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  1. AU="Antonella Lettieri"
  2. AU="Valdiviezo, Jesús"

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  1. Article ; Online: The Differential Roles for Neurodevelopmental and Neuroendocrine Genes in Shaping GnRH Neuron Physiology and Deficiency

    Roberto Oleari / Valentina Massa / Anna Cariboni / Antonella Lettieri

    International Journal of Molecular Sciences, Vol 22, Iss 9425, p

    2021  Volume 9425

    Abstract: Gonadotropin releasing hormone (GnRH) neurons are hypothalamic neuroendocrine cells that control sexual reproduction. During embryonic development, GnRH neurons migrate from the nose to the hypothalamus, where they receive inputs from several afferent ... ...

    Abstract Gonadotropin releasing hormone (GnRH) neurons are hypothalamic neuroendocrine cells that control sexual reproduction. During embryonic development, GnRH neurons migrate from the nose to the hypothalamus, where they receive inputs from several afferent neurons, following the axonal scaffold patterned by nasal nerves. Each step of GnRH neuron development depends on the orchestrated action of several molecules exerting specific biological functions. Mutations in genes encoding for these essential molecules may cause Congenital Hypogonadotropic Hypogonadism (CHH), a rare disorder characterized by GnRH deficiency, delayed puberty and infertility. Depending on their action in the GnRH neuronal system, CHH causative genes can be divided into neurodevelopmental and neuroendocrine genes. The CHH genetic complexity, combined with multiple inheritance patterns, results in an extreme phenotypic variability of CHH patients. In this review, we aim at providing a comprehensive and updated description of the genes thus far associated with CHH, by dissecting their biological relevance in the GnRH system and their functional relevance underlying CHH pathogenesis.
    Keywords GnRH neurons ; congenital hypogonadotropic hypogonadism ; Kallmann syndrome ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 612
    Language English
    Publishing date 2021-08-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Semaphorin Regulation by the Chromatin Remodeler CHD7

    Antonella Lettieri / Roberto Oleari / Alyssa J. J. Paganoni / Cristina Gervasini / Valentina Massa / Alessandro Fantin / Anna Cariboni

    Frontiers in Cell and Developmental Biology, Vol

    An Emerging Genetic Interaction Shaping Neural Cells and Neural Crest in Development and Cancer

    2021  Volume 9

    Abstract: CHD7 is a chromatin remodeler protein that controls gene expression via the formation of multi-protein complexes with specific transcription factors. During development, CHD7 controls several differentiation programs, mainly by acting on neural ... ...

    Abstract CHD7 is a chromatin remodeler protein that controls gene expression via the formation of multi-protein complexes with specific transcription factors. During development, CHD7 controls several differentiation programs, mainly by acting on neural progenitors and neural crest (NC) cells. Thus, its roles range from the central nervous system to the peripheral nervous system and the organs colonized by NC cells, including the heart. Accordingly, mutated CHD7 is linked to CHARGE syndrome, which is characterized by several neuronal dysfunctions and by malformations of NC-derived/populated organs. Altered CHD7 has also been associated with different neoplastic transformations. Interestingly, recent evidence revealed that semaphorins, a class of molecules involved in developmental and pathological processes similar to those controlled by CHD7, are regulated by CHD7 in a context-specific manner. In this article, we will review the recent insights that support the existence of genetic interactions between these pathways, both during developmental processes and cancer progression.
    Keywords CHD7 ; chromatin remodeler ; semaphorins ; development ; cancer ; Biology (General) ; QH301-705.5
    Subject code 571
    Language English
    Publishing date 2021-04-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Autism-linked NLGN3 is a key regulator of gonadotropin-releasing hormone deficiency

    Roberto Oleari / Antonella Lettieri / Stefano Manzini / Alyssa Paganoni / Valentina André / Paolo Grazioli / Marco Busnelli / Paolo Duminuco / Antonio Vitobello / Christophe Philippe / Varoona Bizaoui / Helen L. Storr / Federica Amoruso / Fani Memi / Valeria Vezzoli / Valentina Massa / Peter Scheiffele / Sasha R. Howard / Anna Cariboni

    Disease Models & Mechanisms, Vol 16, Iss

    2023  Volume 3

    Keywords gnrh neurons ; transcriptome ; nlgn3 ; neuritogenesis ; delayed puberty ; autism spectrum disorder ; Medicine ; R ; Pathology ; RB1-214
    Language English
    Publishing date 2023-03-01T00:00:00Z
    Publisher The Company of Biologists
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: LAM Cells as Potential Drivers of Senescence in Lymphangioleiomyomatosis Microenvironment

    Clara Bernardelli / Silvia Ancona / Melania Lazzari / Antonella Lettieri / Piera Selvaggio / Valentina Massa / Cristina Gervasini / Fabiano Di Marco / Raffaella Chiaramonte / Elena Lesma

    International Journal of Molecular Sciences, Vol 23, Iss 7040, p

    2022  Volume 7040

    Abstract: Senescence is a stress-response process characterized by the irreversible inhibition of cell proliferation, associated to the acquisition of a senescence-associated secretory phenotype (SASP), that may drive pathological conditions. ... ...

