A Review of Prostanoid Receptors: Expression, Characterization, Regulation, and Mechanism of Action

Biringer, Roger G.

doi:10.1007/s12079-020-00585-0

Cited by 38 publications

(29 citation statements)

References 201 publications

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“…Previous studies have shown that the EP3 receptor modulates multiple intracellular signaling pathways by coupling different types of heterotrimeric G proteins [ 29 ]. As shown in Fig.…”

Section: Resultsmentioning

confidence: 99%

EP3 Receptor Deficiency Improves Vascular Remodeling and Cognitive Impairment in Cerebral Small Vessel Disease

Liu¹,

Tang²,

Yang³

et al. 2022

Aging and disease

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Aging and hypertension are major risk factors for cerebral small vessel disease (CSVD). Anti-hypertensive therapy has achieved effective; however, incomplete results in treating CSVD, suggesting the need for additional treatments. Targeting abnormal inflammatory responses has become a topic of research interest. Small artery remodeling is the main pathological feature of CSVD. Inhibition of the E-prostanoid 3 (EP3) receptor has been shown to attenuate vascular remodeling in peripheral organs; however, little is known about its role in CSVD. Therefore, we investigated whether the deletion of EP3 attenuates the development of CSVD in an animal model-- stroke-prone renovascular hypertensive rat (RHRsp). We found that the cerebral small arteries of RHRsp exhibited increased EP3 expression. Despite no alleviation of hypertension, the deletion of EP3 still attenuated the cerebral small artery remodeling of RHRsp, as evidenced by reduced overexpression of extracellular matrix (ECM) in the vessel. In vitro experiments indicated that EP3 deletion regulated the expression of ECM by downregulating TGF-β1/Smad signaling. Furthermore, the Morris water maze test and magnetic resonance test demonstrated that EP3 knockout attenuated cognitive impairment of the RHRsp, possibly through increased cerebral blood flow. Together, our results indicate that the deletion of EP3 attenuates vascular remodeling and vascular cognitive impairment induced by hypertension, and blockade of the EP3 receptor may be a promising strategy for the treatment of CSVD.

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“…Previous studies have shown that the EP3 receptor modulates multiple intracellular signaling pathways by coupling different types of heterotrimeric G proteins [ 29 ]. As shown in Fig.…”

Section: Resultsmentioning

confidence: 99%

EP3 Receptor Deficiency Improves Vascular Remodeling and Cognitive Impairment in Cerebral Small Vessel Disease

Liu¹,

Tang²,

Yang³

et al. 2022

Aging and disease

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“…Therefore, HPLC-MS/MS analysis of eicosanoids was performed in our study, in order to compare the release of these lipid signaling molecules from epithelial (parental) and transformed cells with the mesenchymal phenotype. Although the production of several eicosanoids with anti-inflammatory and pro-resolution activities, such as lipoxin LXA4 [32], PGD2, and PGJ2 [37], was increased in the transformed cells, a massive increase in prostaglandins and HETEs with pro-carcinogenic and pro-inflammatory effects, especially PGE 2 [27], was observed. For example, 12-HETE and 20-HETE have been implicated in cell proliferation, inhibition of apoptosis, angiogenesis, and invasion/metastasis [38].…”

Section: Discussionmentioning

confidence: 99%

“…Numerous lipid species, including sphingolipids and eicosanoids, have been shown to play important roles in carcinogenesis, both as lipid signaling molecules and as modulators of the structure/functions of cell membranes [20,31,32]. This study aimed: (1) to compare the SL and GSL content in the human bronchial epithelial cell line HBEC-12KT and in their BaP-transformed counterpart, HBEC-12KT-B1 cells with acquired mesenchymal status [30], in order to identify possible links between SL/GSL concentrations and the expression of genes related to SL/GSL metabolism; (2) to compare SL/GSL composition in exosomes released from both cell lines and to explore possible relationships between the SL/GSL profiles in exosomes and the mesenchymal epithelial cell phenotype, respectively.…”

Section: Discussionmentioning

confidence: 99%

“…Prostaglandins and other eicosanoids represent another group of lipid signaling molecules involved in cancer progression, cardiovascular diseases, and other pathological processes [31,32]. Induction of CerP and S1P synthesis might also be involved in induction of eicosanoid metabolism [28,29], thus linking SLs and eicosanoid production.…”

