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#30387843   2018/10/29 To Up

Apelin‑13 ameliorates metabolic and cardiovascular disorders in a rat model of type 2 diabetes with a high‑fat diet.

Apelin has been reported to be associated with multiple physiological processes in the cardiovascular system. The aim of the present study was to investigate the effects of Apelin‑13 administration on cardiac function, hyperglycemia, insulin resistance (IR), dyslipidemia, endothelial function, inflammation and glucose metabolism in type 2 diabetic Goto‑Kakizaki (GK) rats, and compare the protective effects of Apelin‑13 with metformin or atorvastatin. In the present study, type 2 diabetes was induced in male Goto‑Kakizaki (GK) rats fed with high‑fat diet (HFD). Simultaneously, the rats were treated with metformin (350 mg/kg/d, by gavage), atorvastatin (50 mg/kg/d, by gavage) or Apelin‑13 (200 µg/kg/d, intraperitoneal injection) once daily for 4 consecutive weeks. Hemodynamic parameters were examined by RM6240BD multi‑channel physiological signal monitoring. Fasting plasma glucose (FPG), fasting insulin (FINS), homeostasis model assessment for insulin resistance (HOMA‑IR), total cholesterol (TC), triglyceride (TG), high density lipoprotein‑cholesterol (HDL‑C), low density lipoprotein‑cholesterol (LDL‑C), endothelin‑1 (ET‑1), nitric oxide (NO), constitutive nitric oxide synthase (cNOS) activity, tumor necrosis factor‑α (TNF‑α), leptin and Apelin‑12 levels were measured. Western blotting was performed to determine the levels of Apelin‑12, glucose transporter 4 (GLUT4) and phosphorylated (p)‑5'adenosine monophosphate‑activated protein kinase (AMPK) α2. It was demonstrated that Apelin‑13 decreased heart rate, left ventricular end‑diastolic pressure, FPG, FINS, HOMA‑IR, TC, TG, LDL‑C, ET‑1, TNF‑α and leptin, whereas it increased the rise and fall of maximum rate of left ventricular pressure, HDL‑C, NO, cNOS activity and Apelin‑12 compared with the GK‑HFD group. In addition, GLUT4 and p‑AMPKα2 levels in myocardial tissues were elevated by administration of Apelin‑13. This protective effect of Apelin‑13 was comparable to that of metformin or atorvastatin. Overall, the present study demonstrated that administration ofApelin‑13 may be a promising therapeutic agent for the treatment of type 2 diabetes and metabolic syndrome.
Meng Li, Huijuan Fang, Jian Hu

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#29901077   2018/06/05 To Up

Apelin‑13 attenuates ER stress‑associated apoptosis induced by MPP+ in SH‑SY5Y cells.

Apelin‑13, a neuropeptide that acts as a ligand for a putative receptor related to the angiotensin II type receptor, elicits neuroprotective effects in numerous neurological conditions, such as Huntington's disease and cerebral ischemia. Parkinson's disease (PD), one of the most prevalent neurodegenerative diseases, is caused by damage to neurons in the brain; however, the underlying mechanism remains unclear. The present study explored the effects of apelin‑13 on SH‑SY5Y human neuroblastoma cells treated with 1‑methyl‑4‑phenylpyridine (MPP+). Cell growth, cell viability, and apoptosis were measured by real‑time cell analysis, the Cell Counting Kit‑8 assay, and flow cytometry, respectively. In addition, the expression levels of extracellular signal‑regulated kinase (ERK) 1/2, p38 mitogen‑activated protein kinase (MAPK), glucose‑regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), and cleaved caspase‑12 were assessed by western blotting. MPP+ treatment decreased the viability of SH‑SY5Y cells and increased their apoptosis; however, these changes were attenuated by pretreatment with apelin‑13. Treatment with MPP+ for 24 h significantly increased the expression levels of phospho‑ERK1/2, phospho‑p38, GRP78, CHOP, and cleaved caspase‑12 in SH‑SY5Y cells. Pretreatment with apelin‑13 significantly attenuated the upregulation of GRP78, CHOP and cleaved caspase‑12 in MPP+‑treated SH‑SY5Y cells, and significantly enhanced the expression levels of phospho‑ERK1/2. Taken together, the present results support a model in which apelin‑13 inhibits MPP+‑induced apoptosis of SH‑SY5Y cells by decreasing the expression of GRP78, CHOP, and cleaved caspase‑12, and by increasing the expression of phospho‑ERK1/2. The present findings suggest that apelin‑13 may be useful for the treatment of PD.
Yunlu Jiang, Haiqing Liu, Bingyuan Ji, Zhengwen Wang, Chunmei Wang, Chunqing Yang, Yanyou Pan, Jing Chen, Baohua Cheng, Bo Bai

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#29254197   2017/10/13 To Up

Apelin13/APJ promotes proliferation of colon carcinoma by activating Notch3 signaling pathway.

