Anti-coagulation effect of Fc fragment against anti-β2-GP1 antibodies in mouse models with APS

Xie, Weidong; Zhang, Yaou; Bu, Chujie; Shi-jing, Sun; Hu, Shaoliang; Cai, Guoping

doi:10.1016/j.intimp.2010.10.018

Cited by 4 publications

(2 citation statements)

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“…For LPS mice, wild-type mice received a single injection with an ultra-low dose of LPS (1 µg/kg body weight, Sigma) on day 3 or 11 of pregnancy [17] , [18] . β2GPI mice had a weekly subcutaneous injection with complete Freund's adjuvant-dissolved human β2GPI (25 µg per mouse, Sigma) in the back 3 weeks before mating and incomplete Freund's adjuvant-dissolved β2GPI 2 weeks and 1 week before mating [19] . Wild-type mice in the control group and transgenic mice in the ApoC3+NS group were injected daily with physiological saline from day 3 or 11 of pregnancy.…”

Section: Methodsmentioning

confidence: 99%

Fatty Acid Oxidation Changes and the Correlation with Oxidative Stress in Different Preeclampsia-Like Mouse Models

et al. 2014

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BackgroundLong-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) expression is decreased in placenta of some cases of preeclampsia (PE) which may result in free fatty acid (FFA) increased. High FFA level will induce oxidative stress, so abnormal long-chain fatty acid-oxidation may participate in the pathogenesis of PE through oxidative stress pathway.MethodsPE-like groups were ApoC3 transgenic mice with abnormal fatty acid metabolism, classical PE-like models with injection of Nw-nitro-L-arginine-methyl ester (L-NA) or lipopolysaccharide (LPS) and the antiphospholipid syndrome (APS) mouse model with β2GPI injection (ApoC3+NS, ApoC3+L-NA, L-NA, LPS and β2GPI groups). The control group was wild-type mice with normal saline injection. Except for β2GPI mice, the other mice were subdivided into pre-implantation (Pre) and mid-pregnancy (Mid) subgroups by injection time.ResultsAll PE-like groups showed hypertension and proteinuria except ApoC3+NS mice only showed hypertension. Serum FFA levels increased significantly except in LPS group compared to controls (P<0.05). LCHAD mRNA and protein expression in the liver and placenta was significantly higher for ApoC3+NS, ApoC3+L-NA and β2GPI mice and lower for L-NA mice than controls (P<0.05) but did not differ between LPS mice and controls. P47phox mRNA and protein expression in the liver significantly increased in all PE-like groups except LPS group, while P47phox expression in the placenta only significantly increased in L-NA and β2GPI groups.ConclusionsAbnormal long-chain fatty acid-oxidation may play a different role in different PE-like models and in some cases participate in the pathogenesis of PE through oxidative stress pathway.

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Section: Methodsmentioning

confidence: 99%

Fatty Acid Oxidation Changes and the Correlation with Oxidative Stress in Different Preeclampsia-Like Mouse Models

et al. 2014

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“…For the LPS mice, wild-type mice received a single injection with an ultra-low dose of Lipopolysaccharide (LPS) (1 µg/kg body weight, Sigma) [14,15]. The β2GPI mice were subcutaneously injected weekly with complete Freund's adjuvant-dissolved human β2 glycoprotein I (β2GPI) (25 µg per mouse, Sigma) in the back 3 weeks before mating and incomplete Freund's adjuvant-dissolved β2GPI 2 weeks and 1 week before mating [16]. Wild-type mice in the control group and transgenic mice in the ApoC3+NS group were injected daily with physiological saline from day 7 or 11 of pregnancy.…”

Section: Establishment and Identification Of Animal Modelsmentioning

confidence: 99%

Mitochondrial Long Chain Fatty Acid Oxidation Related Enzyme Changes in Different Preeclampsia-Like Mouse Models

Ding¹,

Yang²

2013

J Hypertens

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IntroductionPreeclampsia is a serious obstetric complication and a major cause of maternal and perinatal mortality and its pathogenesis is still unclear. We and other researchers have proven that long-chain Fatty Acid Oxidation (FAO) is associated with some forms of preeclampsia.Most fatty acids in the human body are long-chain fatty acids. The β-oxidation of fatty acids occurs in the mitochondria. After activation of long-chain fatty acids, they need assistance from carnitine as a carrier and catalysis of carnitine palmitoyltransferase I (CPT I) in the outer mitochondrial membrane and carnitine palmitoyltransferase II (CPT II) in the inner mitochondrial membrane to enter into the mitochondria [1]. Long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) is a component of the mitochondrial trifunctional protein and is capable of catalyzing the third step of β-oxidation [2]. So CPT I, CPT II and LCHAD are key enzymes in the long-chain FAO process, and defects or dysfunction of which can result in disorders in longchain fatty acid transport into the mitochondria or oxidation, further resulting in inefficient energy release from FAO and affecting cell function.In a normal pregnancy, prolactin and estrogen increase the activity of hormone sensitive lipase, resulting in increased fat mobilization, increased maternal plasma Free Fatty Acids (FFA) and increased hepatic uptake of fatty acids. In the past, FAO was generally considered unimportant in placental and fetal development; however, a recent study found that this was not the case. Shekhawat et al. found that LCHAD and six other fatty acid β-oxidation enzymes were abundantly expressed in the placenta, indicating the long-chain FAO played an important role in placental development and energy supply [3]. Oey et al. found Very Long Chain Acyl-Coenzyme a Dehydrogenase (VLCAD) and LCHAD mRNA highly expressed during different stages in the embryo and fetal heart, liver and other tissues, and there were strong VLCAD, LCHAD and CPT II enzyme activities [4]. So long-chain FAO exists not only in the placenta, but also in embryonic tissues, and plays an important role in early development of the fetus. Thus, in a normal pregnancy placental and fetal development also requires FAO as an energy supply.Previous studies have found that LCHAD was associated with some forms of preeclampsia. Bartha and colleagues reported that LCHAD mRNA expression decreased in the placenta of preeclampsia patients compared with controls, and that the FAO ability of the placenta in preeclampsia patients was reduced [5]. Robinson et al. found that the plasma of preeclampsia patients could lead to lipid droplet aggregation in cultured human umbilical vein endothelial cells and decreased mitochondrial dehydrogenase activity [6]. In our previous studies we also found LCHAD expression decreased in the placenta with earlyonset severe preeclampsia, but there was no significant difference between late-onset preeclampsia and the control groups [7]. In animal experiments, we found that LCHAD expression was signifi...

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Long-chain fatty acid oxidation changes in a β2 glycoprotein I-induced preeclampsia-like mouse model

Ding¹,

Yang²,

Han³

et al. 2014

Placenta

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Anti-coagulation effect of Fc fragment against anti-β2-GP1 antibodies in mouse models with APS

Cited by 4 publications

References 21 publications

Fatty Acid Oxidation Changes and the Correlation with Oxidative Stress in Different Preeclampsia-Like Mouse Models

Fatty Acid Oxidation Changes and the Correlation with Oxidative Stress in Different Preeclampsia-Like Mouse Models

Mitochondrial Long Chain Fatty Acid Oxidation Related Enzyme Changes in Different Preeclampsia-Like Mouse Models

Long-chain fatty acid oxidation changes in a β2 glycoprotein I-induced preeclampsia-like mouse model

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