte apoptosis in response to I/R 3,4 . Although the majority of studies have indicated that the sex hormone-estrogen is cardioprotective, the cardiac effects of testosterone remain controversial.…”

Section: Introductionmentioning

confidence: 95%

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