Interplay among cardiotrophin-1, prostaglandins, and vascular endothelial growth factor in rat liver regeneration

Beraza, Naiara; Marqués, Juan Martín; Martı́nez-Ansó, Eduardo; Íñiguez, María; Prieto, Jesús; Bustos, Matilde

doi:10.1002/hep.20590

Cited by 42 publications

(24 citation statements)

References 44 publications

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“…15,16,33,37 Our results and those of other studies showed that CT-1 receptors are present in cardiac fibroblasts, VSMCs, ECs, monocytes, and macrophages. 11,[13][14][15] Several lines of evidence have shown that foam cell formation and CD36 and ACAT1 expression in macrophages and the migration and proliferation of VSMCs are mediated via ERK-1/2.…”

Section: Discussionsupporting

confidence: 83%

Stimulatory Effects of Cardiotrophin 1 on Atherosclerosis

Konii

Sato²,

Kikuchi³

et al. 2013

Hypertension

111

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A therosclerosis is a pathological injury-to-response process that is initiated by early inflammatory responses of vascular endothelial cells (ECs).1 Endothelial inflammation is characterized by increased production of proatherogenic molecules and inflammatory cytokines in ECs, and monocyte adhesion and infiltration into the neointima lesion, followed by oxidized low-density lipoprotein-induced transformation of macrophages into foam cells.2 Accumulation of cholesterol ester in macrophages is a hallmark of foam cell formation. 2This accumulation depends on the balance between the uptake of oxidized low-density lipoprotein via CD36 and the efflux of free cholesterol controlled by ATP-binding cassette transporter A1 (ABCA1), ATP-binding cassette transporter G1, or scavenger receptor class B type I (SR-BI).3 To protect the cells from the toxicity that would result from excessive free cholesterol accumulation, the free cholesterol is esterified to cholesterol ester by acyl-CoA:cholesterol acyltransferase-1 (ACAT1).3 Cholesterol ester stored in lipid droplets can be removed from cells only after hydrolysis to free cholesterol by neutral cholesterol ester hydrolase. 4 Apart from accumulation of macrophage-derived foam cells, the migration and proliferation of vascular smooth muscle cells (VSMCs) followed by extracellular matrix (ECM) production play crucial roles in the development of atherosclerotic lesions. 1Cardiotrophin 1 (CT-1), a 201-aa member of the interleukin-6 cytokine family, was originally cloned from embryoid bodies as a 21.5-kDa protein capable of inducing hypertrophy in neonatal cardiomyocytes. 5 Human and mouse CT-1 share 80% amino acid sequence identity and exhibit cross-species activity.6 Subsequent studies confirmed that plasma concentrations of CT-1 are elevated in various cardiorenal diseases, such as hypertension, ischemic heart disease, heart failure, and chronic renal disease.7-10 CT-1 exerts cardiovascular remodeling induced by hypertensive and ischemic heart diseases and congestive heart failure, through its receptor complex glycoprotein 130 (gp130) and leukemia inhibitory factor receptor (LIFR).11-14 Recently, CT-1 has been shown to be expressed in the intima in the early stages of atherosclerotic lesions in human carotid artery.15 CT-1 stimulates the synthesis of inflammatory cytokines and proatherogenic molecules, such as interleukin-6, Abstract-Cardiotrophin 1 (CT-1), an interleukin-6 family cytokine, was recently shown to be expressed in the intima of early atherosclerotic lesions in the human carotid artery. CT-1 stimulates proatherogenic molecule expression in human vascular endothelial cells and monocyte migration. However, it has not been reported whether CT-1 accelerates atherosclerosis. This study was performed to examine the stimulatory effects of CT-1 on human macrophage foam cell formation and vascular smooth muscle cell migration and proliferation in vitro, and on the development of atherosclerotic lesions in apolipoprotein E-deficient (ApoE −/− ) mice in vivo. CT-1 was express...