The link between Apelin (APL)/APL receptor (APJ) and Jagged (JAG)/Notch signaling pathways in colorectal cancer (CRC) has been poorly investigated. APL/APJ system, a potent angiogenic factor, is up-regulated in a variety of cancers. It contributes to tumor angiogenesis, and correlates with progression of malignancy. JAG/Notch signaling also contributes to progression, proliferation and metastasis of multiple cancers, including CRC. Here we tested the hypothesis that APL/APJ system promotes CRC proliferation by up-regulating Notch3, thus allowing further binding of JAG1 to Notch3.
Tong Chen, Ning Liu, Guang-Meng Xu, Tong-Jun Liu, Ying Liu, Yan Zhou, Si-Bo Huo, Kai Zhang

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#29115618   2017/10/27 To Up

Apelin‑13 promotes cell proliferation in the H9c2 cardiomyoblast cell line by triggering extracellular signal‑regulated kinase 1/2 and protein kinase B phosphorylation.

Apelin‑13 (APL‑13), a peptide hormone that serves as a ligand for G‑protein coupled receptors, has been demonstrated to be highly expressed in left ventricular hypertrophy rat models. It has been implicated in cardio‑protection under pathological states. The present study aimed to assess the physiological proliferation effect of APL‑13 in cultured H9c2 cardiomyoblast cells, and to elucidate the underlying mechanisms. Cell proliferation was determined by MTT assay. The extracellular signal‑regulated kinase (ERK) 1/2 and protein kinase B (Akt) signaling pathway was identified, and protein expression levels were detected using western blot analysis. The results demonstrated that APL‑13 markedly increased cell proliferation. Western blotting results suggested that APL‑13 significantly enhanced the expression of phosphoinositide ERK1/2 and Akt activation in a dose‑dependent manner. U0126 (10 µM; ERK1/2 inhibitor) and/or 10 µM LY294002 (Akt inhibitor) were used to help to determine the APL‑signaling mechanism. As a result, LY294002 and U0126 partially blocked the APL‑13 induced H9c2 proliferation. In conclusion, these data suggested that APL‑13 has a proliferative effect on myocardium cells via the Akt and ERK1/2 signaling pathways, and provide potential novel pharmaceutical targets for cardiovascular disease.
Luhua Yin, Pu Zhang, Chao Li, Jiafeng Si, Yongmei Wang, Xuemei Zhang, Deqing Zhang, Huanyi Zhang, Cong Lin

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#28627589   2017/06/09 To Up

Effect of the spinal apelin‑APJ system on the pathogenesis of chronic constriction injury‑induced neuropathic pain in rats.

Apelin is hypothesized to serve a dual function in pain processing. Spinal administration of apelin induces hyperalgesia, while opioid receptors are implicated in the antinociceptive effects of apelin in acute nociceptive models. However, whether the apelin‑apelin receptor (APJ) system is involved in neuropathic pain remains to be elucidated. The present study aimed to evaluate the impact and mechanism of the spinal apelin‑APJ system in neuropathic pain. Chronic constriction injury (CCI) of the sciatic nerve produced sustained spinal apelin and APJ upregulation, which was associated with mechanical allodynia and heat hyperalgesia development in the hind‑paw plantar surface. Immunofluorescence demonstrated that apelin and APJ were localized to the superficial dorsal horns. In order to further clarify the function of the apelin‑APJ system, a single intrathecal administration of ML221, an APJ antagonist, was used; this transiently reduced CCI‑induced pain hypersensitivity. However, apelin‑13 (the isoform which binds most strongly to APJ) exhibited no effect on the nociceptive response, suggesting an essential role for the spinal apelin‑APJ system in neuropathic pain sensitization. The present study demonstrated that a single application of ML221 alleviated mechanical allodynia and heat hyperalgesia 7 days following CCI, in a dose‑dependent manner. Intraspinal delivery of ML221, at the onset of and in fully‑established neuropathic pain, persistently attenuated CCI‑induced pain hypersensitivity, indicating that the apelin‑APJ system was involved in initiating and maintaining pain. It was demonstrated, using immunoblotting, that intrathecal ML221 downregulated phosphorylated extracellular signal‑related kinase (ERK) in the rat spinal cord dorsal horn, suggesting that the effect of apelin on neuropathic pain may be mediated via ERK signaling. The results of the present study suggested that the spinal apelin‑APJ system may drive neuropathic pain. Inhibition of APJ may provide novel pharmacological interventions for neuropathic pain.
Qingming Xiong, Wanyou He, Hanbing Wang, Jun Zhou, Yajun Zhang, Jian He, Chengxiang Yang, Bin Zhang

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#27109054   2016/04/22 To Up

Apelin-13 protects against myocardial infarction-induced myocardial fibrosis.

