Toxicological Research
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2023
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IF 2.3
Tian Jie,Mu Ying,Ma Lili
This study investigated whether chemerin/chemokine-like receptor 1 (CMKLR1) pathway participate in cisplatin‐induced spiral ganglion neuron (SGN) damage. Middle cochlear turn was collected from C57BL/6 mice and the SGNs were cultured. Cisplatin, 2-(anaphthoyl) ethyltrimethylammonium iodide (α-NETA), or recombinant mouse chemerin was added into the medium for the treatment. Relative mRNA and protein expression was determined by RT-PCR, ELISA and Western blot, respectively. In cultured mouse cochlear SGNs, the treatment of cisplatin enhanced the secretion of chemerin and CMKLR1. Recombinant chemerin promoted but α-NETA inhibited chemerin/CMKLR1 pathway in cisplatin stimulated SGNs. Cisplatin-induced apoptosis and inflammation response in SGNs were enhanced by recombinant chemerin while inhibited by α-NETA. Recombinant chemerin promoted but α-NETA inhibited NF-κB signal in cisplatin stimulated SGNs. In conclusion, chemerin/CMKLR1 pathway regulated apoptosis and inflammation response in cisplatin-induced SGN injury through NF-κB signaling pathway.
研究领域:
神经科学
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药理学
·
耳鼻喉科
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DOI
PubMed
高影响因子
Metallomics
·
2018
·Vol. 10
·期 6
·838-845
·
IF 4.069
Sun Pengcheng,Wang Song,Wang Jian,Sun Jing,Peng Min,Shi Ping
Chemerin exhibits a tumor-inhibitory role in hepatocellular carcinoma. However, the effect of chemerin on essential metal elements in hepatic cells remains unclear. In our study, the contents of six important metal ions, including potassium, calcium, sodium, magnesium, iron and zinc, were detected in human hepatoma SMMC7721 and immortal hepatic QSG7701 cells by ICP-AES. The data showed that chemerin only decreases the content of intracellular iron in SMMC7721 cells. The reduction was due to the blockage of iron entry through the decrease in the mRNA levels of divalent metal transporter 1, iron regulatory proteins and transferrin receptors. Furthermore, the reduction of the cellular iron content induced alterations of p53–p27–p21 signaling to arrest the cell cycle at S phase in SMMC7721 cells treated by chemerin. Conversely, iron addition led to recovery from the inhibitory effect of chemerin on SMMC7721 cells. The results suggest that chemerin plays an important role in inhibiting the cell proliferation of hepatocellular carcinomas by interfering with cellular iron homeostasis in this type of tumors.
研究领域:
肿瘤学
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细胞生物学
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分子生物学
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PubMed
高影响因子
Lipids in Health and Disease
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2023
·Vol. 22
·期 1
·1-14
·
IF 4.5
Tan Lunbo,Ouyang Zijun,Chen Zhilong,Sun Fen,Guo Haichun,Wang Feng,Mulder Monique,Sun Yuan,Lu Xifeng,Zhang Jian V.,Danser A. H. Jan,Verdonk Koen,Fan Xiujun,Yang Qing
Background The adipokine chemerin regulates adipogenesis and the metabolic function of both adipocytes and liver. Chemerin is elevated in preeclamptic women, and overexpression of chemerin in placental trophoblasts induces preeclampsia-like symptoms in mice. Preeclampsia is known to be accompanied by dyslipidemia, albeit via unknown mechanisms. Here, we hypothesized that chemerin might be a contributor to dyslipidemia. Methods Serum lipid fractions as well as lipid-related genes and proteins were determined in pregnant mice with chemerin overexpression in placental trophoblasts and chemerin-overexpressing human trophoblasts. In addition, a phospholipidomics analysis was performed in chemerin-overexpressing trophoblasts. Results Overexpression of chemerin in trophoblasts increased the circulating and placental levels of cholesterol rather than triglycerides. It also increased the serum levels of lysophosphatidic acid, high-density lipoprotein cholesterol (HDL-C), and and low-density lipoprotein cholesterol (LDL-C), and induced placental lipid accumulation. Mechanistically, chemerin upregulated the levels of peroxisome proliferator-activated receptor g, fatty acid-binding protein 4, adiponectin, sterol regulatory element-binding protein 1 and 2, and the ratio of phosphorylated extracellular signal-regulated protein kinase (ERK)1/2 / total ERK1/2 in the placenta of mice and human trophoblasts. Furthermore, chemerin overexpression in human trophoblasts increased the production of lysophospholipids and phospholipids, particularly lysophosphatidylethanolamine. Conclusions Overexpression of placental chemerin production disrupts trophoblast lipid metabolism, thereby potentially contributing to dyslipidemia in preeclampsia.
