دورية أكاديمية
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Disruption of the Rab7-Dependent Final Common Pathway of Endosomal and Autophagic Processing Results in a Severe Podocytopathy.

التفاصيل البيبلوغرافية
العنوان: Disruption of the Rab7-Dependent Final Common Pathway of Endosomal and Autophagic Processing Results in a Severe Podocytopathy.
المؤلفون: Vöing K; Department of Internal Medicine and Nephrology, University Hospital of Münster, Medical Clinic D, Munster, Germany., Michgehl U; Department of Internal Medicine and Nephrology, University Hospital of Münster, Medical Clinic D, Munster, Germany., Mertens ND; Department of Internal Medicine and Nephrology, University Hospital of Münster, Medical Clinic D, Munster, Germany., Picciotto C; Department of Internal Medicine and Nephrology, University Hospital of Münster, Medical Clinic D, Munster, Germany., Maywald ML; Department of Internal Medicine and Nephrology, University Hospital of Münster, Medical Clinic D, Munster, Germany., Goretzko J; Research Group Regulatory Mechanisms of Inflammation, Institute of Medical Biochemistry, Centre for Molecular Biology of Inflammation, University of Muenster, Muenster, Germany., Waimann S; Department of Internal Medicine and Nephrology, University Hospital of Münster, Medical Clinic D, Munster, Germany., Gilhaus K; Department of Internal Medicine and Nephrology, University Hospital of Münster, Medical Clinic D, Munster, Germany., Rogg M; Institute of Surgical Pathology, Faculty of Medicine, Medical Center-University of Freiburg, Freiburg, Germany.; Freiburg Institute for Advanced Studies (FRIAS), University of Freiburg, Freiburg, Germany., Schell C; Institute of Surgical Pathology, Faculty of Medicine, Medical Center-University of Freiburg, Freiburg, Germany.; Freiburg Institute for Advanced Studies (FRIAS), University of Freiburg, Freiburg, Germany., Klingauf J; Institute of Medical Physics and Biophysics, University of Muenster, Muenster, Germany., Tsytsyura Y; Institute of Medical Physics and Biophysics, University of Muenster, Muenster, Germany., Hansen U; Institute for Musculoskeletal Medicine (IMM), University of Muenster, Muenster, Germany., van Marck V; Department of Pathology, University Hospital Muenster Muenster, Germany., Edinger AL; Department of Developmental & Cell Biology, University of California, Irvine, California., Vollenbröker B; Department of Internal Medicine and Nephrology, University Hospital of Münster, Medical Clinic D, Munster, Germany., Rescher U; Research Group Regulatory Mechanisms of Inflammation, Institute of Medical Biochemistry, Centre for Molecular Biology of Inflammation, University of Muenster, Muenster, Germany., Braun DA; Department of Internal Medicine and Nephrology, University Hospital of Münster, Medical Clinic D, Munster, Germany., George B; Department of Internal Medicine and Nephrology, University Hospital of Münster, Medical Clinic D, Munster, Germany., Weide T; Department of Internal Medicine and Nephrology, University Hospital of Münster, Medical Clinic D, Munster, Germany., Pavenstädt H; Department of Internal Medicine and Nephrology, University Hospital of Münster, Medical Clinic D, Munster, Germany.
المصدر: Journal of the American Society of Nephrology : JASN [J Am Soc Nephrol] 2023 Jul 01; Vol. 34 (7), pp. 1191-1206. Date of Electronic Publication: 2023 Apr 05.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Wolters Kluwer Health, on behalf of the American Society of Nephrology Country of Publication: United States NLM ID: 9013836 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1533-3450 (Electronic) Linking ISSN: 10466673 NLM ISO Abbreviation: J Am Soc Nephrol Subsets: MEDLINE
أسماء مطبوعة: Publication: 2023- : Hagerstown, MD : Wolters Kluwer Health, on behalf of the American Society of Nephrology
Original Publication: Baltimore, MD : Williams & Wilkins, c1990-
مواضيع طبية MeSH: Kidney Glomerulus*/pathology , Podocytes*/metabolism, Animals ; Mice ; Humans ; Endosomes ; Drosophila ; Kidney ; Mammals
مستخلص: Significance Statement: Endocytosis, recycling, and degradation of proteins are essential functions of mammalian cells, especially for terminally differentiated cells with limited regeneration rates and complex morphology, such as podocytes. To improve our understanding on how disturbances of these trafficking pathways are linked to podocyte depletion and slit diaphragm (SD) injury, the authors explored the role of the small GTPase Rab7, which is linked to endosomal, lysosomal, and autophagic pathways, using as model systems mice and Drosophila with podocyte-specific or nephrocyte-specific loss of Rab7, and a human podocyte cell line depleted for Rab7. Their findings point to maturation and fusion events during endolysosomal and autophagic maturation as key processes for podocyte homeostasis and function and identify altered lysosomal pH values as a putative novel mechanism for podocytopathies.
Background: Endocytosis, recycling, and degradation of proteins are essential functions of mammalian cells, especially for terminally differentiated cells with limited regeneration rates, such as podocytes. How disturbances within these trafficking pathways may act as factors in proteinuric glomerular diseases is poorly understood.
Methods: To explore how disturbances in trafficking pathways may act as factors in proteinuric glomerular diseases, we focused on Rab7, a highly conserved GTPase that controls the homeostasis of late endolysosomal and autophagic processes. We generated mouse and Drosophila in vivo models lacking Rab7 exclusively in podocytes or nephrocytes, and performed histologic and ultrastructural analyses. To further investigate Rab7 function on lysosomal and autophagic structures, we used immortalized human cell lines depleted for Rab7.
Results: Depletion of Rab7 in mice, Drosophila , and immortalized human cell lines resulted in an accumulation of diverse vesicular structures resembling multivesicular bodies, autophagosomes, and autoendolysosomes. Mice lacking Rab7 developed a severe and lethal renal phenotype with early-onset proteinuria and global or focal segmental glomerulosclerosis, accompanied by an altered distribution of slit diaphragm proteins. Remarkably, structures resembling multivesicular bodies began forming within 2 weeks after birth, prior to the glomerular injuries. In Drosophila nephrocytes, Rab7 knockdown resulted in the accumulation of vesicles and reduced slit diaphragms. In vitro , Rab7 knockout led to similar enlarged vesicles and altered lysosomal pH values, accompanied by an accumulation of lysosomal marker proteins.
Conclusions: Disruption within the final common pathway of endocytic and autophagic processes may be a novel and insufficiently understood mechanism regulating podocyte health and disease.
(Copyright © 2023 by the American Society of Nephrology.)
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تواريخ الأحداث: Date Created: 20230406 Date Completed: 20230705 Latest Revision: 20240702
رمز التحديث: 20240702
مُعرف محوري في PubMed: PMC10356157
DOI: 10.1681/ASN.0000000000000126
PMID: 37022133
قاعدة البيانات: MEDLINE
الوصف
تدمد:1533-3450
DOI:10.1681/ASN.0000000000000126