Section: Hplc-ms/ms Analysis Of Eicosanoids Released From Transformed and Parental Hbec-12kt Cellsmentioning

confidence: 99%

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Changes in Sphingolipid Profile of Benzo[a]pyrene-Transformed Human Bronchial Epithelial Cells Are Reflected in the Altered Composition of Sphingolipids in Their Exosomes

Machala

Slavík

Kováč

et al. 2021

IJMS

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Sphingolipids (SLs), glycosphingolipids (GSLs), and eicosanoids are bioactive lipids, which play important roles in the etiology of various diseases, including cancer. However, their content and roles in cancer cells, and in particular in the exosomes derived from tumor cells, remain insufficiently characterized. In this study, we evaluated alterations of SL and GSL levels in transformed cells and their exosomes, using comparative HPLC-MS/MS analysis of parental human bronchial epithelial cells HBEC-12KT and their derivative, benzo[a]pyrene-transformed HBEC-12KT-B1 cells with the acquired mesenchymal phenotype. We examined in parallel SL/GSL contents in the exosomes released from both cell lines. We found significant alterations of the SL/GSL profile in the transformed cell line, which corresponded well with alterations of the SL/GSL profile in exosomes derived from these cells. This suggested that a majority of SLs and GSLs were transported by exosomes in the same relative pattern as in the cells of origin. The only exceptions included decreased contents of sphingosin, sphingosin-1-phosphate, and lactosylceramide in exosomes derived from the transformed cells, as compared with the exosomes derived from the parental cell line. Importantly, we found increased levels of ceramide phosphate, globoside Gb3, and ganglioside GD3 in the exosomes derived from the transformed cells. These positive modulators of epithelial–mesenchymal transition and other pro-carcinogenic processes might thus also contribute to cancer progression in recipient cells. In addition, the transformed HBEC-12KT-B1 cells also produced increased amounts of eicosanoids, in particular prostaglandin E2. Taken together, the exosomes derived from the transformed cells with specifically upregulated SL and GSL species, and increased levels of eicosanoids, might contribute to changes within the cancer microenvironment and in recipient cells, which could in turn participate in cancer development. Future studies should address specific roles of individual SL and GSL species identified in the present study.

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“…NO produces vasodilation by stimulat-ing soluble guanylate cyclase, leading to an increase in cyclic guanosine monophosphate (cGMP) [83]. Classically, PGI 2 exerts its vasodilation through activating PGI 2 receptor coupled to the Gαs protein-adenylyl cyclase pathway to produce cyclic adenosine monophosphate (cAMP) [84,85]. The mechanism underlying H 2 S-induced vasodilation remains not fully understood, potentially involving activation of K + channels [86].…”

Section: Release Of Endothelium-derived Vasodilatorsmentioning

confidence: 99%

Uteroplacental Circulation in Normal Pregnancy and Preeclampsia: Functional Adaptation and Maladaptation

Zhang

2021

IJMS

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Uteroplacental blood flow increases as pregnancy advances. Adequate supply of nutrients and oxygen carried by uteroplacental blood flow is essential for the well-being of the mother and growth/development of the fetus. The uteroplacental hemodynamic change is accomplished primarily through uterine vascular adaptation, involving hormonal regulation of myogenic tone, vasoreactivity, release of vasoactive factors and others, in addition to the remodeling of spiral arteries. In preeclampsia, hormonal and angiogenic imbalance, proinflammatory cytokines and autoantibodies cause dysfunction of both endothelium and vascular smooth muscle cells of the uteroplacental vasculature. Consequently, the vascular dysfunction leads to increased vascular resistance and reduced blood flow in the uteroplacental circulation. In this article, the (mal)adaptation of uteroplacental vascular function in normal pregnancy and preeclampsia and underlying mechanisms are reviewed.

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A Review of Prostanoid Receptors: Expression, Characterization, Regulation, and Mechanism of Action

Cited by 38 publications

References 201 publications

EP3 Receptor Deficiency Improves Vascular Remodeling and Cognitive Impairment in Cerebral Small Vessel Disease

EP3 Receptor Deficiency Improves Vascular Remodeling and Cognitive Impairment in Cerebral Small Vessel Disease

Changes in Sphingolipid Profile of Benzo[a]pyrene-Transformed Human Bronchial Epithelial Cells Are Reflected in the Altered Composition of Sphingolipids in Their Exosomes

Uteroplacental Circulation in Normal Pregnancy and Preeclampsia: Functional Adaptation and Maladaptation

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