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Article ; Online: Advancements in kidney organoids and tubuloids to study (dys)function.

Dilmen, E / Orhon, I / Jansen, J / Hoenderop, J G J

2023 Volume 34, Issue 4, Page(s) 299–311

Abstract: The rising prevalence of kidney diseases urges the need for novel therapies. Kidney organoids and tubuloids are advanced in vitro models and have recently been described as promising tools to study kidney (patho)physiology. Recent developments have shown ...

Abstract	The rising prevalence of kidney diseases urges the need for novel therapies. Kidney organoids and tubuloids are advanced in vitro models and have recently been described as promising tools to study kidney (patho)physiology. Recent developments have shown their application in disease modeling, drug screening, and nephrotoxicity. These applications rely on their ability to mimic (dys)function in vitro including endocrine activity and drug, electrolyte, and water transport. This review provides an overview of these emerging kidney models and focuses on the most recent developments that utilize their functional capabilities. In addition, we cover current limitations and provide future perspectives for this rapidly evolving field, including what these functional properties mean for translational and personalized medicine now and in the future.
MeSH term(s)	Humans ; Kidney ; Organoids
Language	English
Publishing date	2023-10-19
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	30122-x
ISSN	1879-3088 ; 0962-8924
ISSN (online)	1879-3088
ISSN	0962-8924
DOI	10.1016/j.tcb.2023.09.005
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Article: Differentiated mouse kidney tubuloids as a novel

Olde Hanhof, C J A / Dilmen, E / Yousef Yengej, F A / Latta, F / Ammerlaan, C M E / Schreurs, J / Hooijmaijers, L / Jansen, J / Rookmaaker, M B / Orhon, I / Verhaar, M C / Hoenderop, J G

Frontiers in cell and developmental biology

2023 Volume 11, Page(s) 1086823

Abstract: Kidney tubuloids are cell models that are derived from human or mouse renal epithelial cells and show high similarities with ... ...

Abstract	Kidney tubuloids are cell models that are derived from human or mouse renal epithelial cells and show high similarities with their
Language	English
Publishing date	2023-01-25
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2023.1086823
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Article: Assays to Monitor Autophagy Progression in Cell Cultures.

Orhon, Idil / Reggiori, Fulvio

Cells

2017 Volume 6, Issue 3

Abstract: The vast number of implications of autophagy in multiple areas of life sciences and medicine has attracted the interest of numerous scientists that aim to unveil the role of this process in specific physiological and pathological contexts. Cell cultures ... ...

Abstract	The vast number of implications of autophagy in multiple areas of life sciences and medicine has attracted the interest of numerous scientists that aim to unveil the role of this process in specific physiological and pathological contexts. Cell cultures are one of the most frequently used experimental setup for the investigation of autophagy. As a result, it is essential to assess this highly regulated molecular pathway with efficient and reliable methods. Each method has its own advantages and disadvantages. Here, we present a review summarizing the most established assays used to monitor autophagy induction and progression in cell cultures, in order to guide researchers in the selection of the most optimal solution for their experimental setup and design.
Language	English
Publishing date	2017-07-07
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2661518-6
ISSN	2073-4409
ISSN	2073-4409
DOI	10.3390/cells6030020
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Article ; Online: Monitoring of Autophagy and Cell Volume Regulation in Kidney Epithelial Cells in Response to Fluid Shear Stress.

Lazari, Maria M / Orhon, Idil / Codogno, Patrice / Dupont, Nicolas

Methods in molecular biology (Clifton, N.J.)

2019 Volume 1880, Page(s) 331–340

Abstract: Fluidic shear stress applied to epithelial cells inside the kidney tubules affects cell size in an autophagy-related manner. Here, we describe the technical equipment that we routinely use to apply shear stress on cells, as well as immunoblotting, ... ...

