Apelin/APJ system: A critical regulator of vascular smooth muscle cell

Abstract

APJ, an orphan G protein-coupled receptor, is first identified through homology cloning in 1993. Apelin is endogenous ligand of APJ extracted from bovine stomach tissue in 1998. Apelin/APJ system is widely expressed in many kinds of cells such as endothelial cells, cardiomyocytes, especially vascular smooth muscle cell. Vascular smooth muscle cell (VSMC), an integral part of the vascular wall, takes part in many normal physiological processes. Our experiment firstly finds that apelin/APJ system enhances VSMC proliferation by ERK1/2-cyclin D1 signal pathway. Accumulating studies also show that apelin/APJ system plays a pivotal role in mediating the function of VSMC. In this paper, we review the exact role of apelin/APJ system in VSMC, including induction of proliferation and migration, enhance of contraction and relaxation, inhibition of calcification. Furthermore, we discuss the role of apelin/APJ system in vascular diseases, such as atherosclerosis, hypertension, and chronic kidney disease (CKD) from the point of VSMC. Above all, apelin/APJ system is a promising target for managing vascular disease.

Apelin and apelin receptor expression in renal cell carcinoma

“…The apelin receptor is a G-protein-coupled receptor which binds a number of substances (apelin, APELA, ELABELA, Toddler) with many important functions in the cardio-vascular system, such as cardiac development, vasomotor tone, angiogenesis, myocardial inotropy, prevention of fibrosis and remodelling. 6,7,[14][15][16][17] Recently, it was identified as an essential gene for cancer immunotherapy, which can modulate interferon-γ responses in tumours and the effector function of CD8 + T cells. 5 The loss of its function could reduce the efficacy of cancer immunotherapies.…”

“…4 Recently, the apelin receptor (coded by the APLNR gene) was identified as prerequisite for successful cancer immunotherapy, with APLNR deficiency associated with immunotherapy failure. 5 Since apelin (APLN) and the apelin receptor have long been known to play important roles in vascular physiology, 6,7 emerging evidence of their importance in oncological diseases is not surprising. [8][9][10][11] Given the paucity of data concerning the role of APLN and APLNR in renal cell carcinoma 12 and the importance of immune evasion mechanisms of this tumour, our study aimed to investigate the expression of APLN and APLNR in RCC and its association with clinicopathological parameters and survival.…”

Cyclin G2 Is Involved in the Proliferation of Placental Trophoblast Cells and Their Interactions with Endothelial Cells

“…Moreover, placental cyclin D1 expression is decreased in women with fetal intrauterine growth restriction (IUGR) and preeclampsia complicated with IUGR [ 44 ], suggesting that abnormal regulation of cyclin D1 disturbs cell proliferation and compromises placental development. Because it is a link between growth signaling and cell division, cyclin D1 is a downstream target of several mitotic signals, such as AKT [ 45 ], ERK [ 46 ], NF-κB [ 47 ], and Wnt/β-catenin [ 48 ]. In addition to studying the relationship between CCNG2 and the Wnt/β-catenin signaling pathway [ 28 , 30 ], further research is required to determine whether other signaling pathways participate in the cyclin D1 abnormality mediated by CCNG2 during placental development.…”

Exploring the Modulatory Mechanism of Eleng Capsule in the Treatment of Endometriosis Based on Integrated Strategy of Transcriptomics Combined With Network Pharmacology

“…In other enriched signaling pathways of ELC regulation, 19 down-regulated DEGs were enriched in the calcium signaling pathway. Apelin,as a ligand of the APJ receptor,has functions in angiogenesis and cell proliferation, and is a vasoactive and regulatory peptide [44]. And apelin expression in the ectopic and ectopic endometrium changes periodicall [45].The DEGs in the Apelin signaling pathway are related to muscle contraction, calmodulin binding, and the myosin complex.…”