研究领域:
妇产科学
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内分泌学
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分子生物学
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DOI
PubMed
高影响因子
BIOCHEMICAL PHARMACOLOGY
·
2026
·
IF 6.5
Jianhang Liu,Jie Qiu,Yongyi Dai,Shengnan Fei,Wenjing Sheng,Xijan Wang,Fei Lu,Cheng Sun,Xinzhong Huang
Renal fibrosis is an irreversible pathological process that leads to progressive kidney dysfunction, and effective disease-modifying therapies are still lacking. Chemerin is an adipokine predominantly produced by adipose tissue. In our previous study, we demonstrated that chemerin inhibits ferroptosis in renal tubular epithelial cells and protects the kidney from acute injury. Here, we investigated whether chemerin also exerts nephroprotective effects in chronic kidney disease (CKD). Our results revealed a pronounced reduction in chemerin levels in kidney tissues from individuals with CKD and in a murine model of unilateral ureteral obstruction (UUO). Functionally, exogenous chemerin administration alleviated renal insult and fibrosis in mice undergoing UUO. Moreover, chemerin suppressed M2 macrophage-to-myofibroblast transition (MMT) in the UUO kidneys. In cultured macrophages, chemerin engages chemerin chemokine-like receptor 1 (CMKLR1) to suppress polarization and activation toward M2 phenotype. This inhibitory effect was abolished upon CMKLR1 knockdown. Together, these results indicate that chemerin mitigates kidney injury and fibrosis in CKD, primarily by restraining M2 macrophage polarization and the subsequent MMT.
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PubMed
高影响因子
KIDNEY & BLOOD PRESSURE RESEARCH
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2023
·Vol. 48
·期 1
·405-413
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IF 2.8
Peng Zining,Wang Xueyi,Zhu Qing,Wang Huili,Li Bing,Pang Xinxin,Han Jiarui
Introduction: Diabetic nephropathy (DN) is a common complication in diabetic patients. Chemerin, a novel adipokine, has been associated with renal damage in DN. The chemerin chemokine-like receptor 1 (CMKLR1) has been reported to participate in DN. In this study, we aimed to investigate the effect of a CMKLR1 antagonist, 2-(anaphthoyl)ethyltrimethylammonium iodide (α-NETA), on DN. Methods: To induce diabetes, 8-week-old male C57BL/6J mice were given a single intraperitoneal injection of 65 mg/kg streptozotocin (STZ). Diabetic mice were randomly assigned to receive daily doses of 0, 5, or 10 mg/kg α-NETA for 4 weeks. Results: α-NETA dose-dependently induced body weight and reduced fasting blood glucose levels in STZ-induced diabetic mice. Furthermore, α-NETA significantly reduced the expressions of renal injury markers, including serum creatinine, kidney weight/body weight, urine volume, total proteins, and albumin in the urine, and increased creatinine clearance. Periodic acid-Schiff staining also indicated that α-NETA could effectively ameliorate renal injuries in DN mice. In addition, α-NETA inhibited renal inflammation and the expressions of chemerin and CMKLR1 in mice with DN. Conclusion: In summary, our findings suggested that α-NETA has beneficial effects on the management of DN. Specifically, α-NETA effectively ameliorated renal damage and inflammation in a dose-dependent manner in mice with DN. Thus, targeting the chemerin and CMKLR1 axis with α-NETA may be a promising therapeutic strategy for the treatment of DN
研究领域:
药理学
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肾病学
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糖尿病研究
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PubMed
高影响因子
JOURNAL OF MOLECULAR ENDOCRINOLOGY
·
2026
·
IF 3.1
Xin Ning,Doudou Guo,Qing Huang,Cencen Wang,Yating Li,Yanfen Zhou,Xin Li