Abstract	Fluidic shear stress applied to epithelial cells inside the kidney tubules affects cell size in an autophagy-related manner. Here, we describe the technical equipment that we routinely use to apply shear stress on cells, as well as immunoblotting, immunofluorescence, and three-dimensional cell volume reconstruction techniques used in analysis of the influence of this stress on cells and cellular components. By pointing out details of experimental techniques and potential pitfalls, this review will serve as a guide for those interested in study of how shear stress influences cells.
MeSH term(s)	Animals ; Autophagy/physiology ; Biological Assay/instrumentation ; Biological Assay/methods ; Cell Line ; Cell Size ; Dogs ; Epithelial Cells/cytology ; Epithelial Cells/physiology ; Humans ; Imaging, Three-Dimensional/instrumentation ; Imaging, Three-Dimensional/methods ; Mice ; Microscopy, Fluorescence/instrumentation ; Microscopy, Fluorescence/methods ; Shear Strength/physiology ; Software ; Stress, Mechanical
Language	English
Publishing date	2019-01-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-8873-0_22
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Article ; Online: Autophagy induction during stem cell activation plays a key role in salivary gland self-renewal.

Orhon, Idil / Rocchi, Cecilia / Villarejo-Zori, Beatriz / Serrano Martinez, Paola / Baanstra, Mirjam / Brouwer, Uilke / Boya, Patricia / Coppes, Rob / Reggiori, Fulvio

Autophagy

2021 Volume 18, Issue 2, Page(s) 293–308

Abstract: Relatively quiescent tissues like salivary glands (SGs) respond to stimuli such as injury to expand, replace and regenerate. Resident stem/progenitor cells are key in this process because, upon activation, they possess the ability to self-renew. ... ...

Abstract	Relatively quiescent tissues like salivary glands (SGs) respond to stimuli such as injury to expand, replace and regenerate. Resident stem/progenitor cells are key in this process because, upon activation, they possess the ability to self-renew. Macroautophagy/autophagy contributes to and regulates differentiation in adult tissues, but an important question is whether this pathway promotes stem cell self-renewal in tissues. We took advantage of a 3D organoid system that allows assessing the self-renewal of mouse SGs stem cells (SGSCs). We found that autophagy in dormant SGSCs has slower flux than self-renewing SGSCs. Importantly, autophagy enhancement upon SGSCs activation is a self-renewal feature in 3D organoid cultures and SGs regenerating
MeSH term(s)	Autophagy ; Cell Differentiation ; Cell Self Renewal ; Salivary Glands/physiology ; Stem Cells
Language	English
Publishing date	2021-05-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2021.1924036
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Article ; Online: Primary cilium and autophagy: The avengers of cell-size regulation.

Orhon, Idil / Dupont, Nicolas / Codogno, Patrice

Autophagy

2016 Volume 12, Issue 11, Page(s) 2258–2259

Abstract: The maintenance of cellular homeostasis in response to extracellular stresses by autophagy is vital for the health of various tissues. Extracellular stimuli may include nutrient starvation, endoplasmic reticulum stress, hypoxia, cytotoxic agents, or ... ...

Abstract	The maintenance of cellular homeostasis in response to extracellular stresses by autophagy is vital for the health of various tissues. Extracellular stimuli may include nutrient starvation, endoplasmic reticulum stress, hypoxia, cytotoxic agents, or mechanical stress. The primary cilium (PC) is a microtubule-based sensory organelle that regulates the integration of various extracellular stimuli. The interconnection between macroautophagy/autophagy and the PC is beginning to be illuminated. In this punctum, we discuss our recent study of PC-dependent autophagy in response to fluid flow in kidney epithelial cells. Urinary flow in kidney tubules creates a shear stress that regulates epithelial cell volume. PC-mediated autophagy is necessary for the regulation of cell size. The signal from the PC is transduced by the activation of STK11/LKB1 and by MTOR inhibition. Our results clarify the physiological role of PC-dependent autophagy in the kidney and suggest that autophagy manipulation may provide a route to the treatment of ciliopathies.
MeSH term(s)	Animals ; Autophagy ; Cell Size ; Cilia/metabolism ; Humans ; Signal Transduction ; TOR Serine-Threonine Kinases/metabolism
Chemical Substances	TOR Serine-Threonine Kinases (EC 2.7.1.1)
Language	English
Publishing date	2016-08-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2016.1212790
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Article ; Online: Autophagy and regulation of cilia function and assembly.

