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Published on: January 7, 2016
Effects of Human Recombinant Growth Hormone (rhGH) Treatment on Plasma Extracellular Vesicles in GH-Deficient
Antonello E Rigamonti1, Luca Ferrari2,3, Chiara Favero2
1Department of Clinical Sciences and Community Health, Dipartimento di Eccellenza 2023-2027, University of Milan, 20129 Milan, Italy.
Insights
Recombinant human growth hormone (rhGH) therapy in children with growth hormone deficiency (GHD) selectively alters circulating extracellular vesicles (EVs), particularly those from immune and adipose tissues. These EVs may indicate treatment response and disease severity.
Area of Science:
- Endocrinology and Metabolism
- Cell Biology and Signaling
- Pediatric Growth Disorders
Background:
- Recombinant human growth hormone (rhGH) therapy impacts growth, metabolism, and tissue function in children with growth hormone deficiency (GHD).
- Extracellular vesicles (EVs) mediate inter-organ communication, but their response to rhGH therapy in humans is unstudied.
- Investigating rhGH effects on EV release is crucial for understanding GH-dependent signaling pathways.
Purpose of the Study:
- To investigate the impact of 6-month rhGH therapy on the composition of circulating EVs in children with GHD.
- To assess potential associations between EV subpopulations and clinical, auxological, and metabolic parameters.
- To explore EVs as potential biomarkers for rhGH treatment response and GHD severity.
Main Methods:
- Prospective study of 10 children with GHD treated with rhGH for 6 months.
- Plasma EVs analyzed for size distribution and tissue origin (monocytes, adipose, muscle, endothelium, platelets) at baseline and after treatment.
- Clinical, auxological, and biochemical parameters assessed; statistical analyses included longitudinal and interaction models.
Main Results:
- rhGH therapy improved height velocity, IGF-1, and osteocalcin levels.
- Significant increases in CD14+ (monocyte/macrophage) and FABP+ (adipose) EVs were observed post-treatment.
- More severe GHD correlated with a stronger EV response to rhGH; specific EVs linked to metabolic and growth parameters.
Conclusions:
- Six months of rhGH therapy selectively alters circulating EV composition in GHD children, notably from immune and adipose tissues.
- EVs may play a role in GH-mediated inter-organ communication.
- Tissue-derived EVs show promise as adjunctive biomarkers for rhGH treatment efficacy and GHD severity in pediatric endocrinology.
Abstract:
Background: Recombinant human growth hormone (rhGH) replacement therapy, administered to children with growth hormone deficiency (GHD), exerts pleiotropic effects on growth, metabolism, and tissue functions. Extracellular vesicles (EVs) are emerging mediators of inter-organ communication, but the effects of rhGH therapy on EV release in humans have not yet been investigated. Methods: In a preliminary prospective clinical study, children with GHD (n = 10; F/M = 5/5; age: 11.0 ± 2.7 years) were treated with rhGH for 6 months. Plasma samples were collected at baseline (T0) and after treatment (T6) to characterize the size distribution and tissue-derived composition of circulating EVs. Total EVs and EV subpopulations derived from monocytes/macrophages (CD14+), adipose tissue (FABP+), skeletal muscle (SCG+), endothelium (CD62E+), and platelets (CD42A+) were analyzed. Clinical, auxological/auxometric, and biochemical/metabolic parameters were assessed in parallel. Statistical methods included longitudinal analyses, interaction models, and adjustments for relevant covariates, including insulin-like growth factor 1 (IGF-1) and osteocalcin. Results: After 6 months of rhGH therapy, significant improvements in height velocity (cm/year and SDS) were observed, accompanied by increased circulating IGF-1 and osteocalcin levels. Hormone therapy induced no size-dependent changes in (total) EVs. Significant increases in CD14+ and FABP+ EVs were observed after treatment, without affecting the other tissue-derived EVs. Interaction analyses revealed that children with more severe GHD exhibited a stronger vesiculogenic response to rhGH. Furthermore, specific tissue-derived EVs were associated with metabolic/biochemical and auxological/auxometric parameters, including lipids, insulin resistance, and growth-related measures. Conclusions: When administered for six months, rhGH therapy seems to selectively change tissue-derived composition of circulating EVs in GHD children, particularly those derived from immune cells and adipose tissue. These preliminary findings suggest that EVs might represent an adjunctive component of GH-dependent inter-organ communication and might serve as biomarkers of treatment response and disease severity in pediatric endocrinology.
