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Published on: February 21, 2018
Leukemia inhibitory factor induces a hypertrophic response mediated by gp130 in murine cardiac myocytes
H Matsui1, Y Fujio, K Kunisada
1Department of Medicine III, Osaka University Medical School, Japan.
Insights
Leukemia inhibitory factor (LIF) promotes myocardial hypertrophy in cardiac cells. This cytokine stimulates cell growth and gene expression, suggesting an autocrine/paracrine role in heart development and function.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Cellular Signaling
Background:
- Leukemia inhibitory factor (LIF) is an interleukin-6 related cytokine.
- The role of LIF in myocardial cells requires further investigation.
- Cardiac hypertrophy is a significant pathological process in heart disease.
Purpose of the Study:
- To investigate the effects of LIF on cultured murine cardiac myocytes.
- To determine if LIF influences cardiac cell growth and gene expression.
- To explore the signaling pathways activated by LIF in cardiomyocytes.
Main Methods:
- Primary cell culture of murine cardiac myocytes (fetal and neonatal).
- Stimulation with LIF and assessment of cell size and protein synthesis ([3H] leucine incorporation).
- Quantitative analysis of immediate early gene (c-fos) and cardiac-specific gene (prepro-ANF) mRNA expression.
- Detection of LIF receptor and LIF mRNA expression.
- Analysis of gp130 tyrosine phosphorylation.
Main Results:
- LIF stimulation increased cell size and [3H] leucine incorporation in cardiac myocytes, particularly fetal ones.
- LIF upregulated c-fos and prepro-atrial natriuretic factor (ANF) mRNA expression.
- LIF receptor mRNA was detected in various heart developmental stages and cultured myocytes.
- LIF induced rapid tyrosine phosphorylation of gp130 in cardiac myocytes.
- LIF mRNA was found in both cardiac and non-myocardial heart cells.
Conclusions:
- LIF activates the gp130 signaling pathway in cardiac myocytes.
- LIF acts as an autocrine/paracrine factor to induce myocardial hypertrophy.
- These findings highlight LIF's potential role in cardiac development and disease.
Abstract:
We examined the effects of an interleukin-6 related cytokine, leukemia inhibitory factor (LIF), on myocardial cells using cultured murine cardiac myocytes. LIF stimulation (1 x 10(3) U/ml) for 36 h increased the cell size of neonatal cardiac myocytes and increased [3H] leucine incorporation in both fetal and neonatal cardiac myocytes; the increase was more significant in fetal myocytes. LIF stimulation also increased the expression of c-fos mRNA, one of the immediate early genes. In addition, the expression of prepro-atrial natriuretic factor mRNA, one of the genes expressed in fetal myocardium and reactivated by hypertrophic stimulation, was increased after 48 h of incubation with LIF. LIF receptor mRNA was expressed in fetal, neonatal and adult murine hearts and cultured murine cardiac myocytes. LIF induced the tyrosine phosphorylation of gp130 within 15 min after it was added to cardiac myocytes. In addition, LIF mRNA was expressed in both cardiac myocytes and non-myocardial cells derived from hearts. These results suggest that LIF activates gp130 and induces myocardial hypertrophy by acting as an autocrine/paracrine factor in cardiac myocytes.
