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Article ; Online: The role of acid-labile subunit (ALS) in the modulation of GH-IGF-I action.

Domené, Sabina / Domené, Horacio M

2020 Volume 518, Page(s) 111006

Abstract: Acid-labile subunit (ALS) deficiency (ACLSD) constitutes the first monogenic defect involving a member of the Insulin-like Growth Factor (IGF) binding protein system. The lack of ALS completely disrupts the circulating IGF system. Autocrine/paracrine ... ...

Abstract	Acid-labile subunit (ALS) deficiency (ACLSD) constitutes the first monogenic defect involving a member of the Insulin-like Growth Factor (IGF) binding protein system. The lack of ALS completely disrupts the circulating IGF system. Autocrine/paracrine action of local produced IGF-I could explain the mild effect on growth. In the present work we have revised the more relevant clinical and biochemical consequences of complete ACLSD in 61 reported subjects from 31 families. Low birth weight and/or length, reduced head circumference, height between -2 and -3 SD, pubertal delay and insulin resistance are commonly observed. Partial ACLSD could be present in children initially labeled as idiopathic short stature, presenting low IGF-I levels, suggesting that one functional IGFALS allele is insufficient to stabilize ternary complexes. Dysfunction of the GH-IGF axis observed in ACLSD may eventually result in increased risk for type-2 diabetes and tumor progression. Consequently, long term surveillance is recommended in these patients.
MeSH term(s)	Body Height/drug effects ; Body Height/genetics ; Carrier Proteins/genetics ; Carrier Proteins/pharmacology ; Carrier Proteins/physiology ; Child ; Female ; Glycoproteins/deficiency ; Glycoproteins/genetics ; Glycoproteins/pharmacology ; Glycoproteins/physiology ; Growth Disorders/genetics ; Growth Disorders/metabolism ; Human Growth Hormone/metabolism ; Humans ; Insulin-Like Growth Factor Binding Protein 3/metabolism ; Insulin-Like Growth Factor I/metabolism ; Male ; Puberty, Delayed/genetics ; Puberty, Delayed/metabolism ; Signal Transduction/drug effects ; Signal Transduction/physiology
Chemical Substances	Carrier Proteins ; Glycoproteins ; IGF1 protein, human ; Insulin-Like Growth Factor Binding Protein 3 ; insulin-like growth factor binding protein, acid labile subunit ; Human Growth Hormone (12629-01-5) ; Insulin-Like Growth Factor I (67763-96-6)
Language	English
Publishing date	2020-08-27
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2020.111006
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Article: The role of acid-labile subunit (ALS) in the modulation of GH-IGF-I action

Domené, Sabina / Domené, Horacio M

Molecular and cellular endocrinology. 2020 Dec. 01, v. 518

2020

Abstract	Acid-labile subunit (ALS) deficiency (ACLSD) constitutes the first monogenic defect involving a member of the Insulin-like Growth Factor (IGF) binding protein system. The lack of ALS completely disrupts the circulating IGF system. Autocrine/paracrine action of local produced IGF-I could explain the mild effect on growth.In the present work we have revised the more relevant clinical and biochemical consequences of complete ACLSD in 61 reported subjects from 31 families. Low birth weight and/or length, reduced head circumference, height between −2 and −3 SD, pubertal delay and insulin resistance are commonly observed.Partial ACLSD could be present in children initially labeled as idiopathic short stature, presenting low IGF-I levels, suggesting that one functional IGFALS allele is insufficient to stabilize ternary complexes.Dysfunction of the GH-IGF axis observed in ACLSD may eventually result in increased risk for type-2 diabetes and tumor progression. Consequently, long term surveillance is recommended in these patients.
Keywords	alleles ; autocrine signaling ; endocrinology ; growth retardation ; head circumference ; insulin resistance ; low birth weight ; monitoring ; neoplasm progression ; noninsulin-dependent diabetes mellitus ; risk
Language	English
Dates of publication	2020-1201
Publishing place	Elsevier B.V.
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2020.111006
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Article: Genetic Mutations in the GH/IGF Axis.

