Laura Pozzi

Vita-Salute San Raffaele University

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Nilo Riva

Fondazione IRCCS Istituto Neurologico Carlo Besta

G. Silini

Institute of Biophysics

Angelo Quattrini

San Raffaele University of Rome

Massimo Filippi

Istituto di Ricovero e Cura a Carattere Scientifico San Raffaele

Roberto William Invernizzi

Mario Negri Institute for Pharmacological Research

Federica Agosta

Vita-Salute San Raffaele University

Paola Carrera

Vita-Salute San Raffaele University

R. Samanin

Mario Negri Institute for Pharmacological Research

Teuta Domi

Vita-Salute San Raffaele University

Yuri Falzone

San Raffaele University of Rome

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Istituti di Ricovero e Cura a Carattere Scientifico

125

Vita-Salute San Raffaele University

Istituto di Ricovero e Cura a Carattere Scientifico San Raffaele

University of Milan

San Raffaele University of Rome

IRCCS Ospedale San Raffaele

Sapienza University of Rome

Neuroscience Institute

Mario Negri Institute for Pharmacological Research

National Research Council

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Varia

Acta Haematologica (1972)

D. Ogston Audrey A. Dawson Helen M. Adam E. Palazzo F Oberling

10.1159/000208486

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Case report: coexistence of C9orf72 expansion and progranulin mutation in a case of genetic frontotemporal dementia—clinical features and neuroimaging correlates

Journal of Neurology (2023)

Alma Ghirelli Edoardo Gioele Spinelli Elisa Canu Teuta Domi Silvia Basaia

C9ORF72

Neuroradiology

10.1007/s00415-023-11839-3

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Citations (2)

Nitric Oxide Controls Fat Deposition in Dystrophic Skeletal Muscle by Regulating Fibro-Adipogenic Precursor Differentiation

Stem Cells (2013)

Nicoletta Cordani Viviana Pisa Laura Pozzi Clara Sciorati Emilio Clementi

Abstract Duchenne muscular dystrophy (DMD) is an hereditary disease characterized by loss of muscle fibers and their progressive substitution by fat and fibrous tissue. Mesenchymal fibro-adipogenic progenitors (FAPs) expressing the platelet-derived growth factor receptor alpha (PDGFRα) are an important source of fibrosis and adipogenesis in dystrophic skeletal muscle. Among the therapies suggested for dystrophy are those based on nitric oxide (NO) donating drugs, the administration of which slows disease progression. NO has been shown to act by enhancing the regenerative potential of the diseased muscle. Whether it acts also by inhibiting fibrosis and adipogenesis was not known. Here, we show in vitro that NO regulates FAP fate through inhibition of their differentiation into adipocytes. In mdx mice, an animal model of DMD, treatment with the NO donating drug molsidomine reduced the number of PDGFRα+ cells as well as the deposition of both skeletal muscle fat and connective tissues. Inhibition of adipogenesis was due to NO-induced increased expression of miR-27b leading to downregulation of peroxisome proliferator-activated receptors gamma (Pparγ1) expression in a pathway independent of cGMP generation. These findings reveal an additional effect of NO in dystrophic muscle that conceivably synergizes with its known effects on regeneration improvement and explain why NO-based therapies appear effective in the treatment of muscular dystrophy. Stem Cells 2014;32:874–885

10.1002/stem.1587

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Citations (78)

Polyomavirus genome and polyomavirus enhancer-driven gene expression during myogenesis

Journal of Virology (1989)

Rossella Maione Armando Felsani Laura Pozzi Maurizia Caruso Paolo Amati

The mRNAs for myogenic functions are coordinately transcribed with polyomavirus (Py) early mRNA during in vitro differentiation of mouse C2 myoblast cells. Sequence analysis shows that the A domain of the Py enhancer includes an E1A-like consensus sequence that is also found in the 5' upstream region of two genes expressed during myoblast differentiation: alpha-actin and myosin light chain. Therefore, the coordinate expression of such genes with Py early mRNA may be activated by a common cellular regulatory factor. In the present work, we report that C2 cells surviving Py infection are unable to differentiate and do not express alpha-actin and myosin light-chain mRNAs. Hybrids between such Py-resistant myoblast cells and the parental cells exhibited dominance of the permissibility to Py growth and of the expression of myogenic mRNAs. In C2 cells transiently transfected with a chimeric plasmid (pSVPy12CAT) harboring the bacterial chloramphenicol acetyltransferase (CAT) gene driven by the Py enhancer-promoter region, the CAT gene was expressed irrespective of their stage of differentiation. Moreover, undifferentiated stably transfected cells expressing the CAT gene restricted viral growth. Py-resistant C2 myoblasts transiently transfected with pSVPy12CAT also expressed the CAT gene driven by the Py enhancer. This contradictory finding is similar to results previously obtained by other investigators with cloned genes specific for myogenic functions, and it may be explained by a structural difference between the pSVPy12CAT and the Py genomic organizations in which the viral enhancer operates.

