Cardiotrophin-1 Review

Stejskal, David; Růžička, Viktor

doi:10.5507/bp.2008.002

Cited by 24 publications

(24 citation statements)

References 118 publications

(82 reference statements)

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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: 77%

“…Several studies confirmed the trophic properties of CT-1 in other cell types, such as adult cardiomyocytes, cardiac fibroblasts, hepatocytes, and airway smooth muscle cells. 7,14,31,33 CT-1 induces myocardial hypertrophy and confers protection from ischemia/reperfusion injury through its receptor, gp130/ LIFR complex, followed by activation of the ERK-1/2, Janus kinase/signal transducer and activation of transcription-3, and phosphatidylinositol-3 kinase/Akt pathways.…”

Section: Discussionmentioning

confidence: 99%

“…8,[15][16][17] CT-1 is expressed in the cardiovascular system as well as the thymus, kidney, liver, muscle, and adipose tissue. [31][32][33] Expression of CT-1 is upregulated by mechanical stretching and atherogenic substances, such as angiotensin II, aldosterone, norepinephrine, fibroblast growth factor-2, heparinbinding epidermal growth factor-like growth factor, glucose, and reactive oxygen species. 7,33,34 Vascular media thickness and ECM contents, such as collagen, fibronectin, elastin, and matrix metalloproteinase, in VSMCs were increased by CT-1 treatment in rats.…”

Section: Discussionmentioning

confidence: 99%

“…[31][32][33] Expression of CT-1 is upregulated by mechanical stretching and atherogenic substances, such as angiotensin II, aldosterone, norepinephrine, fibroblast growth factor-2, heparinbinding epidermal growth factor-like growth factor, glucose, and reactive oxygen species. 7,33,34 Vascular media thickness and ECM contents, such as collagen, fibronectin, elastin, and matrix metalloproteinase, in VSMCs were increased by CT-1 treatment in rats. 11,12 Media thickness, wall fibrosis, and inflammation were lower in CT-1-deficient mice than in wild-type controls under a normal diet.…”

Section: Discussionmentioning

confidence: 99%

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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: 77%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Stimulatory Effects of Cardiotrophin 1 on Atherosclerosis

Konii

Sato²,

Kikuchi³

et al. 2013

Hypertension

111

View full text Add to dashboard Cite

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“…19,23) Some studies found increased plasma CT-1 levels in HF patients because of dilated cardiomyopathy, [24][25][26] which indicated there was a significant correlation between up-regulation of CT-1 and left ventricle systolic dysfunction. 27,28) In our study, miR-340 was up-regulated by the stimulation of CT-1, but was not altered in response to ISO. Furthermore, LIF, another member of the IL-6 family, also exhibited the up-regulation effect of miR-340.…”

Section: )mentioning

confidence: 70%

microRNA-340-5p Functions Downstream of Cardiotrophin-1 to Regulate Cardiac Eccentric Hypertrophy and Heart Failure via Target Gene Dystrophin

et al. 2015

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SummaryPathological cardiac hypertrophy inevitably leads to the unfavorable outcomes of heart failure (HF) or even sudden death. microRNAs are key regulation factors participating in many pathophysiological processes. Recently, we observed upregulation of microRNA-340-5p (miR-340) in failing human hearts because of dilated cardiomyopathy, but the functional consequence of miR-340 remains to be clarified.We transfected neonatal cardiomyocytes with miR-340 and found fetal gene expression including Nppa, Nppb and Myh7. We also observed eccentric hypertrophy development upon treatment which was analogous to the phenotype after cardiotrophin-1 (CT-1) stimulation. As a potent inducer of cardiac eccentric hypertrophy, treatment by IL-6 family members CT-1 and leukemia inhibitory factor (LIF) led to the elevation of miR-340. Knockdown of miR-340 using antagomir attenuated fetal gene expression and hypertrophy formation, which means miR-340 could convey the hypertrophic signal of CT-1. To demonstrate the initial factor of miR-340 activation, we constructed a volume overloaded abdominal aorta-inferior vena cava fistula rat HF model. miR-340 and CT-1 were found to be up-regulated in the left ventricle. Dystrophin (DMD), a putative target gene of miR-340 which is eccentric hypertrophy-susceptible, was decreased in this HF model upon Western blotting and immunohistochemistry tests. Luciferase assay constructed in two seed sequence of DMD gene 3'UTR showed decreased luciferase activities, and miR-340 transfected cells resulted in the degradation of DMD.miR-340 is a pro-eccentric hypertrophy miRNA, and its expression is dependent on volume overload and cytokine CT-1 activation. Cardiomyocyte structure protein DMD is a target of miR-340. (Int Heart J 2015; 56: 454-458)

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Osteoclast Secretes Stage‐Specific Key Molecules for Modulating Osteoclast–Osteoblast Communication

Fu,

Shi,

et al. 2024

Journal Cellular Physiology

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In most cases of bone metabolic disorders, such as osteoporosis and osteomalacia, these conditions are often attributed to dysfunctional osteoclasts, leading to their common characterization as “destructors.” In addition to the widely documented regulatory process where osteoblasts direct osteoclastic bone resorption, there is increasing evidence suggesting that osteoclasts also in turn influence osteoblastic bone formation through direct and indirect mechanisms. It is well‐known that differentiation of osteoclasts involves several stages, each characterized by specific cellular features and functions. Stage‐specific key molecules secreted during these stages play a critical role in mediating osteoclast–osteoblast communication. In this review, we described the different stages of osteoclast differentiation and reviewed stage‐specific key molecules involved in osteoclasts‐osteoblasts communication. We highlighted that a detailed understanding of these processes and molecular mechanism could facilitate the development of novel treatments for bone metabolic disorders.

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Cardiotrophin-1 Review

Cited by 24 publications

References 118 publications

Stimulatory Effects of Cardiotrophin 1 on Atherosclerosis

Stimulatory Effects of Cardiotrophin 1 on Atherosclerosis

microRNA-340-5p Functions Downstream of Cardiotrophin-1 to Regulate Cardiac Eccentric Hypertrophy and Heart Failure via Target Gene Dystrophin

Osteoclast Secretes Stage‐Specific Key Molecules for Modulating Osteoclast–Osteoblast Communication

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