Domené, Sabina / Domené, Horacio M

Pediatric endocrinology reviews : PER

2018 Volume 16, Issue Suppl 1, Page(s) 39–62

Abstract: The GH/IGF axis plays an important role in the control of pre and postnatal growth. At least 48 monogenic defects have been described affecting the production, secretion, and action of GH and IGFs. Molecular defects of the GH/IGF axis resulting in short ... ...

Abstract	The GH/IGF axis plays an important role in the control of pre and postnatal growth. At least 48 monogenic defects have been described affecting the production, secretion, and action of GH and IGFs. Molecular defects of the GH/IGF axis resulting in short stature were arbitrarily classified into 4 groups: 1. Combined pituitary hormone deficiency (CPHD) (a. syndromic CPHD and b. non-syndromic CPHD), 2. Isolated GH deficiency (IGHD), 3. GH insensitivity, and 4. IGF-I insensitivity. Genetic diagnosis is obtained in about 30-40% of children with growth retardation, severe IGHD, CPHD, apparent GH or IGF-I insensitivity, and small for gestational age. Increased accessibility to next generation sequencing (NGS) techniques resulted in a significant number of likely pathogenic variants in genes previously associated with short stature as well as in completely novel genes. Functional in vitro assays and in vivo animal models are required to determine the real contribution of these findings.
MeSH term(s)	Dwarfism, Pituitary ; Human Growth Hormone ; Humans ; Hypopituitarism ; Infant, Small for Gestational Age ; Insulin-Like Growth Factor I ; Mutation
Chemical Substances	Human Growth Hormone (12629-01-5) ; Insulin-Like Growth Factor I (67763-96-6)
Language	English
Publishing date	2018-10-31
Publishing country	Israel
Document type	Journal Article
ZDB-ID	2434390-0
ISSN	1565-4753
ISSN	1565-4753
DOI	10.17458/per.vol16.2018.dd.geneticmutationsghigf
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Article ; Online: Physiology of GH action and associated human disorders.

Domené, Horacio M / Wit, Jan M / Frank, Stuart J

Molecular and cellular endocrinology

2020 Volume 520, Page(s) 111078

MeSH term(s)	Animals ; Disease ; Genetic Predisposition to Disease ; Growth Hormone/metabolism ; Growth Hormone/pharmacology ; Humans ; Insulin-Like Growth Factor I/metabolism ; Mice ; Receptors, Somatotropin/metabolism ; Signal Transduction/drug effects
Chemical Substances	Receptors, Somatotropin ; Insulin-Like Growth Factor I (67763-96-6) ; Growth Hormone (9002-72-6)
Language	English
Publishing date	2020-11-07
Publishing country	Ireland
Document type	Editorial ; Introductory Journal Article
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2020.111078
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Article ; Online: Applying Bioinformatic Platforms, In Vitro, and In Vivo Functional Assays in the Characterization of Genetic Variants in the GH/IGF Pathway Affecting Growth and Development.

Domené, Sabina / Scaglia, Paula A / Gutiérrez, Mariana L / Domené, Horacio M

Cells

2021 Volume 10, Issue 8

Abstract: Heritability accounts for over 80% of adult human height, indicating that genetic variability is the main determinant of stature. The rapid technological development of Next-Generation Sequencing (NGS), particularly Whole Exome Sequencing (WES), has ... ...

Abstract	Heritability accounts for over 80% of adult human height, indicating that genetic variability is the main determinant of stature. The rapid technological development of Next-Generation Sequencing (NGS), particularly Whole Exome Sequencing (WES), has resulted in the characterization of several genetic conditions affecting growth and development. The greatest challenge of NGS remains the high number of candidate variants identified. In silico bioinformatic tools represent the first approach for classifying these variants. However, solving the complicated problem of variant interpretation requires the use of experimental approaches such as in vitro and, when needed, in vivo functional assays. In this review, we will discuss a rational approach to apply to the gene variants identified in children with growth and developmental defects including: (i) bioinformatic tools; (ii) in silico modeling tools; (iii) in vitro functional assays; and (iv) the development of in vivo models. While bioinformatic tools are useful for a preliminary selection of potentially pathogenic variants, in vitro-and sometimes also in vivo-functional assays are further required to unequivocally determine the pathogenicity of a novel genetic variant. This long, time-consuming, and expensive process is the only scientifically proven method to determine causality between a genetic variant and a human genetic disease.
MeSH term(s)	Animals ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; Computational Biology/methods ; DNA Copy Number Variations ; Dwarfism/genetics ; Dwarfism/pathology ; Genetic Variation ; Humans ; Insulin-Like Growth Factor I/genetics ; Insulin-Like Growth Factor I/metabolism ; Signal Transduction/genetics ; Transcription Factors/genetics ; Transcription Factors/metabolism
Chemical Substances	Carrier Proteins ; Transcription Factors ; Insulin-Like Growth Factor I (67763-96-6) ; somatotropin-binding protein (W06KFL3RDT)
Language	English
Publishing date	2021-08-12
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10082063
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Article ; Online: Genetic disorders of GH action pathway.

