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1. Heterogeneous bone-marrow stromal progenitors drive myelofibrosis via a druggable alarmin axis

Author

Leimkühler, Nils B., primary, Gleitz, Hélène F.E., additional, Ronghui, Li, additional, Snoeren, Inge A.M., additional, Fuchs, Stijn N.R., additional, Nagai, James S., additional, Banjanin, Bella, additional, Lam, King H., additional, Vogl, Thomas, additional, Kuppe, Christoph, additional, Stalmann, Ursula S.A., additional, Büsche, Guntram, additional, Kreipe, Hans, additional, Gütgemann, Ines, additional, Krebs, Philippe, additional, Banz, Yara, additional, Boor, Peter, additional, Tai, Evelyn Wing-Yin, additional, Brümmendorf, Tim H., additional, Koschmieder, Steffen, additional, Crysandt, Martina, additional, Bindels, Eric, additional, Kramann, Rafael, additional, Costa, Ivan G., additional, and Schneider, Rebekka K., additional

Published
2021
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2. Gli1+ Mesenchymal Stromal Cells Are a Key Driver of Bone Marrow Fibrosis and an Important Cellular Therapeutic Target

Author

Schneider, Rebekka K., primary, Mullally, Ann, additional, Dugourd, Aurelien, additional, Peisker, Fabian, additional, Hoogenboezem, Remco, additional, Van Strien, Paulina M.H., additional, Bindels, Eric M., additional, Heckl, Dirk, additional, Büsche, Guntram, additional, Fleck, David, additional, Müller-Newen, Gerhard, additional, Wongboonsin, Janewit, additional, Ventura Ferreira, Monica, additional, Puelles, Victor G., additional, Saez-Rodriguez, Julio, additional, Ebert, Benjamin L., additional, Humphreys, Benjamin D., additional, and Kramann, Rafael, additional

Published
2018
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3. Mesenchymal Stem Cells in Fibrotic Disease

Author

El Agha, Elie, primary, Kramann, Rafael, additional, Schneider, Rebekka K., additional, Li, Xiaokun, additional, Seeger, Werner, additional, Humphreys, Benjamin D., additional, and Bellusci, Saverio, additional

Published
2017
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4. Gli1 + Mesenchymal Stromal Cells Are a Key Driver of Bone Marrow Fibrosis and an Important Cellular Therapeutic Target

Author

Schneider, Rebekka K., primary, Mullally, Ann, additional, Dugourd, Aurelien, additional, Peisker, Fabian, additional, Hoogenboezem, Remco, additional, Van Strien, Paulina M.H., additional, Bindels, Eric M., additional, Heckl, Dirk, additional, Büsche, Guntram, additional, Fleck, David, additional, Müller-Newen, Gerhard, additional, Wongboonsin, Janewit, additional, Ventura Ferreira, Monica, additional, Puelles, Victor G., additional, Saez-Rodriguez, Julio, additional, Ebert, Benjamin L., additional, Humphreys, Benjamin D., additional, and Kramann, Rafael, additional

Published
2017
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5. Adventitial MSC-like Cells Are Progenitors of Vascular Smooth Muscle Cells and Drive Vascular Calcification in Chronic Kidney Disease

Author

Kramann, Rafael, primary, Goettsch, Claudia, additional, Wongboonsin, Janewit, additional, Iwata, Hiroshi, additional, Schneider, Rebekka K., additional, Kuppe, Christoph, additional, Kaesler, Nadine, additional, Chang-Panesso, Monica, additional, Machado, Flavia G., additional, Gratwohl, Susannah, additional, Madhurima, Kaushal, additional, Hutcheson, Joshua D., additional, Jain, Sanjay, additional, Aikawa, Elena, additional, and Humphreys, Benjamin D., additional

Published
2016
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7. Perivascular Gli1+Progenitors Are Key Contributors to Injury-Induced Organ Fibrosis

Author

Kramann, Rafael, Schneider, Rebekka K., DiRocco, Derek P., Machado, Flavia, Fleig, Susanne, Bondzie, Philip A., Henderson, Joel M., Ebert, Benjamin L., and Humphreys, Benjamin D.

