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143 results on '"Etzrodt, Martin"'

3. Early myeloid lineage choice is not initiated by random PU.1 to GATA1 protein ratios

Author

Hoppe, Philipp S., Schwarzfischer, Michael, Loeffler, Dirk, Kokkaliaris, Konstantinos D., Hilsenbeck, Oliver, Moritz, Nadine, Endele, Max, Filipczyk, Adam, Gambardella, Adriana, Ahmed, Nouraiz, Etzrodt, Martin, Coutu, Daniel L., Rieger, Michael A., Marr, Carsten, Strasser, Michael K., Schauberger, Bernhard, Burtscher, Ingo, Ermakova, Olga, Burger, Antje, Lickert, Heiko, Nerlov, Claus, Theis, Fabian J., and Schroeder, Timm

Subjects
Gene expression -- Analysis, Cell populations -- Research -- Analysis, Transcription factors -- Research -- Analysis, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

The mechanisms underlying haematopoietic lineage decisions remain disputed. Lineage-affiliated transcription factors (1,2) with the capacity for lineage reprogramming (3), positive auto-regulation (4,5) and mutual inhibition (6,7) have been described as [...]

Published
2016

4. Origins of tumor-associated macrophages and neutrophils

Author

Cortez-Retamozo, Virna, Etzrodt, Martin, Newton, Andita, Rauch, Philipp J., Chudnovskiy, Aleksey, Berger, Cedric, Ryan, Russell J. H., Iwamoto, Yoshiko, Marinelli, Brett, Gorbatov, Rostic, Forghani, Reza, Novobrantseva, Tatiana I., Koteliansky, Victor, Figueiredo, Jose-Luiz, Chen, John W., Anderson, Daniel G., Nahrendorf, Matthias, Swirski, Filip K., Weissleder, Ralph, and Pittet, Mikael J.

Published
2012

5. Blood stem cell PU.1 upregulation is a consequence of differentiation without fast autoregulation

Author

Ahmed, Nouraiz, primary, Etzrodt, Martin, additional, Dettinger, Philip, additional, Kull, Tobias, additional, Loeffler, Dirk, additional, Hoppe, Philipp S., additional, Chavez, James S., additional, Zhang, Yang, additional, Camargo Ortega, Germán, additional, Hilsenbeck, Oliver, additional, Nakajima, Hideaki, additional, Pietras, Eric M., additional, and Schroeder, Timm, additional

Published
2021
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7. Unchaining Collective Intelligence for Science, Research, and Technology Development by Blockchain-Boosted Community Participation

Author

Ducrée, Jens, primary, Etzrodt, Martin, additional, Bartling, Sönke, additional, Walshe, Ray, additional, Harrington, Tomás, additional, Wittek, Neslihan, additional, Posth, Sebastian, additional, Wittek, Kevin, additional, Ionita, Andrei, additional, Prinz, Wolfgang, additional, Kogias, Dimitrios, additional, Paixão, Tiago, additional, Peterfi, Iosif, additional, and Lawton, James, additional

Published
2021
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8. Myocardial infarction accelerates atherosclerosis

Author

Dutta, Partha, Courties, Gabriel, Wei, Ying, Leuschner, Florian, Gorbatov, Rostic, Robbins, Clinton S., Iwamoto, Yoshiko, Thompson, Brian, Carlson, Alicia L., Heidt, Timo, Majmudar, Maulik D., Lasitschka, Felix, Etzrodt, Martin, Waterman, Peter, Waring, Michael T., Chicoine, Adam T., van der Laan, Anja M., Niessen, Hans W. M., Piek, Jan J., Rubin, Barry B., Butany, Jagdish, Stone, James R., Katus, Hugo A., Murphy, Sabina A., Morrow, David A., Sabatine, Marc S., Vinegoni, Claudio, Moskowitz, Michael A., Pittet, Mikael J., Libby, Peter, Lin, Charles P., Swirski, Filip K., Weissleder, Ralph, and Nahrendorf, Matthias

Published
2012
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9. Identification of splenic reservoir monocytes and their deployment to inflammatory sites

Author

Swirski, Filip K., Nahrendorf, Matthias, Etzrodt, Martin, Wildgruber, Moritz, Cortez-Retamozo, Virna, Panizzi, Peter, Figueiredo, Jose-Luiz, Kohler, Rainer H., Chudnovskiy, Aleksey, Waterman, Peter, Aikawa, Elena, Mempel, Thorsten R., Libby, Peter, Weissleder, Ralph, and Pittet, Mikael J.