    Abstract Senescence is a stress-response process characterized by the irreversible inhibition of cell proliferation, associated to the acquisition of a senescence-associated secretory phenotype (SASP), that may drive pathological conditions. Lymphangioleiomyomatosis (LAM) is a rare disease in which LAM cells, featuring the hyperactivation of the mammalian Target of Rapamycin Complex 1 (mTORC1) for the absence of tuberin expression, cause the disruption of the lung parenchyma. Considering that LAM cells secrete SASP factors and that mTOR is also a driver of senescence, we deepened the contribution of senescence in LAM cell phenotype. We firstly demonstrated that human primary tuberin-deficient LAM cells (LAM/TSC cells) have senescent features depending on mTOR hyperactivation, since their high positivity to SA-β galactosidase and to phospho-histone H2A.X are reduced by inducing tuberin expression and by inhibiting mTOR with rapamycin. Then, we demonstrated the capability of LAM/TSC cells to induce senescence. Indeed, primary lung fibroblasts (PLFs) grown in LAM/TSC conditioned medium increased the positivity to SA-β galactosidase and to phospho-histone H2A.X, as well as p21 WAF1/CIP1 expression, and enhanced the mRNA expression and the secretion of the SASP component IL-8. Taken together, these data make senescence a novel field of study to understand LAM development and progression.
    Keywords senescence ; LAM ; mTOR ; tuberin ; SASP ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 610
    Language English
    Publishing date 2022-06-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: SEMA6A drives GnRH neuron-dependent puberty onset by tuning median eminence vascular permeability

    Antonella Lettieri / Roberto Oleari / Marleen Hester van den Munkhof / Eljo Yvette van Battum / Marieke Geerte Verhagen / Carlotta Tacconi / Marco Spreafico / Alyssa Julia Jennifer Paganoni / Roberta Azzarelli / Valentina Andre’ / Federica Amoruso / Luca Palazzolo / Ivano Eberini / Leo Dunkel / Sasha Rose Howard / Alessandro Fantin / Ronald Jeroen Pasterkamp / Anna Cariboni

    Nature Communications, Vol 14, Iss 1, Pp 1-

    2023  Volume 20

    Abstract: Abstract Innervation of the hypothalamic median eminence by Gonadotropin-Releasing Hormone (GnRH) neurons is vital to ensure puberty onset and successful reproduction. However, the molecular and cellular mechanisms underlying median eminence development ... ...

    Abstract Abstract Innervation of the hypothalamic median eminence by Gonadotropin-Releasing Hormone (GnRH) neurons is vital to ensure puberty onset and successful reproduction. However, the molecular and cellular mechanisms underlying median eminence development and pubertal timing are incompletely understood. Here we show that Semaphorin-6A is strongly expressed by median eminence-resident oligodendrocytes positioned adjacent to GnRH neuron projections and fenestrated capillaries, and that Semaphorin-6A is required for GnRH neuron innervation and puberty onset. In vitro and in vivo experiments reveal an unexpected function for Semaphorin-6A, via its receptor Plexin-A2, in the control of median eminence vascular permeability to maintain neuroendocrine homeostasis. To support the significance of these findings in humans, we identify patients with delayed puberty carrying a novel pathogenic variant of SEMA6A. In all, our data reveal a role for Semaphorin-6A in regulating GnRH neuron patterning by tuning the median eminence vascular barrier and thereby controlling puberty onset.
    Keywords Science ; Q
    Language English
    Publishing date 2023-12-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article: Iron overload induces hypogonadism in male mice via extrahypothalamic mechanisms

    Macchi, Chiara / Liliana Steffani / Roberto Oleari / Antonella Lettieri / Luca Valenti / Paola Dongiovanni / Antonio Romero-Ruiz / Manuel Tena-Sempere / Anna Cariboni / Paolo Magni / Massimiliano Ruscica

    Molecular and Cellular Endocrinology. 2017,

    2017  

    Abstract: Iron overload leads to multiple organ damage including endocrine organ dysfunctions. Hypogonadism is the most common non-diabetic endocrinopathy in primary and secondary iron overload syndromes.To explore the molecular determinants of iron overload- ... ...

    Abstract Iron overload leads to multiple organ damage including endocrine organ dysfunctions. Hypogonadism is the most common non-diabetic endocrinopathy in primary and secondary iron overload syndromes.To explore the molecular determinants of iron overload-induced hypogonadism with specific focus on hypothalamic derangements. A dysmetabolic male murine model fed iron-enriched diet (IED) and cell-based models of gonadotropin-releasing hormone (GnRH) neurons were used.Mice fed IED showed severe hypogonadism with a significant reduction of serum levels of testosterone (−83%) and of luteinizing hormone (−86%), as well as reduced body weight gain, body fat and plasma leptin. IED mice had a significant increment in iron concentration in testes and in the pituitary. Even if iron challenge of in vitro neuronal models (GN-11 and GT1-7 GnRH cells) resulted in 10- and 5-fold iron content increments, respectively, no iron content changes were found in vivo in hypothalamus of IED mice. Conversely, mice placed on IED showed a significant increment in hypothalamic GnRH gene expression (+34%) and in the intensity of GnRH-neuron innervation of the median eminence (+1.5-fold); similar changes were found in the murine model HFE−/-, resembling human hemochromatosis.IED-fed adult male mice show severe impairment of hypothalamus-pituitary-gonadal axis without a relevant contribution of the hypothalamic compartment, which thus appears sufficiently protected from systemic iron overload.
    Keywords adults ; animal models ; blood serum ; body weight changes ; diet ; gene expression ; gonadotropin-releasing hormone ; humans ; hypothalamus ; innervation ; iron ; iron overload ; leptin ; luteinizing hormone ; males ; mice ; neurons ; testes ; testosterone
    Language English
    Size p. .
    Publishing place Elsevier B.V.
    Document type Article
    Note Pre-press version
    ZDB-ID 187438-x
    ISSN 1872-8057 ; 0303-7207
    ISSN (online) 1872-8057
    ISSN 0303-7207
    DOI 10.1016/j.mce.2017.06.019
    Database NAL-Catalogue (AGRICOLA)

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