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Section: Discussionsupporting

confidence: 83%

Stimulatory Effects of Cardiotrophin 1 on Atherosclerosis

Konii

Sato²,

Kikuchi³

et al. 2013

Hypertension

111

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“…Soon after its discovery, CT-1 was shown to be a potent inducer of the acute phase response in rat primary hepatocytes [2,90] and subsequent studies showed that CT-1 is an essential factor in the defense of the liver against a variety of insults [91][92][93][94][95]. In the liver CT-1 mRNA is expressed by both hepatocytes and non-parenchymal cells [94].…”

Section: Livermentioning

confidence: 97%

Cardiotrophin-1: A multifaceted cytokine

López-Yoldi

Moreno-Aliaga

Bustos

2015

Cytokine & Growth Factor Reviews

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“…rCT-1 was obtained as described elsewhere ( 16 ) and contained <0.04 ng LPS per 1 g of the protein as determined by the Limulus amoebocyte lysate assay (Cambrex, East Rutherford, NJ).…”

Section: Rct-1mentioning

confidence: 99%

Cardiotrophin-1 stimulates lipolysis through the regulation of main adipose tissue lipases

López-Yoldi

Fernández‐Galilea

Laiglesia

et al. 2014

Journal of Lipid Research

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This article is available online at http://www.jlr.org effects by interacting with the glycoprotein 130 (gp130)/ leukemia inhibitory factor receptor heterodimer ( 1 ). Adipose tissue has been identifi ed as a source of CT-1 ( 2 ), and this cytokine is capable of activating major signaling pathways involved in metabolic control in adipocytes ( 3 ). Moreover, it has been reported that CT-1 levels are raised in obesity and metabolic syndrome ( 2 ), suggesting that CT-1 could be a new marker for obesity and related diseases. A recent study by our group has revealed that CT-1 is a key regulator of energy homeostasis, as well as of glucose and lipid metabolism ( 4 ). Thus, chronic recombinant CT-1 (rCT-1) treatment reduced body weight and corrected insulin resistance in ob/ob and high-fat-fed obese mice by reducing food intake and enhancing energy expenditure. Moreover, rCT-1 induced dramatic white adipose tissue remodeling characterized by the upregulation of genes implicated in the control of fatty acid oxidation, mitochondrial biogenesis, and lipolysis. In this context, it has been reported that adipocytes from rCT-1-treated mice exhibited an increased lipolytic response to isoproterenol, while adipocytes from old obese CT-1 -null mice responded poorly to isoproterenol, suggesting that CT-1 might play a role in the regulation of lipolysis ( 4 ). However, the mechanism underlying the lipolytic action of CT-1 still remains unknown.During lipolysis, intracellular triacylglycerol (TAG) is hydrolyzed through the consecutive action of three major lipases: adipose triglyceride lipase (ATGL/desnutrin), Abbreviations: AdPLA , adipocyte phospholipase A2; AICAR, aminoimidazole carboxamide ribonucleotide; ATGL, adipose triglyceride lipase (desnutrin); CGI-58, comparative gene identifi cation-58; cGMP, cyclic guanosine monophosphate; CT-1, cardiotrophin-1; DAG, diacylglycerol; Gi, inhibitory guanine nucleotide binding protein; gp130, glycoprotein 130; Gs, stimulatory guanine nucleotide binding protein; G0S2, G0/G1 switch gene 2; HPTLC, high-performance TLC; HSL, hormone sensitive lipase; IL, interleukin; MAG, monoacylglycerol; PDE3B, phosphodiesterase 3B; PK, protein kinase; rCT-1, recombinant cardiotrophin-1; TAG, triacylglycerol. 1 M. Bustos and M. J. Moreno-Aliaga contributed equally to the work.

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Interplay among cardiotrophin-1, prostaglandins, and vascular endothelial growth factor in rat liver regeneration

Cited by 42 publications

References 44 publications

Stimulatory Effects of Cardiotrophin 1 on Atherosclerosis

Stimulatory Effects of Cardiotrophin 1 on Atherosclerosis

Cardiotrophin-1: A multifaceted cytokine

Cardiotrophin-1 stimulates lipolysis through the regulation of main adipose tissue lipases

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