Subjects
Monocytes -- Properties, Spleen -- Properties, Myocardial ischemia -- Development and progression, Science and technology
Abstract

A current paradigm states that monocytes circulate freely and patrol blood vessels but differentiate irreversibly into dendritic cells (DCs) or macrophages upon tissue entry. Here we show that bona fide undifferentiated monocytes reside in the spleen and outnumber their equivalents in circulation. The reservoir monocytes assemble in clusters in the cords of the subcapsular red pulp and are distinct from macrophages and DCs. In response to ischemic myocardial injury, splenic monocytes increase their motility, exit the spleen en masse, accumulate in injured tissue, and participate in wound healing. These observations uncover a role for the spleen as a site for storage and rapid deployment of monocytes and identify splenic monocytes as a resource that the body exploits to regulate inflammation.

Published
2009

10. A Novel GATA2 Protein Reporter Mouse Reveals Hematopoietic Progenitor Cell Types

Author

Ahmed, Nouraiz, Kunz, Leo, Hoppe, Philipp S., Loeffler, Dirk, Etzrodt, Martin, Ortega, Germán C., Hilsenbeck, Oliver, Anastassiadis, Konstantinos, and Schroeder, Timm

Subjects
Development, Transcription Factor Networks, Cell fate, GATA2, Monocyte and mast cell lineage, Hematopoietic stem and progenitor cells, Transgenic mouse, Fluorescent protein
Abstract

In this study, Schroeder and colleagues generated a GATA2VENUS protein reporter mouse line with normal GATA2 expression and localization, e.g., in the urogenital, auditory, and nervous systems. The authors also profiled GATA2 protein expression across hematopoietic cell types, identified heterogeneity within populations currently assumed to be homogeneous, and demonstrate an earlier monocyte-mast cell lineage bifurcation point., Stem Cell Reports, 15 (2), ISSN:2213-6711

Published
2020

12. Angiotensin II Drives the Production of Tumor-Promoting Macrophages

Author

Cortez-Retamozo, Virna, Etzrodt, Martin, Newton, Andita, Ryan, Russell, Pucci, Ferdinando, Sio, Selena W., Kuswanto, Wilson, Rauch, Philipp J., Chudnovskiy, Aleksey, Iwamoto, Yoshiko, Kohler, Rainer, Marinelli, Brett, Gorbatov, Rostic, Wojtkiewicz, Gregory, Panizzi, Peter, Mino-Kenudson, Mari, Forghani, Reza, Figueiredo, Jose-Luiz, Chen, John W., Xavier, Ramnik, Swirski, Filip K., Nahrendorf, Matthias, Weissleder, Ralph, and Pittet, Mikael J.

Published
2013
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13. Innate Response Activator B Cells Protect Against Microbial Sepsis

Author

Rauch, Philipp J., Chudnovskiy, Aleksey, Robbins, Clinton S., Weber, Georg F., Etzrodt, Martin, Hilgendorf, Ingo, Tiglao, Elizabeth, Figueiredo, Jose-Luiz, Iwamoto, Yoshiko, Theurl, Igor, Gorbatov, Rostic, Waring, Michael T., Chicoine, Adam T., Mouded, Maid, Pittet, Mikael J., Nahrendorf, Matthias, Weissleder, Ralph, and Swirski, Filip K.

Published
2012
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18. Advancing science through incentivizing collaboration, not competition

Author

Etzrodt, Martin

Abstract

Here I highlight some of the current challenges for communication and attribution of scientific achievements relying on a centralized publisher controlled system. I propose to establish decentralized, trusted platforms for the dissemination of scientific information and attribution, which will lead to a more rapid pace of innovation.