Domené, Horacio M / Fierro-Carrión, Gustavo

Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society

2017 Volume 38, Page(s) 19–23

Abstract: While insensitivity to GH (GHI) is characterized by low IGF-I levels, normal or elevated GH levels, and lack of IGF-I response to GH treatment, IGF-I resistance is characterized by elevated IGF-I levels with normal/high GH levels. Several genetic defects ...

Abstract	While insensitivity to GH (GHI) is characterized by low IGF-I levels, normal or elevated GH levels, and lack of IGF-I response to GH treatment, IGF-I resistance is characterized by elevated IGF-I levels with normal/high GH levels. Several genetic defects are responsible for impairment of GH and IGF-I actions resulting in short stature that could affect intrauterine growth or be present in the postnatal period. The genetic defects affecting GH and/or IGF-I action can be divided into five different groups: GH insensitivity by defects affecting the GH receptor (GHR), the intracellular GH signaling pathway (STAT5B, STAT3, IKBKB, IL2RG, PIK3R1), the synthesis of insulin-like growth factors (IGF1, IGF2), the transport/bioavailability of IGFs (IGFALS, PAPPA2), and defects affecting IGF-I sensitivity (IGF1R). Complete GH insensitivity (GHI) was first reported by Zvi Laron and his colleagues in patients with classical appearance of GH deficiency, but presenting elevated levels of GH. The association of GH insensitivity with several clinical sings of immune-dysfunction and autoimmune dysregulation are characteristic of molecular defects in the intracellular GH signaling pathway (STAT5B, STAT3, IKBKB, IL2RG, PIK3R1). Gene mutations in the IGF1 and IGF2 genes have been described in patients presenting intrauterine growth retardation and postnatal short stature. Molecular defects have also been reported in the IGFALS gene, that encodes the acid-labile subunit (ALS), responsible to stabilize circulating IGF-I in ternary complexes, and more recently in the PAPPA2 gen that encodes the pregnancy-associated plasma protein-A2, a protease that specifically cleaves IGFBP-3 and IGFBP-5 regulating the accessibility of IGFs to their target tissues. Mutations in the IGF1R gene resulted in IGF-I insensitivity in patients with impaired intrauterine and postnatal growth. These studies have revealed novel molecular mechanisms of GH insensitivity/primary IGF-I deficiency beyond the GH receptor gene. In addition, they have also underlined the importance of several players of the GH-IGF axis in the complex system that promotes human growth.
MeSH term(s)	Genetic Markers ; Growth Disorders/diagnosis ; Growth Disorders/genetics ; Growth Disorders/metabolism ; Human Growth Hormone/deficiency ; Humans ; Signal Transduction
Chemical Substances	Genetic Markers ; Human Growth Hormone (12629-01-5)
Language	English
Publishing date	2017-12-12
Publishing country	Scotland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1436781-6
ISSN	1532-2238 ; 1096-6374
ISSN (online)	1532-2238
ISSN	1096-6374
DOI	10.1016/j.ghir.2017.12.004
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Article ; Online: An in vivo functional assay to characterize human STAT5B genetic variants during zebrafish development.

