Nicoletta Filigheddu

Università degli Studi del Piemonte Orientale “Amedeo Avogadro”

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Andrea Graziani

Università degli Studi del Piemonte Orientale “Amedeo Avogadro”

Simone Reano

Università degli Studi del Piemonte Orientale “Amedeo Avogadro”

Flavia Prodam

Università degli Studi del Piemonte Orientale “Amedeo Avogadro”

Paolo E. Porporato

University of Turin

Gianluca Baldanzi

Università degli Studi del Piemonte Orientale “Amedeo Avogadro”

Federica Chianale

Bracco (Italy)

Emanuela Agosti

Università degli Studi del Piemonte Orientale “Amedeo Avogadro”

Andrea Scircoli

Università degli Studi del Piemonte Orientale “Amedeo Avogadro”

Ivan Zaggia

Università degli Studi del Piemonte Orientale “Amedeo Avogadro”

Tommaso Raiteri

Università degli Studi del Piemonte Orientale “Amedeo Avogadro”

Cooperative Institutions

Inserm

158

Università degli Studi del Piemonte Orientale “Amedeo Avogadro”

154

Centre National de la Recherche Scientifique

141

University of Michigan–Ann Arbor

126

Harvard University

116

Istituti di Ricovero e Cura a Carattere Scientifico

114

University of Turin

108

Chinese Academy of Sciences

National Institutes of Health

Consejo Superior de Investigaciones Científicas

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Differential Expression of MicroRNAs between Eutopic and Ectopic Endometrium in Ovarian Endometriosis

Journal of Biomedicine and Biotechnology (2010)

Nicoletta Filigheddu Ilaria Gregnanin Paolo E. Porporato Daniela Surico Beatrice Perego

Endometriosis, defined as the presence of endometrial tissue outside the uterus, is a common gynecological disease with poorly understood pathogenesis. MicroRNAs are members of a class of small noncoding RNA molecules that have a critical role in posttranscriptional regulation of gene expression by repression of target mRNAs translation. We assessed differentially expressed microRNAs in ectopic endometrium compared with eutopic endometrium in 3 patients through microarray analysis. We identified 50 microRNAs differentially expressed and the differential expression of five microRNAs was validated by real-time RT-PCR in other 13 patients. We identified in silico their predicted targets, several of which match the genes that have been identified to be differentially expressed in ectopic versus eutopic endometrium in studies of gene expression. A functional analysis of the predicted targets indicates that several of these are involved in molecular pathways implicated in endometriosis, thus strengthening the hypothesis of the role of microRNAs in this pathology.

Pathogenesis

Ectopic expression

10.1155/2010/369549

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Citations (154)

The role of vitamin D in cancer cachexia

Current Opinion in Supportive and Palliative Care (2017)

Fabio Penna Andrea Camperi Maurizio Muscaritoli Nicoletta Filigheddu Paola Costelli

Purpose of review The possibility to use vitamin D supplementation to improve muscle wasting, with particular focus on cancer cachexia, is discussed. Recent findings Vitamin D exerts biological actions on myogenic precursor proliferation and differentiation, impinging on muscle regeneration. However, the effects of VitD supplementation in diseases associated with muscle atrophy, such as cancer cachexia, are poorly investigated. Data obtained in experimental models of cancer cachexia show that the administration of vitamin D to tumor-bearing animals is not able to prevent or delay both muscle wasting and adipose tissue depletion, despite increased expression of muscle vitamin D receptor. Not just vitamin D supplementation impairs muscle damage-induced regeneration, suggesting that upregulation of vitamin D receptor signaling could contribute to muscle wasting. Summary Vitamin D supplementation is likely beneficial to reduce or delay aging-related sarcopenia and osteoporosis, although the available data still put in evidence significant discrepancies. By contrast, VitD supplementation to tumor-bearing animals or to rats with arthritis was shown to be totally ineffective. In this regard, the adoption of VitD treatment in patients with cancer cachexia or other chronic diseases should be carefully evaluated, in particular whenever a regenerative process might be involved.