Published
2018
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29. NfκB signaling dynamics and their target genes differ between mouse blood cell types and induce distinct cell behavior

Author

Kull, Tobias, Wehling, Arne, Etzrodt, Martin, Auler, Markus, Dettinger, Philip, Aceto, Nicola, and Schroeder, Timm

Abstract

Cells can use signaling pathway activity over time (i.e., dynamics) to control cell fates. However, little is known about the potential existence and function of signaling dynamics in primary hematopoietic stem and progenitor cells (HSPCs). Here, we use time-lapse imaging and tracking of single murine HSPCs from GFP-p65/H2BmCherry reporter mice to quantify their nuclear factor κB (NfκB) activity dynamics in response to TNFα and IL1β. We find response dynamics to be heterogeneous between individual cells, with cell type specific dynamics distributions. Transcriptome sequencing of single cells physically isolated after live dynamics quantification shows activation of different target gene programs in cells with different dynamics. Finally, artificial induction of oscillatory NfκB activity causes changes in GMP behavior. Thus, HSPC behavior can be influenced by signaling dynamics, which are tightly regulated during hematopoietic differentiation and enable cell type specific responses to the same signaling inputs.

Published
2024
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30. A microfluidic platform for dynamic cell culture and quantitative time-lapse imaging of non-adherent cells

Author

Dettinger, Philip, primary, Etzrodt, Martin, additional, Frank, Tino, additional, Ahmed, Nouraiz, additional, Reimann, Andreas, additional, Trenzinger, Christoph, additional, Skylaki, Laura, additional, Hilsenbeck, Oliver, additional, Loeffler, Dirk, additional, Kokkaliaris, Konstantinos, additional, Tay, Savas, additional, and Schroeder, Timm, additional

Published
2016
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31. Software tools for single-cell tracking and quantification of cellular and molecular properties

Author

Hilsenbeck, Oliver, primary, Schwarzfischer, Michael, additional, Skylaki, Stavroula, additional, Schauberger, Bernhard, additional, Hoppe, Philipp S, additional, Loeffler, Dirk, additional, Kokkaliaris, Konstantinos D, additional, Hastreiter, Simon, additional, Skylaki, Eleni, additional, Filipczyk, Adam, additional, Strasser, Michael, additional, Buggenthin, Felix, additional, Feigelman, Justin S, additional, Krumsiek, Jan, additional, van den Berg, Adrianus J J, additional, Endele, Max, additional, Etzrodt, Martin, additional, Marr, Carsten, additional, Theis, Fabian J, additional, and Schroeder, Timm, additional

Published
2016
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32. Seamless Combination of Fluorescence-Activated Cell Sorting and Hanging-Drop Networks for Individual Handling and Culturing of Stem Cells and Microtissue Spheroids

Author

Birchler, Axel, primary, Berger, Mischa, additional, Jäggin, Verena, additional, Lopes, Telma, additional, Etzrodt, Martin, additional, Misun, Patrick Mark, additional, Pena-Francesch, Maria, additional, Schroeder, Timm, additional, Hierlemann, Andreas, additional, and Frey, Olivier, additional

Published
2016
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33. Origins of tumor-associated macrophages and neutrophils

Author

Massachusetts Institute of Technology. Department of Chemical Engineering, Koch Institute for Integrative Cancer Research at MIT, Anderson, Daniel Griffith, Cortez-Retamozo, Virna, Etzrodt, Martin, Newton, Andita, Rauch, Philipp J., Chudnovskiy, Aleksey, Berger, Cedric, Ryan, Russell J. H., Iwamoto, Yoshiko, Marinelli, Brett, Gorbatov, Rostic, Forghani, Reza, Novobrantseva, Tatiana I., Kotelianski, Victor E., Figueiredo, Jose Luiz, Chen, John W., Nahrendorf, Matthias, Swirski, Filip K., Weissleder, Ralph, Pittet, Mikael J., Massachusetts Institute of Technology. Department of Chemical Engineering, Koch Institute for Integrative Cancer Research at MIT, Anderson, Daniel Griffith, Cortez-Retamozo, Virna, Etzrodt, Martin, Newton, Andita, Rauch, Philipp J., Chudnovskiy, Aleksey, Berger, Cedric, Ryan, Russell J. H., Iwamoto, Yoshiko, Marinelli, Brett, Gorbatov, Rostic, Forghani, Reza, Novobrantseva, Tatiana I., Kotelianski, Victor E., Figueiredo, Jose Luiz, Chen, John W., Nahrendorf, Matthias, Swirski, Filip K., Weissleder, Ralph, and Pittet, Mikael J.