Chloramphenicol acetyltransferase

Enhancer RNAs

Enhancer trap

10.1128/jvi.63.11.4890-4897.1989

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Citations (10)

[Column chromatography of urinary hydrolysates at various pH values, extracted with several organic solvents].

PubMed (1957)

Laura Pozzi

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NEK1 Variants in a Cohort of Italian Patients With Amyotrophic Lateral Sclerosis

Frontiers in Neuroscience (2022)

Nilo Riva Laura Pozzi Tommaso Russo Giovanni Battista Pipitone Paride Schito

In the last few years, different studies highlighted a significant enrichment of NEK1 loss of function (LoF) variants in amyotrophic lateral sclerosis (ALS), and an additional role for the p.Arg261His missense variant in the disease susceptibility. Several other missense variants have been described so far, whose pathogenic relevance remains however unclear since many of them have been reported in both patients and controls. This study aimed to investigate the presence of NEK1 variants and their correlation with phenotype in a cohort of Italian patients with ALS.We sequenced a cohort of 350 unrelated Italian patients with ALS by next-generation sequencing (NGS) and then we analyzed the clinical features of NEK1 carriers.We detected 20 different NEK1 rare variants (four LoF and 16 missense) in 33 unrelated patients with sporadic ALS (sALS). The four LoF variants (two frameshift and two splice-site variants) were all novel. The p.Arg261His missense variant was enriched in the patients' cohort (p < 0.001). Excluding this variant from counting, the difference in the frequency of NEK1 rare missense variants between patients and controls was not statistically significant. NEK1 carriers had a higher frequency of flail arm (FA) phenotype compared with the other patients of the cohort (29.2% vs. 6.4%). Nine NEK1 carriers (37.5%) also harbored variants in other ALS-related genes.This study confirms that NEK1 LoF and p.Arg261. His missense variants are associated with ALS in an Italian ALS cohort and suggests a correlation between the presence of NEK1 variants and FA phenotype.

10.3389/fnins.2022.833051

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Citations (14)

Immortalization of multipotent growth-factor dependent hemopoietic progenitors from mice transgenic for GATA-1 driven SV40 tsA58 gene.

The EMBO Journal (1994)

Linda Cairns Stefania Crotta Mario Minuzzo Emanuela Moroni Francesca Granucci

Multipotent Stem Cell

10.1002/j.1460-2075.1994.tb06779.x

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Citations (27)

5-HT3 receptor antagonists do not modify cocaine place conditioning or the rise in extracellular dopamine in the nucleus accumbens of rats

Pharmacology Biochemistry and Behavior (1996)

Luigi Cervo Laura Pozzi R. Samanin

10.1016/0091-3057(96)00046-9

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Citations (36)

CCDC 906486: Experimental Crystal Structure Determination

The Cambridge Structural Database (2013)

E.R. Dos Santos Melina A. Mondelli Laura Pozzi R.S. Correa Heloísa Sobreiro Selistre-de-Araújo

An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.

10.5517/cczf8h4

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Deficits in memory and hippocampal long-term potentiation in mice with reduced calbindin D28K expression.

Proceedings of the National Academy of Sciences (1996)

Susanna Molinari Renata Battini Stefano Ferrari Laura Pozzi Simon Killcross

The influx of calcium into the postsynaptic neuron is likely to be an important event in memory formation. Among the mechanisms that nerve cells may use to alter the time course or size of a spike of intracellular calcium are cytosolic calcium binding or "buffering" proteins. To consider the role in memory formation of one of these proteins, calbindin D28K, which is abundant in many neurons, including the CA1 pyramidal cells of the hippocampus, transgenic mice deficient in calbindin D28K have been created. These mice show selective impairments in spatial learning paradigms and fail to maintain long-term potentiation. These results suggest a role for calbindin D28K protein in temporally extending a neuronal calcium signal, allowing the activation of calcium-dependent intracellular signaling pathways underlying memory function.

Calcium in biology

Memory Formation

10.1073/pnas.93.15.8028

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Citations (158)