ArticleInternational journal of molecular medicine2018
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.
Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 9 citations in OpenAlex.
- Synergistic effects of hormones on structural and functional maturation of cardiomyocytes and implications for heart regeneration.Cellular and molecular life sciences : CMLS · 2023Review
- Increased Susceptibility to Cerebral Microhemorrhages Is Associated With Imaging Signs of Microvascular Degeneration in the Retina in an Insulin-Like Growth Factor 1 Deficient Mouse Model of Accelerated Aging.Frontiers in aging neuroscience · 2022Article
- Data Mining and Expression Analysis of Differential lncRNA ADAMTS9-AS1 in Prostate Cancer.Frontiers in genetics · 2019Article
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5 authors at 2 institutions in 1 country.
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Abstract
Ghrelin is an endogenous ligand of growth hormone (GH) secretagogue receptor (GHSR) and has a number of biological effects, including heart protection. The present study aimed to reveal the positive effect of ghrelin on myocardium with hypoxia/reoxygenation (H/R) treatment and the involved molecular mechanisms. Successful construction of lentiviral expression vector (ghrelin‑pLVX‑Puro) was confirmed by colony polymerase chain reaction (PCR) verification. Primary rat cardiac myocytes were isolated and identified by immunofluorescence staining. Existence of red fluorescence of α‑sarcomeric actinin indicated the successful isolation. Following ghrelin transfection and H/R treatment, primary cells were divided into four groups: Control, H/R, empty (empty pLVX‑Puro + H/R) and ghrelin (ghrelin‑pLVX‑Puro + H/R). Cell viability and apoptosis were evaluated by Cell Counting Kit‑8 (CCK‑8) and Hoechst staining, respectively. The cell viability in the ghrelin group was significantly higher than that in the empty control group (P<0.05). The apoptosis rate in the ghrelin group was significantly lower than that in the empty control group (P<0.05). An ex vivo rat cardiac perfusion model was established. Following ghrelin incubation and H/R treatment, ex vivo myocardium was divided into four groups: Control, sham, H/R and ghrelin (ghrelin + H/R). Immunohistochemical analysis demonstrated that ghrelin increased the integrity of cardiac myocytes, and decreased shrinkage and apoptosis. mRNA and protein expression levels of GH, GHSR, insulin‑like growth factor‑1 (IGF‑1), protein kinase B (Akt), phosphorylated Akt (p‑Akt) were determined by reverse transcription (RT)‑PCR, western blot analysis and immunohistochemical analysis. Ghrelin upregulated the mRNA and protein expression levels of GH, GHSR and IGF‑1, and increased the ratio of p‑Akt to Akt protein level (p‑Akt/Akt) in cardiac myocytes and myocardial tissues with H/R treatment. In conclusion, ghrelin protected the myocardium with H/R treatment through upregulating the expression of GH, GHSR and IGF‑1, and promoting the phosphorylation of Akt. This would provide promising insights into the treatment of hypoxic myocardial injury by ghrelin.
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