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Your search keyword '"Puri, Pier Lorenzo"' showing total 287 results
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287 results on '"Puri, Pier Lorenzo"'

1. Smarcd3 is an epigenetic modulator of the metabolic landscape in pancreatic ductal adenocarcinoma

Author

Ferguson, L Paige, Gatchalian, Jovylyn, McDermott, Matthew L, Nakamura, Mari, Chambers, Kendall, Rajbhandari, Nirakar, Lytle, Nikki K, Rosenthal, Sara Brin, Hamilton, Michael, Albini, Sonia, Wartenberg, Martin, Zlobec, Inti, Galván, José A, Karamitopoulou, Eva, Vavinskaya, Vera, Wascher, Alexis, Lowy, Andrew M, Schürch, Christian M, Puri, Pier Lorenzo, Bruneau, Benoit G, Hargreaves, Diana C, and Reya, Tannishtha

Subjects
Stem Cell Research, Rare Diseases, Genetics, Stem Cell Research - Nonembryonic - Non-Human, Digestive Diseases, Pancreatic Cancer, Cancer, 2.1 Biological and endogenous factors, Aetiology, Humans, Mice, Animals, Transcription Factors, Carcinoma, Pancreatic Ductal, Pancreatic Neoplasms, Epigenesis, Genetic
Abstract

Pancreatic cancer is characterized by extensive resistance to conventional therapies, making clinical management a challenge. Here we map the epigenetic dependencies of cancer stem cells, cells that preferentially evade therapy and drive progression, and identify SWI/SNF complex member SMARCD3 as a regulator of pancreatic cancer cells. Although SWI/SNF subunits often act as tumor suppressors, we show that SMARCD3 is amplified in cancer, enriched in pancreatic cancer stem cells and upregulated in the human disease. Diverse genetic mouse models of pancreatic cancer and stage-specific Smarcd3 deletion reveal that Smarcd3 loss preferentially impacts established tumors, improving survival especially in context of chemotherapy. Mechanistically, SMARCD3 acts with FOXA1 to control lipid and fatty acid metabolism, programs associated with therapy resistance and poor prognosis in cancer. These data identify SMARCD3 as an epigenetic modulator responsible for establishing the metabolic landscape in aggressive pancreatic cancer cells and a potential target for new therapies.

Published
2023

3. Conserved transcription factors promote cell fate stability and restrict reprogramming potential in differentiated cells

Author

Missinato, Maria A., Murphy, Sean, Lynott, Michaela, Yu, Michael S., Kervadec, Anaïs, Chang, Yu-Ling, Kannan, Suraj, Loreti, Mafalda, Lee, Christopher, Amatya, Prashila, Tanaka, Hiroshi, Huang, Chun-Teng, Puri, Pier Lorenzo, Kwon, Chulan, Adams, Peter D., Qian, Li, Sacco, Alessandra, Andersen, Peter, and Colas, Alexandre R.

Published
2023
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5. Author Correction: Denervation-activated STAT3–IL-6 signalling in fibro-adipogenic progenitors promotes myofibres atrophy and fibrosis

Author

Madaro, Luca, Passafaro, Magda, Sala, David, Etxaniz, Usue, Lugarini, Francesca, Proietti, Daisy, Alfonsi, Maria Vittoria, Nicoletti, Chiara, Gatto, Sole, De Bardi, Marco, Rojas-García, Ricardo, Giordani, Lorenzo, Marinelli, Sara, Pagliarini, Vittoria, Sette, Claudio, Sacco, Alessandra, and Puri, Pier Lorenzo

Published
2024
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8. The Stat3-Fam3a axis promotes muscle stem cell myogenic lineage progression by inducing mitochondrial respiration.

Author

Sala, David, Cunningham, Thomas J, Stec, Michael J, Etxaniz, Usue, Nicoletti, Chiara, Dall'Agnese, Alessandra, Puri, Pier Lorenzo, Duester, Gregg, Latella, Lucia, and Sacco, Alessandra

Subjects
Cells, Cultured, Mitochondria, Myoblasts, Stem Cells, Animals, Mice, Inbred C57BL, Animals, Newborn, Mice, Knockout, Mice, Cytokines, Signal Transduction, Cell Differentiation, Oxidative Phosphorylation, Cell Lineage, Muscle Development, Male, STAT3 Transcription Factor, Embryo, Mammalian, Muscle, Striated, Newborn, Cells, Cultured, Embryo, Mammalian, Inbred C57BL, Knockout, Muscle, Striated
Abstract

