The Adipokine Chemerin Induces Apoptosis in Cardiomyocytes

Rodríguez-Penas, Diego; Feijóo‐Bandín, Sandra; García-Rúa, Vanessa; Mosquera-Leal, Ana; Durán, Darío; Varela, Alfonso; Portolés, Manuel; Roselló‐Lletí, Esther; Rivera, Miguel; Diéguez, Carlos; Gualillo, Oreste; González-Juanatey, José Ramón; Lago, Francisca

doi:10.1159/000430343

Cited by 47 publications

(42 citation statements)

References 82 publications

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“…Furthermore, chemerin was able to induce functional angiogenesis in these cells . In contrast, other examinations have indicated opposite effects by demonstrating that chemerin promotes apoptosis in human endothelial and vascular smooth muscle cells and murine cardiomyocytes . We assume that chemerin plays a crucial role in the pathophysiology of cardiovascular diseases, but further research is needed addressing the complex underlying mechanisms.…”

Section: Discussionmentioning

confidence: 84%

Serum chemerin is associated with inflammatory and metabolic parameters—results of a population‐based study

Zylla

Pietzner

Kühn

et al. 2017

Obesity

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Objective: This study aimed to confirm existing assumptions about the associations of circulating chemerin with inflammatory and metabolic parameters in a large population-based study. Methods: Data of 3,986 subjects from the Study of Health in Pomerania were analyzed. Residual method was used to investigate the different associations of visceral (VAT) and subcutaneous adipose tissue (SAT) with serum chemerin levels. Multivariable regression models were applied to examine the association of chemerin with high-sensitivity C-reactive protein, fibrinogen, glucose, glycated hemoglobin, lipid profile, blood pressure, diabetes, dyslipidemia, and hypertension. Results: Positive associations with chemerin were observed for VAT and SAT with a stronger relation found for VAT. After adjustment for waist circumference, increased chemerin levels were related to higher inflammatory cytokines and glycated hemoglobin and an unfavorable lipid profile. Logistic regression revealed positive associations of chemerin with dyslipidemia [highest vs. lowest quartile: odds ratio (OR) 1.56 (95% confidence interval (CI) 1.25-1.94)] and hypertension [OR 1.31 (95% CI 1.03-1.68)]. Conclusions: Chemerin levels are significantly linked to inflammation and metabolic syndrome. The majority of the detected associations persisted even after adjustment for waist circumference, suggesting that the relation of chemerin with the analyzed traits cannot be solely explained by an accumulation of adipose tissue.

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Section: Discussionmentioning

confidence: 84%

Serum chemerin is associated with inflammatory and metabolic parameters—results of a population‐based study

Zylla

Pietzner

Kühn

et al. 2017

Obesity

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show abstract

“…There is a lack of data concerning the influence of chemerin on apoptosis. Rodríguez-Penas et al [51] reported that chemerin induces apoptosis, reduces AKT phosphorylation, and increases caspase-9 cleavage in murine cardiomyocytes, suggesting that chemerin plays a role in the physiopathology of cardiac diseases.…”

Section: Discussionmentioning

confidence: 99%

Apelin abrogates the stimulatory effects of 17β-estradiol and insulin-like growth factor-1 on proliferation of epithelial and granulosa ovarian cancer cell lines via crosstalk between APLNR and ERα/IGF1R

2019

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Apelin and chemerin are adipocytokines that play important roles in many physiological and pathological processes throughout the body. Our previous study demonstrated that these two adipokines are expressed and secreted by epithelial and granulosa cancer cell lines. 17β-estradiol (E2) and insulin-like growth factor-1 (IGF-1) are important regulators of ovarian functions, and their roles are well known. This study investigated whether apelin and chemerin regulate proliferation and apoptosis of epithelial (OVCAR-3) and granulosa (COV434) ovarian cancer cell lines by interacting with E2 and IGF-1. Apelin and chemerin did not affect caspase-3 activation in either cell line. However, apelin abrogated the stimulatory effects of E2 on proliferation of OVCAR-3 cells and of IGF-1 on proliferation of COV434 cells independently of ERK1/2 and PI3K via crosstalk of apelin receptor with estrogen receptor alpha and IGF-1 receptor, respectively.

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“…Recently, however, chemerin was reported to be a key regulator of cardiovascular disease, including hypertension, coronary atherosclerosis disease, and myocardial infarction (Kadoglou et al, 2015). In patients with type 2 diabetes, elevated serum levels of chemerin have been associated with heart failure (Zhou et al, 2019) while chemerin was shown to induce murine cardiomyocyte apoptosis through inflammatory processes (Rodriguez-Penas et al, 2015). These results suggest that chemerin plays an important role in DCM by inducing cardiac inflammation.…”

Section: Introductionmentioning

confidence: 99%

Chemerin/CMKLR1 Axis Promotes Inflammation and Pyroptosis by Activating NLRP3 Inflammasome in Diabetic Cardiomyopathy Rat

et al. 2020

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Chemerin and its receptor CMKLR1 (a G-protein-coupled receptor) are inducers of inflammation, and play an important role in diabetic cardiomyopathy (DCM). In this study, we investigated the role of the chemerin/CMKLR1 axis in mediating inflammation and cell death in DCM. Sprague-Dawley rats, treated with a high-fat diet and low-dose of streptozotocin, were used as a DCM model. CMKLR1 expression was knocked down by siRNA (CMKLR1-siRNA) to evaluate the role of CMKLR1 in DCM. Chemerintreated H9c2 cells were used to investigate the factors acting downstream of the chemerin/CMKLR1 axis. LDH release and EthD-III staining were used to measure the ratio of cell death in vitro. CMKLR1-siRNA and siRNA against nucleotide-binding oligomerization domain-like receptors 3 (NLRP3-siRNA) were used to explore the mechanism underlying chemerin-induced inflammation and cell death. The results showed that the expression of chemerin, CMKLR1, NLRP3, pro-caspase-1, activated caspase-1, and mature IL-1β was increased in the DCM model rat. Myocardium of DCM model rats exhibited fibrosis, hypertrophy, a disorganized ultrastructure, and impaired function. Pyroptosis was observed in vivo and in vitro. Silencing of CMKLR1 in vivo attenuated the expression of NLRP3 and activated caspase-1 and IL-1β. CMKLR1-siRNA treatment attenuated cardiac inflammation, fibrosis, hypertrophy, and pyroptosis, and improved cardiac function in vivo. Silencing of either CMKLR1 or NLRP3 suppressed the levels of activated caspase-1, IL-1β, and pyroptosis; however, silencing of both CMKLR1 and NLRP3 further decreased the levels of mature IL-1β and pyroptosis. Overall, the results showed that the chemerin/CMKLR1 axis contributed to the development of DCM and that the NLRP3 inflammasome mediated the chemerin/CMLR1-induced inflammation and pyroptosis. These data indicate that silencing of the CMKLR1 gene might exert a protective effect against DCM.

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The Adipokine Chemerin Induces Apoptosis in Cardiomyocytes

Cited by 47 publications

References 82 publications

Serum chemerin is associated with inflammatory and metabolic parameters—results of a population‐based study

Serum chemerin is associated with inflammatory and metabolic parameters—results of a population‐based study

Apelin abrogates the stimulatory effects of 17β-estradiol and insulin-like growth factor-1 on proliferation of epithelial and granulosa ovarian cancer cell lines via crosstalk between APLNR and ERα/IGF1R

Chemerin/CMKLR1 Axis Promotes Inflammation and Pyroptosis by Activating NLRP3 Inflammasome in Diabetic Cardiomyopathy Rat

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