ERK1/2 mediates lung adenocarcinoma cell proliferation and autophagy induced by apelin-13

Yang, Li; Su, Tao; Lv, Deguan; Xie, Feng; Liu, Wei; Cao, Jun; Sheikh, Irshad Ali; Qin, Xu; Li, Lanfang

doi:10.1093/abbs/gmt140

Cited by 68 publications

(66 citation statements)

References 52 publications

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“…Xie et al [22] indicated that static pressure up-regulated APJ expression to promote cardiomyocyte hypertrophy by autophagy pathway. Yang et al [7] also confirmed that apelin-13 promote autophagy via ERK1/2 signaling pathway. In the present study, we observed the effects of apelin/APJ on the autophagy.…”

Section: Discussionmentioning

confidence: 87%

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Hypoxia promotes bone marrow-derived mesenchymal stem cell proliferation through apelin/APJ/autophagy pathway

Li¹,

Li²,

Zhang³

et al. 2015

ABBS

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Bone marrow-derived mesenchymal stem cells (BMSCs) are a population of multipotent progenitors that have the capacity of proliferation and differentiation into mesenchymal lineage cells. The regulatory peptide apelin is the endogenous ligand for the G protein-coupled receptor APJ. Apelin, which can enhance BMSC proliferation, has mitogenic effects on a wide variety of cell types. We hypothesized that the increased apelin/APJ might be involved in the occurrence and development of hypoxia-induced BMSC proliferation. BMSCs from the bone marrow of 8-to 10-week-old C57BL/6J mice were cultured under either normoxia (21% oxygen) or hypoxia (1% oxygen) condition. Cell proliferation was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and 5-bromo-2 0 -deoxyuridine assay. Expressions of hypoxia-inducible factor (HIF)-1α, apelin, APJ, Beclin-1, and LC3II/LC3I were detected by western blot analysis. Results suggested that hypoxia enhanced the proliferation of BMSC in a time-dependent manner. The expressions of HIF-1α, apelin, APJ, Beclin-1, and LC3II/LC3I were increased in BMSCs induced by hypoxia. Small interfering RNA (siRNA)-HIF-1α that inhibited the hypoxia-induced expressions of apelin, APJ, Beclin-1, and LC3II/ LC3I prevented hypoxia-induced BMSC proliferation. siRNA-APJ that inhibited the hypoxia-induced expressions of Beclin-1 and LC3II/LC3I reversed hypoxia-induced BMSC proliferation. siRNA-Beclin-1 also abolished hypoxia-induced cell proliferation. These data suggested that the apelin/APJ/autophagy signaling pathway might be involved in hypoxia-induced BMSC proliferation.

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Section: Discussionmentioning

confidence: 87%

“…Functionally, apelin can stimulate cell proliferation [6][7][8]. Apelin can promote thymidine incorporation into the DNA in Chinese hamster ovary (CHO) cells.…”

Section: Introductionmentioning

confidence: 99%

Hypoxia promotes bone marrow-derived mesenchymal stem cell proliferation through apelin/APJ/autophagy pathway

Li¹,

Li²,

Zhang³

et al. 2015

ABBS

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“…It is knowledgeable that adhesion, proliferation [53][54][55] , migration [56] and autophagy [57,58] are the characteristics of cells [59][60][61] . [61] .…”

Section: Endoplasmic Reticulum Stress Regulates Cardiovascular Physiomentioning

confidence: 99%

Endoplasmic reticulum stress: a novel mechanism and therapeutic target for cardiovascular diseases

2016

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Endoplasmic reticulum is a principal organelle responsible for folding, post-translational modifications and transport of secretory, luminal and membrane proteins, thus palys an important rale in maintaining cellular homeostasis. Endoplasmic reticulum stress (ERS) is a condition that is accelerated by accumulation of unfolded/misfolded proteins after endoplasmic reticulum environment disturbance, triggered by a variety of physiological and pathological factors, such as nutrient deprivation, altered glycosylation, calcium depletion, oxidative stress, DNA damage and energy disturbance, etc. ERS may initiate the unfolded protein response (UPR) to restore cellular homeostasis or lead to apoptosis. Numerous studies have clarified the link between ERS and cardiovascular diseases. This review focuses on ERS-associated molecular mechanisms that participate in physiological and pathophysiological processes of heart and blood vessels. In addition, a number of drugs that regulate ERS was introduced, which may be used to treat cardiovascular diseases. This review may open new avenues for studying the pathogenesis of cardiovascular diseases and discovering novel drugs targeting ERS.