Muscle Atrophy

10.1097/spc.0000000000000302

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Citations (20)

Both ghrelin deletion and unacylated ghrelin overexpression preserve muscles in aging mice

Endocrine Abstracts (2020)

Emanuela Agosti Feudis Marilisa De Elia Angelino Roberta Belli Teixeira Maraiza Alves

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

10.1530/endoabs.70.oc4.2

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Diacylglycerol kinases are essential for hepatocyte growth factor‐dependent proliferation and motility of Kaposi’s sarcoma cells

Cancer Science (2011)

Gianluca Baldanzi Stefano Pietronave Deborah Locarno Simone Merlin Paolo E. Porporato

Hepatocyte growth factor (HGF) is involved in the pathogenesis of Kaposi’s sarcoma (KS), the most frequent neoplasia in patients with AIDS, characterized by proliferating spindle cells, infiltrating inflammatory cells, angiogenesis, edema, and invasiveness. In vitro , this factor sustains the biological behavior of KS derived cells, after activation of its receptor and the downstream MAPK and AKT signals. In other cell types, namely endothelial and epithelial cells, movement, proliferation, and survival stimulated by HGF and other growth factors and cytokines depend on diacylglycerol kinases (DGK). In an effort to identify new intracellular transducers operative in KS cells, which could represent therapeutic targets, we investigated the role of DGK in KS cell movement and proliferation by treating cells with the DGK pharmacological inhibitor R59949. We report that R59949 strongly inhibits HGF‐induced KS motility, proliferation, and anchorage‐independent growth with only a partial effect on cell adhesion and spreading. R59949 does not affect cell survival, HGF receptor activation, or the classical MAPK and AKT signalling pathways. Furthermore, we carried out an siRNA screen to characterize the DGK isoforms involved in KS motility and anchorage independent growth. Our data indicate a strong involvement of DGK‐δ in KS motility and of DGK‐ι in anchorage‐independent growth. These results indicate that DGK inhibition is sufficient to impair in vitro KS cell proliferation and movement and suggest that selected DGK represent new pharmacological targets to interfere with the malignant properties of KS, independently from the well‐known RAS/MAPK and PI3K/AKT pathways. ( Cancer Sci 2011; 102: 1329–1336)

10.1111/j.1349-7006.2011.01953.x

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Citations (23)

98 Key role of phosphatidylinositol 3-kinase-mediated signals in hepatic preconditioning

Journal of Hepatology (2004)

Rita Carini Maria Grazia De Cesaris Roberta Splendore Gianluca Baldanzi Mariapaola Nitti

10.1016/s0168-8278(04)90098-0

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Ghrelin knockout mice display defective skeletal muscle regeneration and impaired satellite cell self-renewal

Endocrine (2018)

Elia Angelino Simone Reano Alessandro Bollo Michele Ferrara Marilisa De Feudis

Obestatin

Knockout mouse

10.1007/s12020-018-1606-4

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Citations (16)

The Atrophic Effect of 1,25(OH)2 Vitamin D3 (Calcitriol) on C2C12 Myotubes Depends on Oxidative Stress

Antioxidants (2021)

Tommaso Raiteri Ivan Zaggia Simone Reano Andrea Scircoli Laura Salvadori

Dysfunctional mitochondrial metabolism has been linked to skeletal muscle loss in several physio-pathological states. Although it has been reported that vitamin D (VD) supports cellular redox homeostasis by maintaining normal mitochondrial functions, and VD deficiency often occurs in conditions associated with skeletal muscle loss, the efficacy of VD supplementation to overcome muscle wasting is debated. Investigations on the direct effects of VD metabolites on skeletal muscle using C2C12 myotubes have revealed an unexpected pro-atrophic activity of calcitriol (1,25VD), while its upstream metabolites cholecalciferol (VD3) and calcidiol (25VD) have anti-atrophic effects. Here, we investigated if the atrophic effects of 1,25VD on myotubes depend on its activity on mitochondrial metabolism. The impact of 1,25VD and its upstream metabolites VD3 and 25VD on mitochondria dynamics and the activity of C2C12 myotubes was evaluated by measuring mitochondrial content, architecture, metabolism, and reactive oxygen species (ROS) production. We found that 1,25VD induces atrophy through protein kinase C (PKC)-mediated ROS production, mainly of extramitochondrial origin. Consistent with this, cotreatment with the antioxidant N-acetylcysteine (NAC), but not with the mitochondria-specific antioxidant mitoTEMPO, was sufficient to blunt the atrophic activity of 1,25VD. In contrast, VD3 and 25VD have antioxidant properties, suggesting that the efficacy of VD supplementation might result from the balance between atrophic pro-oxidant (1,25VD) and protective antioxidant (VD3 and 25VD) metabolites.

Mitochondrial ROS

Muscle Atrophy

10.3390/antiox10121980

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Citations (9)

Diacylglycerol kinase-α phosphorylation by Src on Y335 is required for activation, membrane recruitment and Hgf-induced cell motility

Oncogene (2007)

Gianluca Baldanzi Santina Cutrupi Federica Chianale Viola F. Gnocchi Elena Rainero

Phosphorylation cascade

10.1038/sj.onc.1210717

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Citations (51)