4 results on '"Maria L, Angelotti"'
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2. Type I interferon–related kidney disorders
- Author
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Lorenzo Lodi, Maria V. Mastrolia, Federica Bello, Giovanni M. Rossi, Maria L. Angelotti, Yanick J. Crow, Paola Romagnani, and Augusto Vaglio
- Subjects
collapsing glomerulopathy ,Kidney Glomerulus ,interferonopathy ,interferon ,Kidney ,Antiviral Agents ,viral nephropathy ,systemic lupus erythematosus ,Nephrology ,Interferon Type I ,Humans ,Lupus Erythematosus, Systemic ,Kidney Diseases ,glomerulonephritis - Abstract
Type I interferon (IFN-I) mediates tissue damage in a wide range of kidney disorders, directly affecting the biology and function of several renal cell types including podocytes, mesangial, endothelial, and parietal epithelial cells. Enhanced IFN-I signaling is observed in the context of viral infections, autoimmunity (e.g., systemic lupus erythematosus), and type 1 interferonopathies, rare monogenic disorders characterized by constitutive activation of the IFN-I pathway. All these IFN-I–related disorders can cause renal dysfunction and share pathogenic and histopathological features. Collapsing glomerulopathy, a histopathological lesion characterized by podocyte loss, collapse of the vascular tuft, and parietal epithelial cell proliferation, is commonly associated with viral infections, has been described in type 1 interferonopathies such as Aicardi-Goutières syndrome and stimulator of IFN genes–associated vasculopathy with onset in infancy, and can also be induced by recombinant IFN therapy. In all these conditions, podocytes and parietal epithelial cells seem to be the primary target of IFN-I–mediated damage. Additionally, immune-mediated glomerular injury is common to viral infections, systemic lupus erythematosus, and type 1 interferonopathies such as coatomer subunit-α syndrome (COPA) and DNASE1L3 deficiency, diseases in which IFN-I apparently promotes immune-mediated kidney injury. Finally, kidney pathology primarily characterized by vascular lesions (e.g., thrombotic microangiopathy and vasculitis) is a hallmark of type 1 interferonopathy adenosine deaminase 2 deficiency as well as of systemic lupus erythematosus, viral infections, and IFN therapy. Defining the nosology, pathogenic mechanisms, and histopathological patterns of IFN-I–related kidney disorders has diagnostic and therapeutic implications, especially considering the likely near-term availability of novel drugs targeting the IFN-I pathway.
- Published
- 2022
- Full Text
- View/download PDF
3. List of Contributors
- Author
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Michael Abecassis, Ahmed Abed, Massimo Abelli, Sarwat Ahmad, Mario Alessiani, Aynaa Alsharidi, Fiorella Altruda, Gabriella Amorese, Andrea Angeletti, Mario Angelico, Roberta Angelico, Maria L. Angelotti, Robert J. Applegate, Anthony Atala, Chiara Attanasio, David Axelrod, Yanik Bababekov, Joydeep Basu, Francesca Becherucci, P. Matthew Belford, Enrico Benedetti, Valentina Benedetti, Ariela Benigni, Timothy A. Bertram, Oriol Bestard, Joshua Blake, Ugo Boggi, Lauren Brasile, Jonathan S. Bromberg, Sophie Brouard, Matthew Brovold, George W. Burke, Mirela Busic, Zeeshan Butt, Silvia Caddeo, Stefano Calzone, Josep M. Campistol, Irene Carmagnola, Fiona Carty, Diego Castanares-Zapatero, Christos E. Chadjichristos, Brooke E. Chambers, Sindhu Chandran, Christos Chatziantoniou, Ashton Chen, Linda Chen, Xiwu Chen, Valeria Chiono, Manuel Chiusa, Gaetano Ciancio, Gianluca Ciardelli, Gino Coletti, Elisabeth Coll, Christine Collienne, Robert B. Colvin, Monica Cortinovis, A. Benedict Cosimi, Paolo Cravedi, Giuseppe D’Amico, Stefano Da Sacco, Richard Danger, Jacques Dantal, Alan J. Davidson, Letizia De Chiara, Johannes W. De Fijter, Gloria de la Rosa, Francis L. Delmonico, Junhong Deng, Corinne Deurdulian, Abritee Dhal, Paolo Dionigi, Beatriz Domínguez-Gil, Marek Drozdzik, Jean-Claude Dussaule, Lauren Edgar, Maria Francesca Egidi, Hany El Hennawy, Karen English, Matthew J. Everly, Sharmila Fagoonee, Elvira Smeralda Famulari, Alan C. Farney, Marina Figliuzzi, Marialuisa Framarino-dei-Malatesta, David E. Fumo, Elena Gagliardini, Lorenzo Gallon, Sanjay K. Gandhi, Michael D. Gautreaux, Anna Geraedts, Domenico Giannese, Pier C. Giulianotti, Michael S. Goligorsky, Adam Griesemar, Josep M. Grinyó, Angelika C. Gruessner, Rainer W.G. Gruessner, Bulang He, Eliot Heher, Bing Ho, Sarah A. Hosgood, Kiyohiko Hotta, Atul Humar, H. David Humes, Giuseppe Iaria, Barbara