Orhon, I / Dupont, N / Pampliega, O / Cuervo, A M / Codogno, P

Cell death and differentiation

2014 Volume 22, Issue 3, Page(s) 389–397

Abstract: Motile and primary cilia (PC) are microtubule-based structures located at the cell surface of many cell types. Cilia govern cellular functions ranging from motility to integration of mechanical and chemical signaling from the environment. Recent studies ... ...

Abstract	Motile and primary cilia (PC) are microtubule-based structures located at the cell surface of many cell types. Cilia govern cellular functions ranging from motility to integration of mechanical and chemical signaling from the environment. Recent studies highlight the interplay between cilia and autophagy, a conserved cellular process responsible for intracellular degradation. Signaling from the PC recruits the autophagic machinery to trigger autophagosome formation. Conversely, autophagy regulates ciliogenesis by controlling the levels of ciliary proteins. The cross talk between autophagy and ciliated structures is a novel aspect of cell biology with major implications in development, physiology and human pathologies related to defects in cilium function.
MeSH term(s)	Animals ; Autophagy/physiology ; Cell Movement/physiology ; Cilia/physiology ; Humans ; Signal Transduction
Language	English
Publishing date	2014-10-31
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1225672-9
ISSN	1476-5403 ; 1350-9047
ISSN (online)	1476-5403
ISSN	1350-9047
DOI	10.1038/cdd.2014.171
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Article ; Online: Autophagy and autophagic flux in tumor cells.

Dupont, Nicolas / Orhon, Idil / Bauvy, Chantal / Codogno, Patrice

Methods in enzymology

2014 Volume 543, Page(s) 73–88

Abstract: Macroautophagy (hereafter referred to as autophagy), a central mechanism mediating the lysosomal degradation of cytoplasmic components, can be stimulated by a wide panel of adverse stimuli, including a panoply of anticancer agents. The central autophagic ...

Abstract	Macroautophagy (hereafter referred to as autophagy), a central mechanism mediating the lysosomal degradation of cytoplasmic components, can be stimulated by a wide panel of adverse stimuli, including a panoply of anticancer agents. The central autophagic organelle is the autophagosome, a double membrane-bound vacuole that sequesters the cytoplasmic material destined to disposal. The ultimate destiny of the autophagosome is to fuse with a lysosome, resulting in the degradation of the autophagic cargo. In this setting, it is important to discriminate whether a particular stimulus actually promotes autophagy or it simply blocks the fusion of autophagosomes with lysosomes. To this aim, the methods that assess autophagy should assess not only the number of autophagosomes but also the so-called autophagic flux, that is, the clearance of the autophagy cargo from the lysosomal compartment. Here, we present a compendium of methods to assess the autophagic flux in cultured malignant cells. This approach should allow for the study of the intimate link between autophagy and oncometabolism in several experimental paradigms.
MeSH term(s)	Autophagy ; Cell Line, Tumor ; Humans ; Molecular Probes ; Neoplasms/immunology ; Neoplasms/pathology
Chemical Substances	Molecular Probes
Language	English
Publishing date	2014
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1557-7988 ; 0076-6879
ISSN (online)	1557-7988
ISSN	0076-6879
DOI	10.1016/B978-0-12-801329-8.00004-0
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Article ; Online: Autophagy induction in atrophic muscle cells requires ULK1 activation by TRIM32 through unanchored K63-linked polyubiquitin chains.

Di Rienzo, M / Antonioli, M / Fusco, C / Liu, Y / Mari, M / Orhon, I / Refolo, G / Germani, F / Corazzari, M / Romagnoli, A / Ciccosanti, F / Mandriani, B / Pellico, M T / De La Torre, R / Ding, H / Dentice, M / Neri, M / Ferlini, A / Reggiori, F /

Kulesz-Martin, M / Piacentini, M / Merla, G / Fimia, G M

Science advances

2019 Volume 5, Issue 5, Page(s) eaau8857

Abstract: Optimal autophagic activity is crucial to maintain muscle integrity, with either reduced or excessive levels leading to specific myopathies. LGMD2H is a muscle dystrophy caused by mutations in the ubiquitin ligase TRIM32, whose function in muscles ... ...

