Exposure to AT1 Receptor Autoantibodies during Pregnancy Increases Susceptibility of the Maternal Heart to Postpartum Ischemia-Reperfusion Injury in Rats

Wang, Huiping; Zhang, Wenhui; Wang, Xiaofang; Zhu, Jin; Zheng, Yanqian; Qin, Xia; Jiang, Zhi

doi:10.3390/ijms150711495

Cited by 15 publications

(13 citation statements)

References 27 publications

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“…Rats administered AT1-AA during pregnancy displayed no differences in cardiac function as compared with normal pregnant rats 16 weeks postpartum in a study conducted by Wang et al 145 However in this study, there were several morphological changes in cardiomyocytes, increased collagen content, and changes in the myocardium structure of rats administered the AT1-AA during pregnancy. 145 These changes were prevented when losartan was administered along with AT1-AA during pregnancy. 145 These data taken together suggest that the AT1-AA may play a pivotal role in the development or pathogenesis of cardiovascular dysfunction and CVDs in the mother.…”

Section: Chronic Inflammation Is a Common Thread That Could Contributcontrasting

confidence: 62%

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Preeclampsia: long-term consequences for vascular health

Amaral¹,

Cunningham²,

Cornelius³

et al. 2015

VHRM

119

137

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Preeclampsia (PE) is a pregnancy-specific syndrome and one of the leading causes of preterm birth, neonatal and maternal morbidity and mortality. This disease is characterized by new onset hypertension usually in the third trimester of pregnancy and is sometimes associated with proteinuria, although proteinuria is not a requirement for the diagnosis of PE. In developing countries, women have a higher risk of death due to PE than more affluent countries and one of the most frequent causes of death is high blood pressure and stroke. Although PE only affects approximately 2%–8% of pregnancies worldwide it is associated with severe complications such as eclampsia, hemorrhagic stroke, hemolysis, elevated liver enzymes and low platelets (HELLP syndrome), renal failure and pulmonary edema. Importantly, there is no “cure” for the disease except for early delivery of the baby and placenta, leaving PE a health care risk for babies born from PE moms. In addition, PE is linked to the development of cardiovascular disease and stroke in women after reproductive age, leaving PE a risk factor for long-term health in women. This review will highlight factors implicated in the pathophysiology of PE that may contribute to long-term effects in women with preeclamptic pregnancies.

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Section: Chronic Inflammation Is a Common Thread That Could Contributcontrasting

confidence: 62%

“… 145 These changes were prevented when losartan was administered along with AT1-AA during pregnancy. 145 These data taken together suggest that the AT1-AA may play a pivotal role in the development or pathogenesis of cardiovascular dysfunction and CVDs in the mother.…”

Section: Chronic Inflammation Is a Common Thread That Could Contributmentioning

confidence: 99%

Preeclampsia: long-term consequences for vascular health

Amaral¹,

Cunningham²,

Cornelius³

et al. 2015

VHRM

119

137

View full text Add to dashboard Cite

show abstract

“…A previous study also reported that mitochondrial structure plays an important role in cardiac function (32). Degradation in mitochondrial structure results in a progressive increase in mitochondrial Ca 2+ sequestration and mitochondrial depolarization, finally leading to cardiac dysfunction (33).…”

Section: Discussionmentioning

confidence: 91%

Tanshinone IIA ameliorates diabetic cardiomyopathy by inhibiting Grp78 and CHOP expression in STZ‑induced diabetes rats

et al. 2019

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Diabetic cardiomyopathy (DCM), one of the common diabetic complications, causes a high rate of mortality in patients with diabetes. Tanshinone IIA (TSIIA), one of the components of Salvia miltiorrhiza (Danshen), has anti-oxidative stress activity and is widely used to treat diabetes-associated diseases. However, its efficacy on DCM remains unclear. The present study aimed to investigate the potential therapeutic function of TSIIA on DCM in an experimental diabetic rat model. Streptozotocin (STZ)-induced diabetic rats were intraperitoneally injected with TSIIA for 6 weeks. The present results indicated that blood glucose concentration was slightly reduced in the low-dose TSIIA treatment group. TSIIA injection was also noted to improve cardiac function, and restore loss of mitochondrial cristae, swollen mitochondrial matrix and disorganized myofibrils in myocardial cells, which are thought to be characteristics of apoptosis. Furthermore, TSIIA injection could increase the activity of superoxide dismutase in STZ-induced diabetic rats, and suppress the endoplasmic reticulum (ER) stress signaling pathway via reducing the expression of glucose-regulated protein 78 and C/EBP homologous protein. These results provide evidence that TSIIA may ameliorate DCM in diabetic rats, possibly via suppressing oxidative stress and ER stress activation.

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“…The AT1-AAs IgG was prepared from the sera of 5 ACS patients with higher AT1-AAs titer separately, purified by affinity chromatography as described previously [ 11 ]. Briefly, the immunoglobulin fractions were loaded on a Sepharose 4B CNBr-activated gel, to which the peptide corresponding to AT1-EC2 was covalently linked [ 20 ]. The antibodies were adsorbed on the affinity column and eluted with 3 mol/L potassium thiocyanate.…”

Section: Methodsmentioning

confidence: 99%

Autoantibodies Targeting AT1 Receptor from Patients with Acute Coronary Syndrome Upregulate Proinflammatory Cytokines Expression in Endothelial Cells Involving NF-κB Pathway

Chen

et al. 2014

Journal of Immunology Research

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Our study intended to prove whether agonistic autoantibodies to angiotensin II type 1 receptor (AT1-AAs) exist in patients with coronary heart disease (CHD) and affect the human endothelial cell (HEC) by upregulating proinflammatory cytokines expression involved in NF-κB pathway. Antibodies were determined by chronotropic responses of cultured neonatal rat cardiomyocytes coupled with receptor-specific antagonists (valsartan and AT1-EC2) as described previously. Interleukin-6 (IL-6), vascular cell adhesion molecule-1 (VCAM-1), and monocyte chemotactic protein-1 (MCP-1) expression were improved at both mRNA and protein levels in HEC, while NF-κB in the DNA level was improved detected by electrophoretic mobility shift assays (EMSA). These improvements could be inhibited by specific AT1 receptor blocker valsartan, NF-κB blocker pyrrolidine dithiocarbamate (PDTC), and specific short peptides from the second extracellular loop of AT1 receptor. These results suggested that AT1-AAs, via the AT1 receptor, induce expression of proinflammatory cytokines involved in the activation of NF-κB. AT1-AAs may play a great role in the pathogenesis of the acute coronary syndrome by mediating vascular inflammatory effects involved in the NF-κB pathway.

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Exposure to AT1 Receptor Autoantibodies during Pregnancy Increases Susceptibility of the Maternal Heart to Postpartum Ischemia-Reperfusion Injury in Rats

Cited by 15 publications

References 27 publications

Preeclampsia: long-term consequences for vascular health

Preeclampsia: long-term consequences for vascular health

Tanshinone IIA ameliorates diabetic cardiomyopathy by inhibiting Grp78 and CHOP expression in STZ‑induced diabetes rats

Autoantibodies Targeting AT1 Receptor from Patients with Acute Coronary Syndrome Upregulate Proinflammatory Cytokines Expression in Endothelial Cells Involving NF-κB Pathway

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