Abstract

Tumor-associated macrophages (TAMs) and tumor-associated neutrophils (TANs) can control cancer growth and exist in almost all solid neoplasms. The cells are known to descend from immature monocytic and granulocytic cells, respectively, which are produced in the bone marrow. However, the spleen is also a recently identified reservoir of monocytes, which can play a significant role in the inflammatory response that follows acute injury. Here, we evaluated the role of the splenic reservoir in a genetic mouse model of lung adenocarcinoma driven by activation of oncogenic Kras and inactivation of p53. We found that high numbers of TAM and TAN precursors physically relocated from the spleen to the tumor stroma, and that recruitment of tumor-promoting spleen-derived TAMs required signaling of the chemokine receptor CCR2. Also, removal of the spleen, either before or after tumor initiation, reduced TAM and TAN responses significantly and delayed tumor growth. The mechanism by which the spleen was able to maintain its reservoir capacity throughout tumor progression involved, in part, local accumulation in the splenic red pulp of typically rare extramedullary hematopoietic stem and progenitor cells, notably granulocyte and macrophage progenitors, which produced CD11b[superscript +] Ly-6C[superscript hi] monocytic and CD11b[superscript +] Ly-6G[superscript hi] granulocytic cells locally. Splenic granulocyte and macrophage progenitors and their descendants were likewise identified in clinical specimens. The present study sheds light on the origins of TAMs and TANs, and positions the spleen as an important extramedullary site, which can continuously supply growing tumors with these cells.

Published
2014

35. Regulation of Monocyte Functional Heterogeneity by miR-146a and Relb

Author

Etzrodt, Martin, Cortez-Retamozo, Virna, Newton, Andita, Zhao, Jimmy, Ng, Aylwin, Wildgruber, Moritz, Romero, Pedro, Wurdinger, Thomas, Xavier, Ramnik, Geissmann, Frédéric, Meylan, Etienne, Nahrendorf, Matthias, Swirski, Filip K., Baltimore, David, Weissleder, Ralph, Pittet, Mikael, Etzrodt, Martin, Cortez-Retamozo, Virna, Newton, Andita, Zhao, Jimmy, Ng, Aylwin, Wildgruber, Moritz, Romero, Pedro, Wurdinger, Thomas, Xavier, Ramnik, Geissmann, Frédéric, Meylan, Etienne, Nahrendorf, Matthias, Swirski, Filip K., Baltimore, David, Weissleder, Ralph, and Pittet, Mikael

Abstract

info:eu-repo/semantics/published

Published
2012

38. Demyelinating Diseases: Myeloperoxidase as an Imaging Biomarker and Therapeutic Target

Author

Forghani, Reza, primary, Wojtkiewicz, Gregory R., additional, Zhang, Yinian, additional, Seeburg, Daniel, additional, Bautz, Benjamin R. M., additional, Pulli, Benjamin, additional, Milewski, Andrew R., additional, Atkinson, Wendy L., additional, Iwamoto, Yoshiko, additional, Zhang, Elizabeth R., additional, Etzrodt, Martin, additional, Rodriguez, Elisenda, additional, Robbins, Clinton S., additional, Swirski, Filip K., additional, Weissleder, Ralph, additional, and Chen, John W., additional

Published
2012
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39. Regulation of Monocyte Functional Heterogeneity by miR-146a and Relb

Author

Etzrodt, Martin, primary, Cortez-Retamozo, Virna, additional, Newton, Andita, additional, Zhao, Jimmy, additional, Ng, Aylwin, additional, Wildgruber, Moritz, additional, Romero, Pedro, additional, Wurdinger, Thomas, additional, Xavier, Ramnik, additional, Geissmann, Frederic, additional, Meylan, Etienne, additional, Nahrendorf, Matthias, additional, Swirski, Filip K., additional, Baltimore, David, additional, Weissleder, Ralph, additional, and Pittet, Mikael J., additional

Published
2012
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40. Extramedullary Hematopoiesis Generates Ly-6C high Monocytes That Infiltrate Atherosclerotic Lesions