Metabolic reprogramming is an active regulator of stem cell fate choices, and successful stem cell differentiation in different compartments requires the induction of oxidative phosphorylation. However, the mechanisms that promote mitochondrial respiration during stem cell differentiation are poorly understood. Here we demonstrate that Stat3 promotes muscle stem cell myogenic lineage progression by stimulating mitochondrial respiration in mice. We identify Fam3a, a cytokine-like protein, as a major Stat3 downstream effector in muscle stem cells. We demonstrate that Fam3a is required for muscle stem cell commitment and skeletal muscle development. We show that myogenic cells secrete Fam3a, and exposure of Stat3-ablated muscle stem cells to recombinant Fam3a in vitro and in vivo rescues their defects in mitochondrial respiration and myogenic commitment. Together, these findings indicate that Fam3a is a Stat3-regulated secreted factor that promotes muscle stem cell oxidative metabolism and differentiation, and suggests that Fam3a is a potential tool to modulate cell fate choices.

Published
2019

12. HDAC-regulated myomiRs control BAF60 variant exchange and direct the functional phenotype of fibro-adipogenic progenitors in dystrophic muscles

Author

Saccone, Valentina, Consalvi, Silvia, Giordani, Lorenzo, Mozzetta, Chiara, Barozzi, Iros, Sandoná, Martina, Ryan, Tammy, Rojas-Muñoz, Agustin, Madaro, Luca, Fasanaro, Pasquale, Borsellino, Giovanna, De Bardi, Marco, Frigè, Gianmaria, Termanini, Alberto, Sun, Xin, Rossant, Janet, Bruneau, Benoit G, Mercola, Mark, Minucci, Saverio, and Puri, Pier Lorenzo

Subjects
Pediatric, Biotechnology, Intellectual and Developmental Disabilities (IDD), Brain Disorders, Duchenne/ Becker Muscular Dystrophy, Stem Cell Research, Human Genome, Rare Diseases, Stem Cell Research - Nonembryonic - Non-Human, Genetics, Muscular Dystrophy, Regenerative Medicine, 2.1 Biological and endogenous factors, Aetiology, Musculoskeletal, Animals, Cellular Reprogramming, Chromatin, Chromatin Assembly and Disassembly, Chromosomal Proteins, Non-Histone, Gene Expression Profiling, Gene Expression Regulation, Histone Deacetylase Inhibitors, Histone Deacetylases, Hydroxamic Acids, Mice, Mice, Inbred mdx, MicroRNAs, Muscle Proteins, Muscle, Skeletal, Muscular Dystrophies, Stem Cells, SWI/SNF chromatin remodeling, BAF60, microRNA, HDAC, FAPs, muscular dystrophy, Biological Sciences, Medical and Health Sciences, Psychology and Cognitive Sciences, Developmental Biology
Abstract

Fibro-adipogenic progenitors (FAPs) are important components of the skeletal muscle regenerative environment. Whether FAPs support muscle regeneration or promote fibro-adipogenic degeneration is emerging as a key determinant in the pathogenesis of muscular diseases, including Duchenne muscular dystrophy (DMD). However, the molecular mechanism that controls FAP lineage commitment and activity is currently unknown. We show here that an HDAC-myomiR-BAF60 variant network regulates the fate of FAPs in dystrophic muscles of mdx mice. Combinatorial analysis of gene expression microarray, genome-wide chromatin remodeling by nuclease accessibility (NA) combined with next-generation sequencing (NA-seq), small RNA sequencing (RNA-seq), and microRNA (miR) high-throughput screening (HTS) against SWI/SNF BAF60 variants revealed that HDAC inhibitors (HDACis) derepress a "latent" myogenic program in FAPs from dystrophic muscles at early stages of disease. Specifically, HDAC inhibition induces two core components of the myogenic transcriptional machinery, MYOD and BAF60C, and up-regulates the myogenic miRs (myomiRs) (miR-1.2, miR-133, and miR-206), which target the alternative BAF60 variants BAF60A and BAF60B, ultimately directing promyogenic differentiation while suppressing the fibro-adipogenic phenotype. In contrast, FAPs from late stage dystrophic muscles are resistant to HDACi-induced chromatin remodeling at myogenic loci and fail to activate the promyogenic phenotype. These results reveal a previously unappreciated disease stage-specific bipotency of mesenchimal cells within the regenerative environment of dystrophic muscles. Resolution of such bipotency by epigenetic intervention with HDACis provides a molecular rationale for the in situ reprogramming of target cells to promote therapeutic regeneration of dystrophic muscles.

