Nuclear Receptors in Vascular Biology

Bishop‐Bailey, David

doi:10.1007/s11883-015-0507-8

Cited by 6 publications

(6 citation statements)

References 56 publications

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“…NRs are involved in the control of numerous physiological activities including metabolism ( 86 , 87 ), reproduction ( 88 , 89 ), cell cycle ( 90 ), vasculature ( 91 , 92 ), brain activity ( 93 , 94 ), circadian rhythm ( 95 – 97 ) and immunity ( 98 – 103 ). NRs have then been widely implicated in the control of inflammatory processes and the control of immune cell activity ( 99 ).…”

Section: Nuclear Receptorsmentioning

confidence: 99%

Nuclear Receptors in the Control of the NLRP3 Inflammasome Pathway

Duez

Pourcet

2021

Front. Endocrinol.

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The innate immune system is the first line of defense specialized in the clearing of invaders whether foreign elements like microbes or self-elements that accumulate abnormally including cellular debris. Inflammasomes are master regulators of the innate immune system, especially in macrophages, and are key sensors involved in maintaining cellular health in response to cytolytic pathogens or stress signals. Inflammasomes are cytoplasmic complexes typically composed of a sensor molecule such as NOD-Like Receptors (NLRs), an adaptor protein including ASC and an effector protein such as caspase 1. Upon stimulation, inflammasome complex components associate to promote the cleavage of the pro-caspase 1 into active caspase-1 and the subsequent activation of pro-inflammatory cytokines including IL-18 and IL-1β. Deficiency or overactivation of such important sensors leads to critical diseases including Alzheimer diseases, chronic inflammatory diseases, cancers, acute liver diseases, and cardiometabolic diseases. Inflammasomes are tightly controlled by a two-step activation regulatory process consisting in a priming step, which activates the transcription of inflammasome components, and an activation step which leads to the inflammasome complex formation and the subsequent cleavage of pro-IL1 cytokines. Apart from the NF-κB pathway, nuclear receptors have recently been proposed as additional regulators of this pathway. This review will discuss the role of nuclear receptors in the control of the NLRP3 inflammasome and the putative beneficial effect of new modulators of inflammasomes in the treatment of inflammatory diseases including colitis, fulminant hepatitis, cardiac ischemia–reperfusion and brain diseases.

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Section: Nuclear Receptorsmentioning

confidence: 99%

Nuclear Receptors in the Control of the NLRP3 Inflammasome Pathway

Duez

Pourcet

2021

Front. Endocrinol.

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“…49,50 We have previously shown that female sex hormones including17b-estradiol and progesterone inhibit IL-1b-induced collagen degradation by corneal fibroblasts as well as the IL-1b-induced phosphorylation of p38 MAPK, but not that of ERK or JNK, in these cells. 16 In addition, the glucocorticoid receptor agonist dexamethasone inhibits IL1b-induced collagen degradation by corneal fibroblasts as well as the IL-1b-induced phosphorylation of ERK and JNK, but not that of p38 MAPK, in these cells.…”

Section: Discussionmentioning

confidence: 99%

Suppression by an RAR-γ Agonist of Collagen Degradation Mediated by Corneal Fibroblasts

Kimura

Zhou

Orita

et al. 2017

Invest. Ophthalmol. Vis. Sci.

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PURPOSE.To examine the role of retinoic acid receptor (RAR) isoforms in interleukin-1b (IL1b)-induced collagen degradation by corneal fibroblasts.METHODS. Primary rabbit corneal fibroblasts embedded in a three-dimensional collagen gel were incubated with or without all-trans retinoic acid (ATRA), the RAR-a agonist Am580, the RAR-b agonist AC55649, or the RAR-c agonist R667. Collagen degradation was determined by measurement of hydroxyproline produced in acid hydrolysates of culture supernatants. Matrix metalloproteinase (MMP) expression was evaluated by immunoblot analysis and gelatin zymography. The phosphorylation of mitogen-activated protein kinases (MAPKs) and the endogenous nuclear factor (NF)-jB inhibitor IjB-a was examined by immunoblot analysis. Cell proliferation was measured with a bromodeoxyuridine incorporation assay, and cell viability was determined by measurement of the release of lactate dehydrogenase. RESULTS.Interleukin-1b-induced collagen degradation by corneal fibroblasts was inhibited by ATRA, Am580, and R667 in a concentration-dependent manner but was unaffected by AC55649, with the inhibitory effects of ATRA and R667 being markedly greater than that of Am580. The IL-1b-induced production of MMP-1, MMP-2, MMP-3, and MMP-9 by corneal fibroblasts was also inhibited by R667 in a concentration-dependent manner. R667 inhibited the IL-1b-induced phosphorylation of IjB-a but not that of MAPKs. R667 had no effect on the proliferation or viability of corneal fibroblasts.CONCLUSIONS. The RAR-c agonist R667 suppressed MMP production and thereby inhibited collagen degradation by corneal fibroblasts exposed to the proinflammatory cytokine IL-1b. These effects of R667 may be mediated by the NF-jB signaling pathway.

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“…PPARβ signalling includes the classical PPAR-RXR pathway to regulate target gene induction and trans-repression of the transcription factor BCL-6 (Lee, et al, 2003) and/or protein kinase PKCα (Ali, Armstrong, et al, 2009;Ali, Hall, Desvergne, Warner, & Mitchell, 2009;Mitchell, et al, 2014). The pharmacological relationship between PGI2 drugs in their interaction with IP versus PPARs is reviewed elsewhere (Belvisi & Mitchell, 2009;Bishop-Bailey, 2015;Mitchell, et al, 2014;. PGI2 drugs include, injectable treprostinil, iloprost, beraprost and newer orally active selexipag (Mitchell, et al, 2014).…”

Section: Pgi2 Drugsmentioning

confidence: 99%

Cyclooxygenases and the cardiovascular system

Mitchell

Kirkby

Ahmetaj‐Shala

et al. 2021

Pharmacology & Therapeutics

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Cyclooxygenase (COX)-1 and COX-2 are centrally important enzymes within the cardiovascular system with a range of diverse, sometimes opposing, functions. Through the production of thromboxane, COX in platelets is a pro-thrombotic enzyme. By contrast, through the production of prostacyclin, COX in endothelial cells is antithrombotic and in the kidney regulates renal function and blood pressure. Drug inhibition of COX within the cardiovascular system is important for both therapeutic intervention with low dose aspirin and for the manifestation of side effects caused by nonsteroidal anti-inflammatory drugs. This review focuses on the role that COX enzymes and drugs that act on COX pathways have within the cardiovascular system and provides an in-depth resource covering COX biology and pharmacology. The review goes on to consider the role of COX in both discrete cardiovascular locations and in associated organs that contribute to cardiovascular health.We discuss the importance of, and strategies to manipulate, the thromboxane: prostacyclin balance.Finally within this review the authors discuss testable COX-2-hypotheses intended to stimulate debate and facilitate future research and therapeutic opportunities within the field.

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Nuclear Receptors in Vascular Biology

Cited by 6 publications

References 56 publications

Nuclear Receptors in the Control of the NLRP3 Inflammasome Pathway

Nuclear Receptors in the Control of the NLRP3 Inflammasome Pathway

Suppression by an RAR-γ Agonist of Collagen Degradation Mediated by Corneal Fibroblasts

Cyclooxygenases and the cardiovascular system

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