In mammals, chemerin and its receptor CMKLR1 might be downstream effectors in response to long photoperiod in the ependymal cells lining the third ventricle in rats. Iodothyronine deiodinase 2 (DIO2) is a main product of the involvement of TSH in photoperiodic signaling. Thus, the potential interplay of TSH and Chemerin/CMKLR1 signaling might exist during photoperiodic changes. Our study aimed to investigate whether Chemerin/CMKLR1 signaling could stimulate DIO2 production and how TSH could affect Chemerin/CMKLR1 signaling in primary rat ependymal cells. Colocalization of Chemerin with its receptor, CMKLR1, was observed using immunohistochemistry assay. The expression of chemerin and CMKLR1 was identified using real-time PCR and western blot analysis respectively. DIO2 expression, which involves a dual signaling pathway (an increase in cAMP levels and phosphorylation of ERK1/2, was detected by western blot assay and enzyme-linked immunosorbent assay (ELISA). Our study showed the potential interaction between Chemerin and CMKLR1 in primary rat ependymal cells. TSH could upregulate the expression of chemerin and CMKLR1 in Chemerin-pretreated primary ependymal cells. In vitro treatment of primary ependymal cells with Chemerin (10 ng/mL) or TSH (60 mIU/mL) could induce an increase in cAMP levels, ERK1/2 phosphorylation and DIO2 expression. Furthermore, we found that TSH could promote the effect of Chemerin/CMKLR1 signaling on DIO2 production through an increase in cAMP level and the phosphorylation of ERK1/2. We concluded that Chemerin/CMKLR1 signaling could enhance DIO2 activity in primary rat ependymal cells in vitro, and this effect could be promoted by TSH through cAMP and phosphorylation of ERK1/2.
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PubMed
高影响因子
Journal of Magnesium and Alloys
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2026
·
IF 15.8
Yuwei Gu,Qi Wang,Shaosheng Jia,Jianan Yu,Lan Chen,Lingchuang Bai,Shaokang Guan
Magnesium alloy stents (MAS) show remarkable application potential for treating cardiovascular diseases, attributable to their superior mechanical properties and biodegradability. However, their clinical applications are significantly hindered by inadequate corrosion resistance and suboptimal blood compatibility. In this study, a multilayer coating was constructed on the Mg-Zn-Y-Nd (ZE21B) alloy to enhance its degradation rate, blood compatibility, and the capacity to promote endothelialization in the field of vascular stent applications. This coating comprised layers of magnesium fluoride, polydopamine, fucoidan, and the chemerin 15 (C15) peptide, achieved through a surface modification technique. The modified ZE21B alloy exhibited increased charge transfer resistance and decreased corrosion current density, suggesting a marked enhancement in its corrosion resistance. Furthermore, the modified alloy demonstrated exceptional blood compatibility, as evidenced by the comparatively low magnitudes of hemolysis, fibrinogen adsorption and denaturation, and platelet adhesion. After fucoidan and C15 peptide were grafted on samples, the coating notably promoted key biological behaviors of endothelial cells (ECs), including adhesion, proliferation, migration, and nitric oxide (NO) release. In contrast, it could efficiently restrain smooth muscle cell adhesion and proliferation. The ECs on the fucoidan and C15 peptide modified ZE21B alloy exhibited obvious competitive growth advantages over SMCs in a co-culture system. Furthermore, the introduction of the C15 peptide had endowed the ZE21B alloy with anti-inflammatory properties through regulating the M2 polarization of macrophages. This study offered a highly promising approach for the development of degradable MAS endowed with outstanding corrosion resistance and vascular histocompatibility.
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高影响因子
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