Imberti, Juan Carlos Izpisua Belmonte, Ina Jochmans, Ravi Katari, Panagiotis Kavvadas, Tatsuo Kawai, Carlos Kengla, Tristan Keys, Amritha Kidiyoor, Kengo Kidokoro, Deepali Kumar, Michael A. Kutcher, Quirino Lai, Pierre-François Laterre, Céleste Lebbé, Christophe Legendre, Rachel Lennon, Peng Li, Jen-Jar Lin, Melissa H. Little, Xiongbing Lu, John W. Ludlow, Beatriz Mahíllo, Rosalinde Masereeuw, Rafael Matesanz, Mirjana S. Matovinovic, Benedetta Mazzinghi, Serge Cedrick Mbiandjeu Toya, Scott McEwen, Fabio Melandro, Loredana Melchiorri, Madhav C. Menon, Majid Mirzazadeh, Samantha Montag, Robert A. Montgomery, Virginie Montiel, Nuria Montserrat, Marina Morigi, Christian C. Morrill, Michel Mourad, Sean V. Murphy, Patricia Murray, Tiziana Nardo, Paolo A. Netti, Mark Nguyen, Michael L. Nicholson, John M. O’Callaghan, Linda Ohler, Giuseppe Orlando, Kenji Osafune, Tetsu Oura, Anna Peired, Andrea Peloso, Zhenzhen Peng, Norberto Perico, Laura Perin, Vittorio Perrone, Paul Persad, János Peti-Peterdi, Astgik Petrosyan, Andrea Pietrabissa, Christopher J. Pino, Jacques Pirenne, Francesco Pisani, Rutger J. Ploeg, Esteban Porrini, Ambra Pozzi, Alberto Pugliese, Luigi Pugliese, Ton J. Rabelink, Teresa Rampino, Michael A. Rees, Marlies E.J. Reinders, Andrea Remuzzi, Giuseppe Remuzzi, Anne Riquier-Brison, Raquel G. Roca, Jeffrey Rogers, Paola Romagnani, Ivy A. Rosales, Norman D. Rosenblum, Cinzia Rota, Piero Ruggenenti, Francesca Ruini, Junichiro Sageshima, Fadi El Salem, Shaifali Sandal, Veronika Sander, Ilaria Santeramo, Renato M. Santos, Minnie Sarwal, Jigesh Shah, Aneesha A. Shetty, Lorenzo Silengo, Eric Siskind, Anton Skaro, Renaud Snanoudj, Shay Soker, Andrew M. South, Goce Spasovski, Robert J. Stratta, Charles Strom, Bart Stubenitsky, Riccardo Tamburrini, Qizhi Tang, Ekamol Tantissattamo, Masayuki Tasaki, Hisham Tchelepi, Elena Ticozzelli, Opas Traitanon, Matias Trillini, Ivo Tzvetanov, María O. Valentín, Flavio Vincenti, Fabio Vistoli, Jelle Vriend, Stephen J. Walker, Jason A. Wertheim, David F. Williams, Bettina Wilm, Martijn J. Wilmer, Rebecca A. Wingert, Xavier Wittebole, Yun Xia, Christodoulos Xinaris, Kazuhiko Yamada, Takashi Yokoo, Shinya Yokote, Maarten L. Zandvliet, Roy Zent, Yuanyuan Zhang, David X. Zhao, Lihui Zhao, and Susan Y. Zhao
- Published
- 2017
- Full Text
- View/download PDF
4. The antiviral cytokines IFN-α and IFN-β modulate parietal epithelial cells and promote podocyte loss: implications for IFN toxicity, viral glomerulonephritis, and glomerular regeneration
- Author
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Adriana, Migliorini, Maria L, Angelotti, Shrikant R, Mulay, Onkar O, Kulkarni, Jana, Demleitner, Alexander, Dietrich, Costanza, Sagrinati, Lara, Ballerini, Anna, Peired, Stuart J, Shankland, Helen, Liapis, Paola, Romagnani, and Hans-Joachim, Anders
- Subjects
Cell Death ,Cell Survival ,Podocytes ,Kidney Glomerulus ,Interferon-alpha ,Cell Differentiation ,Epithelial Cells ,HIV Infections ,Interferon-beta ,Mice, SCID ,Antiviral Agents ,Mice ,Glomerulonephritis ,Cell Movement ,Doxorubicin ,Animals ,Humans ,Regeneration ,Female ,Cells, Cultured ,Cell Proliferation - Abstract
Interferon (IFN)-α and IFN-β are the central regulators of antiviral immunity but little is known about their roles in viral glomerulonephritis (eg, HIV nephropathy). We hypothesized that IFN-α and IFN-β would trigger local inflammation and podocyte loss. We found that both IFNs consistently activated human and mouse podocytes and parietal epithelial cells to express numerous IFN-stimulated genes. However, only IFN-β significantly induced podocyte death and increased the permeability of podocyte monolayers. In contrast, only IFN-α caused cell-cycle arrest and inhibited the migration of parietal epithelial cells. Both IFNs suppressed renal progenitor differentiation into mature podocytes. In Adriamycin nephropathy, injections with either IFN-α or IFN-β aggravated proteinuria, macrophage influx, and glomerulosclerosis. A detailed analysis showed that only IFN-β induced podocyte mitosis. This did not, however, lead to proliferation, but was associated with podocyte loss via podocyte detachment and/or mitotic podocyte death (mitotic catastrophe). We did not detect TUNEL-positive podocytes. Thus, IFN-α and IFN-β have both common and differential effects on podocytes and parietal epithelial cells, which together promote glomerulosclerosis by enhancing podocyte loss while suppressing podocyte regeneration from local progenitors.
- Published
- 2012
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