Author

Robbins, Clinton S., primary, Chudnovskiy, Aleksey, additional, Rauch, Philipp J., additional, Figueiredo, Jose-Luiz, additional, Iwamoto, Yoshiko, additional, Gorbatov, Rostic, additional, Etzrodt, Martin, additional, Weber, Georg F., additional, Ueno, Takuya, additional, van Rooijen, Nico, additional, Mulligan-Kehoe, Mary Jo, additional, Libby, Peter, additional, Nahrendorf, Matthias, additional, Pittet, Mikael J., additional, Weissleder, Ralph, additional, and Swirski, Filip K., additional

Published
2012
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42. Early myeloid lineage choice is not initiated by random PU.1 to GATA1 protein ratios

Author

Hoppe, Philipp S., Schwarzfischer, Michael, Loeffler, Dirk, Kokkaliaris, Konstantinos D., Hilsenbeck, Oliver, Moritz, Nadine, Endele, Max, Filipczyk, Adam, Gambardella, Adriana, Ahmed, Nouraiz, Etzrodt, Martin, Coutu, Daniel L., Rieger, Michael A., Marr, Carsten, Strasser, Michael K., Schauberger, Bernhard, Burtscher, Ingo, Ermakova, Olga, Bürger, Antje, Lickert, Heiko, Nerlov, Claus, Theis, Fabian J., and Schroeder, Timm

Abstract

The mechanisms underlying haematopoietic lineage decisions remain disputed. Lineage-affiliated transcription factors with the capacity for lineage reprogramming, positive auto-regulation and mutual inhibition have been described as being expressed in uncommitted cell populations. This led to the assumption that lineage choice is cell-intrinsically initiated and determined by stochastic switches of randomly fluctuating cross-antagonistic transcription factors. However, this hypothesis was developed on the basis of RNA expression data from snapshot and/or population-averaged analyses. Alternative models of lineage choice therefore cannot be excluded. Here we use novel reporter mouse lines and live imaging for continuous single-cell long-term quantification of the transcription factors GATA1 and PU.1 (also known as SPI1). We analyse individual haematopoietic stem cells throughout differentiation into megakaryocytic–erythroid and granulocytic–monocytic lineages. The observed expression dynamics are incompatible with the assumption that stochastic switching between PU.1 and GATA1 precedes and initiates megakaryocytic–erythroid versus granulocytic–monocytic lineage decision-making. Rather, our findings suggest that these transcription factors are only executing and reinforcing lineage choice once made. These results challenge the current prevailing model of early myeloid lineage choice.

Published
2017
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43. Different Capacity of Monocyte Subsets to Phagocytose Iron-Oxide Nanoparticles

Author

Settles, Marcus, primary, Etzrodt, Martin, additional, Kosanke, Katja, additional, Schiemann, Matthias, additional, Zimmermann, Alexander, additional, Meier, Reinhard, additional, Braren, Rickmer, additional, Huber, Armin, additional, Rummeny, Ernst J., additional, Weissleder, Ralph, additional, Swirski, Filip K., additional, and Wildgruber, Moritz, additional

Published
2011
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45. Behavior of Endogenous Tumor-Associated Macrophages Assessed In Vivo Using a Functionalized Nanoparticle

Author

Leimgruber, Antoine, primary, Berger, Cedric, additional, Cortez-Retamozo, Virna, additional, Etzrodt, Martin, additional, Newton, Andita P., additional, Waterman, Peter, additional, Figueiredo, Jose Luiz, additional, Kohler, Rainer H., additional, Elpek, Natalie, additional, Mempel, Thorsten R., additional, Swirski, Filip K., additional, Nahrendorf, Matthias, additional, Weissleder, Ralph, additional, and Pittet, Mikael J., additional

Published
2009
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48. Regulation of Monocyte Functional Heterogeneity by miR-146aand Relb

Author

Etzrodt, Martin, Cortez-Retamozo, Virna, Newton, Andita, Zhao, Jimmy, Ng, Aylwin, Wildgruber, Moritz, Romero, Pedro, Wurdinger, Thomas, Xavier, Ramnik, Geissmann, Frederic, Meylan, Etienne, Nahrendorf, Matthias, Swirski, Filip K., Baltimore, David, Weissleder, Ralph, and Pittet, Mikael J.