Abstract	Optimal autophagic activity is crucial to maintain muscle integrity, with either reduced or excessive levels leading to specific myopathies. LGMD2H is a muscle dystrophy caused by mutations in the ubiquitin ligase TRIM32, whose function in muscles remains not fully understood. Here, we show that TRIM32 is required for the induction of muscle autophagy in atrophic conditions using both in vitro and in vivo mouse models. Trim32 inhibition results in a defective autophagy response to muscle atrophy, associated with increased ROS and MuRF1 levels. The proautophagic function of TRIM32 relies on its ability to bind the autophagy proteins AMBRA1 and ULK1 and stimulate ULK1 activity via unanchored K63-linked polyubiquitin. LGMD2H-causative mutations impair TRIM32's ability to bind ULK1 and induce autophagy. Collectively, our study revealed a role for TRIM32 in the regulation of muscle autophagy in response to atrophic stimuli, uncovering a previously unidentified mechanism by which ubiquitin ligases activate autophagy regulators.
MeSH term(s)	Adaptor Proteins, Signal Transducing/antagonists & inhibitors ; Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Autophagy ; Autophagy-Related Protein-1 Homolog/metabolism ; Cell Line ; Cell Transdifferentiation ; Humans ; Lysine/metabolism ; Mice ; Mice, Knockout ; Muscular Dystrophies, Limb-Girdle/metabolism ; Muscular Dystrophies, Limb-Girdle/pathology ; Myoblasts/cytology ; Myoblasts/metabolism ; Protein Binding ; RNA Interference ; RNA, Small Interfering/metabolism ; Ubiquitin-Protein Ligases/antagonists & inhibitors ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitination
Chemical Substances	Adaptor Proteins, Signal Transducing ; Ambra1 protein, mouse ; RNA, Small Interfering ; TRIM32 protein, mouse (EC 2.3.2.27) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Autophagy-Related Protein-1 Homolog (EC 2.7.11.1) ; Lysine (K3Z4F929H6)
Language	English
Publishing date	2019-05-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.aau8857
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Article ; Online: Chloroquine inhibits autophagic flux by decreasing autophagosome-lysosome fusion.

Mauthe, Mario / Orhon, Idil / Rocchi, Cecilia / Zhou, Xingdong / Luhr, Morten / Hijlkema, Kerst-Jan / Coppes, Robert P / Engedal, Nikolai / Mari, Muriel / Reggiori, Fulvio

Autophagy

2018 Volume 14, Issue 8, Page(s) 1435–1455

Abstract: Macroautophagy/autophagy is a conserved transport pathway where targeted structures are sequestered by phagophores, which mature into autophagosomes, and then delivered into lysosomes for degradation. Autophagy is involved in the pathophysiology of ... ...

Abstract	Macroautophagy/autophagy is a conserved transport pathway where targeted structures are sequestered by phagophores, which mature into autophagosomes, and then delivered into lysosomes for degradation. Autophagy is involved in the pathophysiology of numerous diseases and its modulation is beneficial for the outcome of numerous specific diseases. Several lysosomal inhibitors such as bafilomycin A
MeSH term(s)	Animals ; Autophagosomes/drug effects ; Autophagosomes/metabolism ; Autophagosomes/ultrastructure ; Autophagy/drug effects ; Cell Line, Tumor ; Chloroquine/pharmacology ; Endocytosis/drug effects ; Endosomes/drug effects ; Endosomes/metabolism ; Endosomes/ultrastructure ; ErbB Receptors/metabolism ; Female ; Golgi Apparatus/drug effects ; Golgi Apparatus/metabolism ; Golgi Apparatus/ultrastructure ; Humans ; Hydroxychloroquine/pharmacology ; Lysosomes/drug effects ; Lysosomes/metabolism ; Lysosomes/ultrastructure ; Macrolides/pharmacology ; Membrane Fusion/drug effects ; Mice, Inbred C57BL ; Proteolysis/drug effects ; Sequestosome-1 Protein/metabolism
Chemical Substances	Macrolides ; Sequestosome-1 Protein ; Sqstm1 protein, mouse ; Hydroxychloroquine (4QWG6N8QKH) ; Chloroquine (886U3H6UFF) ; bafilomycin A1 (88899-55-2) ; ErbB Receptors (EC 2.7.10.1)
Keywords	covid19
Language	English
Publishing date	2018-07-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2018.1474314
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