Abstract

Mesenchymal stem cells (MSCs) reside in the perivascular niche of many organs, including kidney, lung, liver, and heart, although their roles in these tissues are poorly understood. Here, we demonstrate that Gli1 marks perivascular MSC-like cells that substantially contribute to organ fibrosis. In vitro, Gli1+cells express typical MSC markers, exhibit trilineage differentiation capacity, and possess colony-forming activity, despite constituting a small fraction of the platelet-derived growth factor-β (PDGFRβ)+cell population. Genetic lineage tracing analysis demonstrates that tissue-resident, but not circulating, Gli1+cells proliferate after kidney, lung, liver, or heart injury to generate myofibroblasts. Genetic ablation of these cells substantially ameliorates kidney and heart fibrosis and preserves ejection fraction in a model of induced heart failure. These findings implicate perivascular Gli1+MSC-like cells as a major cellular origin of organ fibrosis and demonstrate that these cells may be a relevant therapeutic target to prevent solid organ dysfunction after injury.

Published
2015
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8. SARS-CoV-2 infects the human kidney and drives fibrosis in kidney organoids

Author

Jansen, Jitske, Reimer, Katharina Charlotte, Nagai, James Shiniti, Varghese, Finny S., Overheul, Gijs J., de Beer, Marit, Roverts, Rona, Daviran, Deniz, Fermin, Liline A.S., Willemsen, Brigith, Beukenboom, Marcel, Djudjaj, Sonja, von Stillfried, Saskia, van Eijk, Larissa E., Mastik, Mirjam, Bulthuis, Marian, Dunnen, Wilfred den, van Goor, Harry, Hillebrands, Jan-Luuk, Triana, Sergio Heli, Alexandrov, Theodore, Timm, Marie-Cherelle, Tideman van den Berge, Bartholomeus, van den Broek, Martijn, Nlandu, Quincy, Heijnert, Joelle, Bindels, Eric M.J., Hoogenboezem, Remco M., Mooren, Fieke, Kuppe, Christoph, Miesen, Pascal, Grünberg, Katrien, Ijzermans, Ties, Steenbergen, Eric J., Czogalla, Jan, Schreuder, Michiel F., Sommerdijk, Nico, Akiva, Anat, Boor, Peter, Puelles, Victor G., Floege, Jürgen, Huber, Tobias B., van Rij, Ronald P., Costa, Ivan G., Schneider, Rebekka K., Smeets, Bart, and Kramann, Rafael

Abstract

Kidney failure is frequently observed during and after COVID-19, but it remains elusive whether this is a direct effect of the virus. Here, we report that SARS-CoV-2 directly infects kidney cells and is associated with increased tubule-interstitial kidney fibrosis in patient autopsy samples. To study direct effects of the virus on the kidney independent of systemic effects of COVID-19, we infected human induced pluripotent stem cell-derived kidney organoids with SARS-CoV-2. Single cell RNA-sequencing indicated injury and dedifferentiation of infected cells with activation of pro-fibrotic signaling pathways. Importantly, SARS-CoV-2 infection also led to increased collagen 1 protein expression in organoids. A SARS-CoV-2 protease inhibitor was able to ameliorate the infection of kidney cells by SARS-CoV-2. Our results suggest that SARS-CoV-2 can directly infect kidney cells and induce cell injury with subsequent fibrosis. These data could explain both acute kidney injury in COVID-19 patients and the development of chronic kidney disease in Long-COVID.