Abstract

Monocytes serve as a central defense system against infection and injury but can also promote pathological inflammatory responses. Considering the evidence that monocytes exist in at least two subsets committed to divergent functions, we investigated whether distinct factors regulate the balance between monocyte subset responses in vivo. We identified a microRNA (miRNA), miR-146a, which is differentially regulated both in mouse (Ly-6Chi/Ly-6Clo) and human (CD14hi/CD14loCD16+) monocyte subsets. The single miRNA controlled the amplitude of the Ly-6Chimonocyte response during inflammatory challenge whereas it did not affect Ly-6Clocells. miR-146a-mediated regulation was cell-intrinsic and depended on Relb, a member of the noncanonical NF-κB/Rel family, which we identified as a direct miR-146atarget. These observations not only provide mechanistic insights into the molecular events that regulate responses mediated by committed monocyte precursor populations but also identify targets for manipulating Ly-6Chimonocyte responses while sparing Ly-6Clomonocyte activity.

Published
2012
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49. Blood stem cell PU.1 upregulation is a consequence of differentiation without fast autoregulation

Author

Ahmed, Nouraiz, Etzrodt, Martin, Dettinger, Philip, Kull, Tobias, Loeffler, Dirk, Hoppe, Philipp S., Chavez, James S., Zhang, Yang, Camargo Ortega, Germán, Hilsenbeck, Oliver, Nakajima, Hideaki, Pietras, Eric M., and Schroeder, Timm

Abstract

Transcription factors (TFs) regulate cell fates, and their expression must be tightly regulated. Autoregulation is assumed to regulate many TFs’ own expression to control cell fates. Here, we manipulate and quantify the (auto)regulation of PU.1, a TF controlling hematopoietic stem and progenitor cells (HSPCs), and correlate it to their future fates. We generate transgenic mice allowing both inducible activation of PU.1 and noninvasive quantification of endogenous PU.1 protein expression. The quantified HSPC PU.1 dynamics show that PU.1 up-regulation occurs as a consequence of hematopoietic differentiation independently of direct fast autoregulation. In contrast, inflammatory signaling induces fast PU.1 up-regulation, which does not require PU.1 expression or its binding to its own autoregulatory enhancer. However, the increased PU.1 levels induced by inflammatory signaling cannot be sustained via autoregulation after removal of the signaling stimulus. We conclude that PU.1 overexpression induces HSC differentiation before PU.1 up-regulation, only later generating cell types with intrinsically higher PU.1.

Published
2022
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50. Myocardial Infarction Accelerates Atherosclerosis

Author

Leuschner, Florian, Robbins, Clinton, Iwamoto, Yoshiko, Thompson, Brian, Carlson, Alicia L., Heidt, Timo, Lasitschka, Felix, Etzrodt, Martin, Waterman, Peter, Waring, Michael T., Chicoine, Adam T., van der Laan, Anja M., Niessen, Hans W.M., Piek, Jan J., Rubin, Barry B., Butany, Jagdish, Katus, Hugo A., Murphy, Sabina A., Pittet, Mikael J., Lin, Charles P., Dutta, Partha, Courties, Gabriel P, Wei, Ying, Gorbatov, Rostic, Majmudar, Maulik D, Stone, James Robert, Morrow, David Andrew, Sabatine, Marc Steven, Vinegoni, Claudio, Moskowitz, Michael Arthur, Libby, Peter, Swirski, Filip K., Weissleder, Ralph, and Nahrendorf, Matthias

Abstract

During progression of atherosclerosis, myeloid cells destabilize lipid-rich plaque in the arterial wall and cause its rupture, thus triggering myocardial infarction and stroke. Survivors of acute coronary syndromes have a high risk of recurrent events for unknown reasons. Here we show that the systemic response to ischemic injury aggravates chronic atherosclerosis. After myocardial infarction or stroke, apoE\(^{−/−}\) mice developed larger atherosclerotic lesions with a more advanced morphology. This disease acceleration persisted over many weeks and was associated with markedly increased monocyte recruitment. When seeking the source of surplus monocytes in plaque, we found that myocardial infarction liberated hematopoietic stem and progenitor cells from bone marrow niches via sympathetic nervous system signaling. The progenitors then seeded the spleen yielding a sustained boost in monocyte production. These observations provide new mechanistic insight into atherogenesis and provide a novel therapeutic opportunity to mitigate disease progression.

Published
2012
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