Landi, Estefanía / Karabatas, Liliana / Rodríguez Gomez, Tomás / Salatino, Lucía / Scaglia, Paula / Ramírez, Laura / Keselman, Ana / Braslavsky, Débora / Sanguineti, Nora / Pennisi, Patricia / Rey, Rodolfo A / Bergadá, Ignacio / Jasper, Héctor G / Domené, Horacio M / Plazas, Paola V / Domené, Sabina

Human molecular genetics

2023 Volume 32, Issue 15, Page(s) 2473–2484

Abstract: Growth hormone (GH) binding to GH receptor activates janus kinase 2 (JAK2)-signal transducer and activator of transcription 5b (STAT5b) pathway, which stimulates transcription of insulin-like growth factor-1 (IGF1), insulin-like growth factor binding ... ...

Abstract	Growth hormone (GH) binding to GH receptor activates janus kinase 2 (JAK2)-signal transducer and activator of transcription 5b (STAT5b) pathway, which stimulates transcription of insulin-like growth factor-1 (IGF1), insulin-like growth factor binding protein 3 (IGFBP3) and insulin-like growth factor acid-labile subunit (IGFALS). Although STAT5B deficiency was established as an autosomal recessive disorder, heterozygous dominant-negative STAT5B variants have been reported in patients with less severe growth deficit and milder immune dysfunction. We developed an in vivo functional assay in zebrafish to characterize the pathogenicity of three human STAT5B variants (p.Ala630Pro, p.Gln474Arg and p.Lys632Asn). Overexpression of human wild-type (WT) STAT5B mRNA and its variants led to a significant reduction of body length together with developmental malformations in zebrafish embryos. Overexpression of p.Ala630Pro, p.Gln474Arg or p.Lys632Asn led to an increased number of embryos with pericardial edema, cyclopia and bent spine compared with WT STAT5B. Although co-injection of WT and p.Gln474Arg and WT and p.Lys632Asn STAT5B mRNA in zebrafish embryos partially or fully rescues the length and the developmental malformations in zebrafish embryos, co-injection of WT and p.Ala630Pro STAT5B mRNA leads to a greater number of embryos with developmental malformations and a reduction in body length of these embryos. These results suggest that these variants could interfere with endogenous stat5.1 signaling through different mechanisms. In situ hybridization of zebrafish embryos overexpressing p.Gln474Arg and p.Lys632Asn STAT5B mRNA shows a reduction in igf1 expression. In conclusion, our study reveals the pathogenicity of the STAT5B variants studied.
MeSH term(s)	Animals ; Humans ; Zebrafish/genetics ; Zebrafish/metabolism ; STAT5 Transcription Factor/genetics ; STAT5 Transcription Factor/metabolism ; Growth Hormone ; Signal Transduction/genetics ; RNA, Messenger ; Insulin-Like Growth Factor I/genetics
Chemical Substances	STAT5 Transcription Factor ; Growth Hormone (9002-72-6) ; RNA, Messenger ; Insulin-Like Growth Factor I (67763-96-6) ; STAT5B protein, human
Language	English
Publishing date	2023-04-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1108742-0
ISSN	1460-2083 ; 0964-6906
ISSN (online)	1460-2083
ISSN	0964-6906
DOI	10.1093/hmg/ddad078
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Article ; Online: Novel Insulin-Like Growth Factor 1 Gene Mutation: Broadening of the Phenotype and Implications for Insulin Resistance.

Giacomozzi, Claudio / Martin, Ayelen / Fernández, María Celia / Gutiérrez, Mariana / Iascone, Maria / Domené, Horacio M / Dominici, Fernando P / Bergadá, Ignacio / Cangiano, Biagio / Persani, Luca / Pennisi, Patricia A

The Journal of clinical endocrinology and metabolism

2022 Volume 108, Issue 6, Page(s) 1355–1369

Abstract: Context: Insulin-like growth factor (IGF)1 gene mutations are extremely rare causes of pre- and postnatal growth retardation. Phenotype can be heterogenous with varying degrees of neurosensory deafness, cognitive defects, glucose metabolism impairment ... ...