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“…Moreover, in our experiments a modest increase in pressure suggests that apelin is not always one of the strongest inotropic compounds as sometimes it has been reported [74,41]. On the other hand, chronic apelin administration may be a key factor leading to tumorigenesis [117,118]. Independently of the duration and intensity of the effect on contractility, it must be kept in mind that at present the use of inotropic drugs is quite limited, because of their poor long term therapeutic effectiveness.…”

Section: Is Apelin a Therapeutic Tool?mentioning

confidence: 47%

Effects of apelin on the cardiovascular system

et al. 2015

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Apelin is an endogenous peptide acting on the APJ receptor. It consists of several isoforms characterised by different numbers of aminoacids. The number of aminoacids in the active isoforms range from 36 to 12. Apelin-13 and, to a lesser extent, apelin-36 are considered the most active isoforms with the greatest activity on the cardiovascular homeostasis. The effects normally exerted by the basal level of endogenous apelin, can be enhanced not only by its up-regulation, but may also by its exogenous administration. The present review considers the effects of apelin on various aspects of the cardiovascular function, such as cardiac development, vasomotor tone, angiogenesis, myocardial inotropy in healthy and failing hearts as well as the prevention of ischemia-reperfusion injury, cardiac fibrosis and remodeling. Also the biphasic changes of apelin level during the evolution of heart failure are considered. Although the positive inotropic effect exerted by apelin in normal and failing hearts would suggest the use of this peptide in the treatment of heart failure, the limited duration and extent of its effect do not support this possibility, unless a long lasting (6 hours) infusion is performed to overcome the limit of its short life. However, although the data on the characteristics of the inotropic activity do not provide a strong support for the treatment of active heart failure, apelin may be used in the prevention of heart failure because of its activity in limiting the consequences of myocardial ischemia such as infarct size and cardiac remodeling. KeywordsApelin/APJ system, heart failure, ischemia-reperfusion injury, contractility, cardiac protection, Reninangiotensin system 2 The apelin/APJ system Apelin In 1998 Tatemoto et al. discovered the endogenous peptide capable of binding the G protein-coupled receptor (GPCR) APJ [1,2], which at that time was considered an orphan receptor becaue its ligand was unknown. The just discovered ligand was called, apelin e.g APj Endogenous LIgaNd. Apelin is expressed in hearts, lungs, kidneys, liver, adipose tissue, gastrointestinal tract, brain, adrenal glands, endothelium, and human plasma. The gene of apelin is located on chromosome X [3] and encodes a 77 aminoacid sequence called pre-pro-apelin [4]. Upon cleavage by a family of endopeptidases, pre-pro-apelin generates several C-terminal fragments of various size, which are classified on the basis of the number of aminoacids. The active isoforms range from 36 to 12 aminoacids. As fragments shorter than 12 aminoacids are biologically inactive, it appears evident that the Cterminal 12 aminoacids are essential for receptor binding, whereas the N-terminal sequence modulates the interaction with the receptor [5]. At present it is recognized that, although different isoforms display similar functions, active isoforms differ in tissue distribution, potency and receptor binding affinity [6]. Apelin-13 and, to a lesser extent, apelin-36 have been considered the most active isoforms with the greatest activity on the cardi...

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ERK1/2 mediates lung adenocarcinoma cell proliferation and autophagy induced by apelin-13

Cited by 68 publications

References 52 publications

Hypoxia promotes bone marrow-derived mesenchymal stem cell proliferation through apelin/APJ/autophagy pathway

Hypoxia promotes bone marrow-derived mesenchymal stem cell proliferation through apelin/APJ/autophagy pathway

Endoplasmic reticulum stress: a novel mechanism and therapeutic target for cardiovascular diseases

Effects of apelin on the cardiovascular system

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