Ghrelin protects the myocardium with hypoxia/reoxygenation treatment through upregulating the expression of growth hormone, growth hormone secretagogue receptor and insulin-like growth factor-1, and promoting the phosphorylation of protein kinase�B

Liu, Yang; Liu, Yanling; Li, Guolin; Gu, Guixiong

doi:10.3892/ijmm.2018.3886

Cited by 5 publications

(3 citation statements)

References 33 publications

(37 reference statements)

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“…In agreement with previously published data, the results of RPPA analysis (Fig. 4) showed that activation of GHSR‐1a strongly affects the pattern of cellular protein phosphorylation (69, 70). This suggests that ghrelin‐induced signaling cascades may affect transcription and translation factors such as NF‐κB, ERK, mTOR, and eEF2.…”

Section: Discussionsupporting

confidence: 92%

Short‐chain fatty acids and microbiota metabolites attenuate ghrelin receptor signaling

et al. 2019

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The gastrointestinal microbiota is emerging as a unique and inexhaustible source for metabolites with potential to modulate G-protein coupled receptors (GPCRs). The ghrelin receptor [growth hormone secretagogue receptor (GHSR)-1a] is a GPCR expressed throughout both the gut and the brain and plays a crucial role in maintaining energy balance, metabolism, and the central modulation of food intake, motivation, reward, and mood. To date, few studies have investigated the potential of the gastrointestinal microbiota and its metabolites to modulate GPCR signaling. Here we investigate the ability of short-chain fatty acids (SCFAs), lactate, and different bacterial strains, including Bifidobacterium and Lactobacillus genera, to modulate GHSR-1a signaling. We identify, for what is to our knowledge the first time, a potent effect of microbiota-derived metabolites on GHSR-1a signaling with potential significant consequences for host metabolism and physiology. We show that SCFAs, lactate, and bacterial supernatants are able to attenuate ghrelin-mediated signaling through the GHSR-1a. We suggest a novel route of communication between the gut microbiota and the host via modulation of GHSR-1a receptor signaling. Together, this highlights the emerging therapeutic potential in the exploration of the microbiota metabolome in the specific targeting of key GPCRs, with pleiotropic actions that span both the CNS and periphery.

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Section: Discussionsupporting

confidence: 92%

Short‐chain fatty acids and microbiota metabolites attenuate ghrelin receptor signaling

et al. 2019

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“…Moreover, other studies demonstrate that even four weeks after MI, intracellular calcium transients and contractile function could be improved via long-term treatment with Gh, which might at least partially be attributed to the increased protein levels of SERCA-2 upon treatment observed in this study [ 280 ]. An upregulation of Gh and Igf1 and subsequently increased phosphorylated AKT levels are also suggested to underlie the cardioprotective effect of ghrelin treatment [ 109 ] in cardiomyocytes undergoing hypoxia and reoxygenation [ 178 ]. Surprisingly, the growth hormone-releasing hormone (GHRH) agonist JI-38 is reported to promote cardiac repair after MI, independently of Gh or Igf1 [ 141 ], suggesting a direct signaling pathway of GHRH.…”

Section: Hormone-based Strategies For Cardiac Regenerationmentioning

confidence: 99%

Synergistic effects of hormones on structural and functional maturation of cardiomyocytes and implications for heart regeneration

Galow

Brenmoehl

Hoeflich

2023

Cell. Mol. Life Sci.

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The limited endogenous regenerative capacity of the human heart renders cardiovascular diseases a major health threat, thus motivating intense research on in vitro heart cell generation and cell replacement therapies. However, so far, in vitro-generated cardiomyocytes share a rather fetal phenotype, limiting their utility for drug testing and cell-based heart repair. Various strategies to foster cellular maturation provide some success, but fully matured cardiomyocytes are still to be achieved. Today, several hormones are recognized for their effects on cardiomyocyte proliferation, differentiation, and function. Here, we will discuss how the endocrine system impacts cardiomyocyte maturation. After detailing which features characterize a mature phenotype, we will contemplate hormones most promising to induce such a phenotype, the routes of their action, and experimental evidence for their significance in this process. Due to their pleiotropic effects, hormones might be not only valuable to improve in vitro heart cell generation but also beneficial for in vivo heart regeneration. Accordingly, we will also contemplate how the presented hormones might be exploited for hormone-based regenerative therapies. Graphical abstract

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“…9) Thus, we aimed to explore the functions of circ-USP39 in the progression of AMI. Since the occurrence of AMI is mainly related to hypoxia induced by ischemia, 10,11) we further explored the concrete mechanism of circ-USP39 in hypoxia-induced cardiomyocyte injury.…”

mentioning

confidence: 99%

Silencing of Hsa_circ_0055440 Alleviates Hypoxia-Induced Cardiomyocyte Injury by Regulating the MiR-499b-5p/ACSL1 Axis

Yan

Zhou

2023

Int. Heart J.

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Circular RNAs (circRNAs) are a new type of regulatory RNAs, which are involved in various cardiac processes. However, the role of circRNA hsa_circ_0055440 (circ-USP39) in acute myocardial infarction regulation has not been studied yet.This study aims to explore the effect of circ-USP39 on hypoxia-induced cardiomyocyte injury.The head-to-tail splicing of circ-USP39 was verified by agarose gel electrophoresis. AC16 cell viability was detected using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays. The apoptosis of the AC16 cell was determined by flow cytometry and detection of caspase-3 activity. The levels of creatine kinasemuscle/brain and cTnl were evaluated by specific detection kits. The interactions between miR-499b-5p and circ-USP39 (or acyl-CoA synthetase long-chain family member-1 (ACSL1)) were verified by luciferase reporter assays.After confirming the circular characteristics of circ-USP39, we further found that the circ-USP39 expression was upregulated in hypoxia-induced cardiomyocytes and the circ-USP39 knockdown facilitated the viability of hypoxia-induced AC16, while suppressing cardiomyocyte apoptosis and injury. Importantly, circ-USP39 negatively regulated miR-499b-5p expression. As a downstream target of miR-499b-5p, ACSL1 partially counteracted the protective effect of circ-USP39 depletion on cardiomyocyte injury.Silencing of circ-USP39 alleviates hypoxia-induced cardiomyocyte injury via the miR-499b-5p/ACSL1 axis.

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Ghrelin protects the myocardium with hypoxia/reoxygenation treatment through upregulating the expression of growth hormone, growth hormone secretagogue receptor and insulin-like growth factor-1, and promoting the phosphorylation of protein kinase�B

Cited by 5 publications

References 33 publications

Short‐chain fatty acids and microbiota metabolites attenuate ghrelin receptor signaling

Short‐chain fatty acids and microbiota metabolites attenuate ghrelin receptor signaling

Synergistic effects of hormones on structural and functional maturation of cardiomyocytes and implications for heart regeneration

Silencing of Hsa_circ_0055440 Alleviates Hypoxia-Induced Cardiomyocyte Injury by Regulating the MiR-499b-5p/ACSL1 Axis

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