Published
2014

18. Histological effects of givinostat in boys with Duchenne muscular dystrophy

Author

Bettica, Paolo, Petrini, Stefania, D'Oria, Valentina, D'Amico, Adele, Catteruccia, Michela, Pane, Marika, Sivo, Serena, Magri, Francesca, Brajkovic, Simona, Messina, Sonia, Vita, Gian Luca, Gatti, Barbara, Moggio, Maurizio, Puri, Pier Lorenzo, Rocchetti, Maurizio, De Nicolao, Giuseppe, Vita, Giuseppe, Comi, Giacomo P., Bertini, Enrico, and Mercuri, Eugenio

Published
2016
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29. HDAC2 Blockade by Nitric Oxide and Histone Deacetylase Inhibitors Reveals a Common Target in Duchenne Muscular Dystrophy Treatment

Author

Colussi, Claudia, Mozzetta, Chiara, Gurtner, Aymone, Illi, Barbara, Rosati, Jessica, Straino, Stefania, Ragone, Gianluca, Pescatori, Mario, Zaccagnini, Germana, Antonini, Annalisa, Minetti, Giulia, Martelli, Fabio, Piaggio, Giulia, Gallinari, Paola, Steinkuhler, Christian, Clementi, Emilio, Dell'Aversana, Carmela, Altucci, Lucia, Mai, Antonello, Capogrossi, Maurizio C., Puri, Pier Lorenzo, and Gaetano, Carlo

Published
2008
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30. Stat3 signaling controls satellite cell expansion and skeletal muscle repair

Author

Tierney, Matthew Timothy, Aydogdu, Tufan, Sala, David, Malecova, Barbora, Gatto, Sole, Puri, Pier Lorenzo, Latella, Lucia, and Sacco, Alessandra

Subjects
Muscles -- Regeneration, Stem cells -- Research -- Analysis -- Physiological aspects, Biological sciences, Health
Abstract

The progressive loss of muscle regenerative capacity with age or disease results in part from a decline in the number and function of satellite cells, the direct cellular contributors to muscle repair (1-11). However, little is known about the molecular effectors underlying satellite cell impairment and depletion. Elevated levels of inflammatory cytokines, including interleukin-6 (IL-6), are associated with both age-related and muscle-wasting conditions (12-15). The levels of STAT3, a downstream effector of IL-6, are also elevated with muscle wasting (16, 17), and STAT3 has been implicated in the regulation of self-renewal and stem cell fate in several tissues (18-21). Here we show that IL-6-activated Stat3 signaling regulates satellite cell behavior, promoting myogenic lineage progression through myogenic differentiation 1 (Myodl) regulation. Conditional ablation of Stat3 in Pax7-expressing satellite cells resulted in their increased expansion during regeneration, but compromised myogenic differentiation prevented the contribution of these cells to regenerating myofibers. In contrast, transient Stat3 inhibition promoted satellite cell expansion and enhanced tissue repair in both aged and dystrophic muscle. The effects of STAT3 inhibition on cell fate and proliferation were conserved in human myoblasts. The results of this study indicate that pharmacological manipulation of STAT3 activity can be used to counteract the functional exhaustion of satellite cells in pathological conditions, thereby maintaining the endogenous regenerative response and ameliorating muscle-wasting diseases., Chronic inflammation is a hallmark of several muscle-wasting diseases and impairs the normal regenerative response. IL-6 is among the inflammatory cytokines present during the initial stages of muscle repair and [...]

Published
2014

31. Human skeletal muscle CD90+ fibro-adipogenic progenitors are associated with muscle degeneration in type 2 diabetic patients

Author

Farup, Jean, Just, Jesper, de Paoli, Frank, Lin, Lin, Jensen, Jonas Brorson, Billeskov, Tine, Roman, Ines Sanchez, Cömert, Cagla, Møller, Andreas Buch, Madaro, Luca, Groppa, Elena, Fred, Rikard Göran, Kampmann, Ulla, Gormsen, Lars C., Pedersen, Steen B., Bross, Peter, Stevnsner, Tinna, Eldrup, Nikolaj, Pers, Tune H., Rossi, Fabio M.V., Puri, Pier Lorenzo, and Jessen, Niels

Published
2021
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32. Studying arrhythmogenic right ventricular dysplasia with patient-specific iPSCs

Author

Kim, Changsung, Wong, Johnson, Wen, Jianyan, Wang, Shirong, Wang, Cheng, Spiering, Sean, Kan, Natalia G., Forcales, Sonia, Puri, Pier Lorenzo, Leone, Teresa C., Marine, Joseph E., Calkins, Hugh, Kelly, Daniel P., Judge, Daniel P., and Chen, Huei-Sheng Vincent

Subjects
Heart diseases -- Observations, Genetic disorders -- Research, Stem cells -- Testing, Cardiomyopathy -- Observations, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Cellular reprogramming of somatic cells to patient-specific induced pluripotent stem cells (iPSCs) enables in vitro modelling of human genetic disorders for pathogenic investigations and therapeutic screens (1-7). However, using iPSC-derived [...]