Abstract	Context: Insulin-like growth factor (IGF)1 gene mutations are extremely rare causes of pre- and postnatal growth retardation. Phenotype can be heterogenous with varying degrees of neurosensory deafness, cognitive defects, glucose metabolism impairment and short stature. Objective: This study describes a 12.6-year-old girl presenting with severe short stature and insulin resistance, but with normal hearing and neurological development at the lower limit of normal. Methods: DNA was obtained from the proband and both parents for whole exome sequencing (WES). In silico analysis was performed to predict the impact of the IGF1 variant on IGF1 and insulin receptors (IGF1R and IR) signaling. Phosphorylation of the IGF1R at activating Tyr residues and cell proliferation analyses were used to assess the ability of each subject's IGF1 to bind and activate IGF1R. Results: The proband had low immunoreactive IGF1 in serum and WES revealed a novel homozygous IGF1 missense variant (c.247A>T), causing a change of serine 83 for cysteine (p.Ser83Cys; p.Ser35Cys in mature peptide). The proband's parents were heterozygous for this mutation. In silico analyses indicated the pathogenic potential of the variant with electrostatic variations with the potential of hampering the interaction with the IGF1R but strengthening the binding to IR. The mutant IGF1 protein had a significantly reduced activity on in vitro bioassays. Conclusion: We describe a novel IGF1 mutation leading to severe loss of circulating IGF1 immunoreactivity and bioactivity. In silico modeling predicts that the mutant IGF1 could interfere with IR signaling, providing a possible explanation for the severe insulin resistance observed in the patient. The absence of significant hearing and neurodevelopmental involvement in the present case is unusual and broadens the clinical spectrum of IGF1 mutations.
MeSH term(s)	Humans ; Insulin-Like Growth Factor I/genetics ; Insulin-Like Growth Factor I/metabolism ; Insulin Resistance/genetics ; Receptor, IGF Type 1/genetics ; Receptor, IGF Type 1/metabolism ; Mutation ; Mutation, Missense ; Dwarfism/genetics ; Phenotype
Chemical Substances	Insulin-Like Growth Factor I (67763-96-6) ; Receptor, IGF Type 1 (EC 2.7.10.1)
Language	English
Publishing date	2022-12-16
Publishing country	United States
Document type	Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3029-6
ISSN	1945-7197 ; 0021-972X
ISSN (online)	1945-7197
ISSN	0021-972X
DOI	10.1210/clinem/dgac738
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Article: Same Phenotype in Children with Growth Hormone Deficiency and Resistance.

Ioimo, Irene / Guarracino, Carmen / Meazza, Cristina / Domené, Horacio M / Bozzola, Mauro

Case reports in pediatrics

2018 Volume 2018, Page(s) 5902835

Abstract: By definition, about 2.5% of children show a short stature due to several causes. Two clinical conditions are characterized by serum IGF-I low levels, idiopathic GH deficiency (IGHD), and GH insensitivity (GHI), and the phenotypic appearance of these ... ...

Abstract	By definition, about 2.5% of children show a short stature due to several causes. Two clinical conditions are characterized by serum IGF-I low levels, idiopathic GH deficiency (IGHD), and GH insensitivity (GHI), and the phenotypic appearance of these patients may be very similar. We studied two children with short stature and similar phenotypes. The first case showed frontal bossing, doll face, acromicria, and truncal obesity, with a GH peak <0.05 ng/ml after stimuli and undetectable serum IGF-I levels. After PCR amplification of the whole
Language	English
Publishing date	2018-04-15
Publishing country	United States
Document type	Case Reports
ZDB-ID	2659094-3
ISSN	2090-6811 ; 2090-6803
ISSN (online)	2090-6811
ISSN	2090-6803
DOI	10.1155/2018/5902835
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Article ; Conference proceedings: The XIX Annual Meeting of the Latin American Society for Pediatric Endocrinology (SLEP) Mar del Plata October 13-17, 2007.

Domené, Horacio M / Jasper, Héctor G

Pediatric endocrinology reviews : PER

2008 Volume 5, Issue 4, Page(s) 915–921

MeSH term(s)	Child ; Endocrine System Diseases/physiopathology ; Endocrine System Diseases/therapy ; Endocrinology ; Humans ; Latin America ; Pediatrics
Language	English
Publishing date	2008-06
Publishing country	Israel
Document type	Congresses
ZDB-ID	2434390-0
ISSN	1565-4753
ISSN	1565-4753
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