Published
2021
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9. Gli1+Mesenchymal Stromal Cells Are a Key Driver of Bone Marrow Fibrosis and an Important Cellular Therapeutic Target

Author

Schneider, Rebekka K., Mullally, Ann, Dugourd, Aurelien, Peisker, Fabian, Hoogenboezem, Remco, Van Strien, Paulina M.H., Bindels, Eric M., Heckl, Dirk, Büsche, Guntram, Fleck, David, Müller-Newen, Gerhard, Wongboonsin, Janewit, Ventura Ferreira, Monica, Puelles, Victor G., Saez-Rodriguez, Julio, Ebert, Benjamin L., Humphreys, Benjamin D., and Kramann, Rafael

Published
2018
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10. Gli1+Mesenchymal Stromal Cells Are a Key Driver of Bone Marrow Fibrosis and an Important Cellular Therapeutic Target

Author

Schneider, Rebekka K., Mullally, Ann, Dugourd, Aurelien, Peisker, Fabian, Hoogenboezem, Remco, Van Strien, Paulina M.H., Bindels, Eric M., Heckl, Dirk, Büsche, Guntram, Fleck, David, Müller-Newen, Gerhard, Wongboonsin, Janewit, Ventura Ferreira, Monica, Puelles, Victor G., Saez-Rodriguez, Julio, Ebert, Benjamin L., Humphreys, Benjamin D., and Kramann, Rafael

Abstract

Bone marrow fibrosis (BMF) develops in various hematological and non-hematological conditions and is a central pathological feature of myelofibrosis. Effective cell-targeted therapeutics are needed, but the cellular origin of BMF remains elusive. Here, we show using genetic fate tracing in two murine models of BMF that Gli1+mesenchymal stromal cells (MSCs) are recruited from the endosteal and perivascular niche to become fibrosis-driving myofibroblasts in the bone marrow. Genetic ablation of Gli1+cells abolished BMF and rescued bone marrow failure. Pharmacological targeting of Gli proteins with GANT61 inhibited Gli1+cell expansion and myofibroblast differentiation and attenuated fibrosis severity. The same pathway is also active in human BMF, and Gli1 expression in BMF significantly correlates with the severity of the disease. In addition, GANT61 treatment reduced the myofibroblastic phenotype of human MSCs isolated from patients with BMF, suggesting that targeting of Gli proteins could be a relevant therapeutic strategy.

Published
2017
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11. SARS-CoV-2 infects the human kidney and drives fibrosis in kidney organoids.

Author

Jansen J, Reimer KC, Nagai JS, Varghese FS, Overheul GJ, de Beer M, Roverts R, Daviran D, Fermin LAS, Willemsen B, Beukenboom M, Djudjaj S, von Stillfried S, van Eijk LE, Mastik M, Bulthuis M, Dunnen WD, van Goor H, Hillebrands JL, Triana SH, Alexandrov T, Timm MC, van den Berge BT, van den Broek M, Nlandu Q, Heijnert J, Bindels EMJ, Hoogenboezem RM, Mooren F, Kuppe C, Miesen P, Grünberg K, Ijzermans T, Steenbergen EJ, Czogalla J, Schreuder MF, Sommerdijk N, Akiva A, Boor P, Puelles VG, Floege J, Huber TB, van Rij RP, Costa IG, Schneider RK, Smeets B, and Kramann R

Subjects
Fibrosis, Humans, Kidney, Organoids pathology, Post-Acute COVID-19 Syndrome, COVID-19 complications, SARS-CoV-2
Abstract

Kidney failure is frequently observed during and after COVID-19, but it remains elusive whether this is a direct effect of the virus. Here, we report that SARS-CoV-2 directly infects kidney cells and is associated with increased tubule-interstitial kidney fibrosis in patient autopsy samples. To study direct effects of the virus on the kidney independent of systemic effects of COVID-19, we infected human-induced pluripotent stem-cell-derived kidney organoids with SARS-CoV-2. Single-cell RNA sequencing indicated injury and dedifferentiation of infected cells with activation of profibrotic signaling pathways. Importantly, SARS-CoV-2 infection also led to increased collagen 1 protein expression in organoids. A SARS-CoV-2 protease inhibitor was able to ameliorate the infection of kidney cells by SARS-CoV-2. Our results suggest that SARS-CoV-2 can directly infect kidney cells and induce cell injury with subsequent fibrosis. These data could explain both acute kidney injury in COVID-19 patients and the development of chronic kidney disease in long COVID., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2021 The Author(s). Published by Elsevier Inc. All rights reserved.)

Published
2022
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