Published
2013

43. Stage-specific modulation of skeletal myogenesis by inhibitors of nuclear deacetylases

Author

Lezzi, Simona, Cossu, Giulio, Nervi, Clara, Sartorelli, Vittorio, and Puri, Pier Lorenzo

Subjects
Gene expression -- Research, Muscle cells -- Genetic aspects, Science and technology
Abstract

Nuclear acetyltransferases promote and deacetylases inhibit skeletal muscle-gene expression, suggesting the potential effectiveness of deacetylase inhibitors (DIs) in modulating skeletal myogenesis. Surprisingly, previous studies have indicated that DIs suppress myogenesis. The recent observations that histone deacetylases associate with the muscle-regulatory proteins MyoD and MEF2C only in undifferentiated myoblasts prompted us to evaluate the effect of DIs at distinct stages of the myogenic program. We found that exposure of established rodent and human muscle cells to distinct DIs has stage-specific effects. Exposure of undifferentiated skeletal myoblasts to DIs, followed by incubation in differentiation medium, enhanced the expression of muscle-specific reporters and increased the levels of endogenous muscle proteins, leading to a dramatic increase in the formation of multinucleated myotubes. By contrast, simultaneous exposure of muscle cells to differentiation medium and DIs inhibited the myogenic program. Likewise, embryos exposed in utero to nonteratogenic doses of DI at the early stages of somitic myogenesis (embryonic day 8.5) exhibited an increased number of somites and augmented expression of a muscle-specific transgene as well as endogenous muscle genes. The functional effects induced by DIs were mirrored by changes in the state of acetylation of histones present at a muscle-gene enhancer and of MyoD itself. These results represent the first evidence that DIs can enhance muscle differentiation and suggest the rationale for their use in manipulating adult and embryonic skeletal myogenesis. deacetylase inhibitors | gene expression | MyoD | skeletal muscle differentiation | embryos

Published
2002

45. Induction of terminal differentiation by constitutive activation of p38 MAP kinase in human rhabdomyosarcoma cells

Author

Puri, Pier Lorenzo, Wu, Zhenguo, Zhang, Peilin, Wood, Lauren D., Bhakta, Kunjan S., Han, Jiahuai, Feramisco, James R., Karin, Michael, and Wang, Jean Y.J.

Subjects
Cytochemistry -- Research, Rhabdomyosarcoma -- Genetic aspects, Protein kinases -- Physiological aspects, Mitogens -- Physiological aspects, Cell differentiation -- Research, Biological sciences
Abstract

Terminal differentiation by constitutive activation of p38 mitogen-activated protein (MAP) kinase in rhabdomyosarcoma (RMS) cells and its induction are discussed. RMS comes from muscle precursors. The block in RMS of the differentiation program is a paradox. The deregulated proliferation exists despite MyoD expression. MyoD inhibits proliferation of cells and promotes muscle differentiation. A lack of a factor needed for MyoD activity in RMS has been implicated before, and it has now been shown that p38 MAPK activaction, necessary for muscle differentiation is lacking in RMS cells.

Published
2000

48. Regulation of histone acetyltransferases p300 and PCAF by the bHLH protein twist and adenoviral oncoprotein E1A

Author

Hamamori, Yasuo, Sartorelli, Vittorio, Ogryzko, Vasily, Puri, Pier Lorenzo, Wu, Hung-Yi, Wang, Jean Y.J., Nakatani, Yoshihiro, and Kedes, Larry

Subjects
Histones -- Research, Proteins -- Research, Genetic transcription -- Research, Transferases -- Research, Biological sciences
Abstract

The regulation of the p300 and p300/CBP-associated factor (PCAF) histone acetyltransferases (HAT) was investigated. Results showed that the basic helix-loop-helix protein Twist directly binds two independent HAT domains and regulates the HAT activities of p300 and PCAF. It was also found that the N terminus of the Twist is the primary domain interacting with p300 and PCAF and that the effects of the Twist are imitated by the adenovirus E1A protein.

Published
1999

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