Myocardial infarction is a serious health threat. Apelin is an endogenous ligand of angiotensin II receptor-like 1 (APJ) and the apelin/APJ system is associated with various types of heart disease. However, whether apelin protects against myocardial infarction‑induced myocardial fibrosis remains unclear. The present study aimed to investigate the function of apelin‑13 during myocardial infarction‑induced myocardial fibrosis, and to determine the mechanism underlying the effects of apelin‑13. Apelin‑13 was demonstrated to improve left ventricular function and results of hematoxylin and eosin staining, Masson's trichrome staining and western blotting showed that apelin‑13 attenuated myocardial fibrosis. Further mechanistic investigation was performed by enzyme‑linked immunosorbent assay, western blotting and electrophoretic mobility shift assay. The results demonstrated that apelin‑13 inhibited the activation of nuclear factor (NF)‑κB signaling in vitro and in vivo. To the best of our knowledge, the present study was the first to demonstrate that apelin‑13 may attenuate myocardial infarction‑induced myocardial fibrosis, and that this protective function may be mediated by inhibition of NF‑κB signaling. The present study suggests a theoretical basis for the effects of apelin‑13 and provides insight into the potential clinical application of apelin-13.
Xuemin Zhang, Wenyu Hu, Feng Feng, Jian Xu, Fang Wu

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#26135903   2015/06/30 To Up

Apelin-13 induces MCF-7 cell proliferation and invasion via phosphorylation of ERK1/2.

Apelin-13 is extensively expressed in various tissues, particularly breast tissue. Apelin‑13 has been shown to promote tumor proliferation in various types of cancer, including hepatocellular, lung and ovarian cancer. However, the effect and molecular mechanism of apelin‑13 in breast cancer cells remains unclear. The present study investigated the effect of apelin‑13 on MCF‑7. Therefore, cell proliferation was determined by MTT and flow cytometry analysis. The results revealed that apelin‑13 markedly increased cell proliferation. Transwell assays demonstrated that apelin‑13 increased MCF‑7 cell invasion. Apelin‑13 also markedly increased the expression of cyclin D1, extracellular matrix metalloproteinase‑1 and amplified in breast cancer 1 (AIB1) in a dose‑dependent manner by polymerase chain reaction assays. To study the molecular mechanism, cell proliferation, invasion and cyclin D1 were inhibited by pre‑treatment with 10 µM of PD98059 (ERK(1/2) inhibitor). Western blotting results suggested that apelin‑13 significantly enhances the expression of p‑ERK(1/2) in a concentration‑dependent manner. In conclusion, the results suggest that apelin‑13 promoted MCF-7 cell proliferation and invasion via the ERK1/2/AIB1 signaling pathway.
Xuewei Peng, Fengyu Li, Ping Wang, Shengnan Jia, Lili Sun, Hongliang Huo

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#24573187   2014/02/25 To Up

Apelin-13 stimulates angiogenesis by promoting cross‑talk between AMP-activated protein kinase and Akt signaling in myocardial microvascular endothelial cells.

Currently, there is major interest in the functions of apelin-13, an endogenous ligand for the orphan G-protein coupled receptor APJ, a receptor that closely resembles the angiotensin receptor AT1. In the present study, the role of apelin-13 in angiogenesis and its mechanism as a novel angiogenic factor in myocardial microvascular endothelial cells (MMVECs) was investigated. It was revealed that apelin-13 can promote proliferation, migration and tube formation in MMVECs. In addition, apelin-13 dose dependently stimulated the phosphorylation of AMP-activated protein kinase (AMPK) and endothelial nitric oxide synthase (eNOS) at Thr-172 and Ser-1179, respectively. The treatment with the AMPK (compound C) and protein kinase Akt/protein kinase B (Akt; LY294002) inhibitor significantly suppressed the apelin‑13-induced AMPK, Akt and eNOS phosphorylation. They also inhibited the apelin13‑stimulated endothelial cell migration and tube formation. Therefore, we hypothesize that apelin-13 promotes angiogenesis through the modulation of AMPK and Akt signaling in MMVECs.
Xiaoman Yang, Wei Zhu, Pu Zhang, Kankai Chen, Lijie Zhao, Jingbo Li, Meng Wei, Mingya Liu

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#24316062   2013/12/05 To Up

Tumour co-expression of apelin and its receptor is the basis of an autocrine loop involved in the growth of colon adenocarcinomas.

Using a cancer profiling array, our laboratory has shown that apelin gene is up-regulated in half of colon adenocarcinomas. We have therefore postulated that apelin signalling might play a prominent role in the growth of colon tumours. We first confirmed by immunohistochemistry that apelin peptide is overexpressed in human colon adenomas and adenocarcinomas. We also observed a significant overexpression of apelin receptor (APJ) in adjacent sections. We then demonstrated that several colorectal cancer cell lines also expressed apelin and its receptor, the highest gene and peptide expression being detected in LoVo cells. In this cell line, the expression and functionality of apelin receptor were revealed by apelin-induced adenylyl cyclase inhibition and Akt phosphorylation. In addition, apelin clearly protected LoVo cells from apoptosis by inactivating a caspase-dependent pathway and decreasing the degradation of poly ADP ribose polymerase protein (PARP). Finally, treatment of these tumour cells by the (F13A)apelin13 receptor antagonist significantly reduced their proliferation rate. Altogether, these data suggest the existence of an autocrine loop by which constitutive activation of apelin signalling should participate in the growth of colon adenocarcinomas. Accordingly, apelin signalling is a promising pharmacological target for the treatment of human colon adenomas and adenocarcinomas.
François-Xavier Picault, Carline Chaves-Almagro, Fabrice Projetti, Hervé Prats, Bernard Masri, Yves Audigier

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