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Identification of Haptoglobin as a Readout of rhGH Therapy in GH Deficiency
Marilisa De Feudis1, Gillian Elisabeth Walker2, Giulia Genoni2
1Department of Translational Medicine, University of Piemonte Orientale, Novara, Italy.
Insights
Growth hormone deficiency (GHD) involves inflammation and cardiovascular risks. This study identifies haptoglobin (Hp) as a key molecule modulated by GHD and growth hormone (GH) therapy, suggesting its potential as a biomarker.
Area of Science:
- Biochemistry
- Endocrinology
- Molecular Biology
Background:
- Growth hormone deficiency (GHD) is associated with cardiovascular risks and low-grade inflammation.
- Identifying molecules modulated by GHD is crucial for understanding its pathophysiology.
Purpose of the Study:
- To investigate plasma proteomic changes in children with GHD.
- To identify molecules directly affected by GHD and growth hormone (GH) therapy.
- To explore the role of haptoglobin (Hp) in GHD-related inflammation.
Main Methods:
- Plasma proteomics using two-dimensional electrophoresis in 10 children with GHD before and after 1 year of recombinant human GH (rhGH) treatment.
- Comparison with 14 matched controls.
- In vitro studies using human hepatoma (HepG2) cells to validate findings.
Main Results:
- Haptoglobin (Hp) isoforms α and β were identified as key modulated proteins.
- Elevated Hp levels in GHD patients were reduced by GH treatment.
- GH and IGF-1 inhibited IL-6-induced Hp secretion in HepG2 cells; pegvisomant restored Hp secretion.
Conclusions:
- Haptoglobin (Hp) plays a role in the inflammatory state of GHD.
- Hp may serve as a biomarker for GH treatment efficacy.
- Further research is needed to define molecular pathways and other contributing factors in GH's downregulation of Hp.
Background:
GH deficiency (GHD) is characterized by a cluster of cardiovascular risk factors and subtle inflammation. We aimed to demonstrate, through a proteomic approach, molecules directly modulated by GHD and involved in the inflammatory state.
Methods:
Ten children with isolated GHD were studied before and after 1 year of treatment with rhGH and compared with 14 matched controls. A two-dimensional electrophoresis plasma proteomics analysis was performed at baseline and after GH treatment to identify the top molecules modulated by GH. In vitro studies on human hepatoma (HepG2) cells were performed to validate the data.
Results:
Twelve of 20 proteomic spots were predicted to be isoforms α and β of haptoglobin (Hp) and confirmed by liquid chromatography tandem mass spectrometry and Western immunoblot analyses. Hp levels were higher in patients with GHD than controls at baseline (P < 0.001) and were reduced following GH treatment (P < 0.01). In HepG2 cells, both GH and IGF-1 were able to downregulate IL-6-induced Hp secretion. Moreover, Hp secretion was restored in pegvisomant-treated HepG2 cells.
Conclusions:
Hp is a molecule acting in the inflammatory state of GHD and a possible biomarker for GH treatment. Nevertheless, the contribution of other factors and the molecular pathways involved in the GH downregulation of Hp remain to be clearly defined.
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