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31 results on '"Schafer, Marissa J."'

1. An untapped window of opportunity for glioma: targeting therapy-induced senescence prior to recurrence

Author

Riviere-Cazaux, Cecile, Carlstrom, Lucas P., Neth, Bryan J., Olson, Ian E., Rajani, Karishma, Rahman, Masum, Ikram, Samar, Mansour, Moustafa A., Mukherjee, Bipasha, Warrington, Arthur E., Short, Susan C., von Zglinicki, Thomas, Brown, Desmond A., Burma, Sandeep, Tchkonia, Tamar, Schafer, Marissa J., Baker, Darren J., Kizilbash, Sani H., Kirkland, James L., and Burns, Terry C.

Published
2023
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3. Targeting senescent cells alleviates obesity‐induced metabolic dysfunction

Author

Palmer, Allyson K, Xu, Ming, Zhu, Yi, Pirtskhalava, Tamar, Weivoda, Megan M, Hachfeld, Christine M, Prata, Larissa G, van Dijk, Theo H, Verkade, Esther, Casaclang‐Verzosa, Grace, Johnson, Kurt O, Cubro, Hajrunisa, Doornebal, Ewald J, Ogrodnik, Mikolaj, Jurk, Diana, Jensen, Michael D, Chini, Eduardo N, Miller, Jordan D, Matveyenko, Aleksey, Stout, Michael B, Schafer, Marissa J, White, Thomas A, Hickson, LaTonya J, Demaria, Marco, Garovic, Vesna, Grande, Joseph, Arriaga, Edgar A, Kuipers, Folkert, von Zglinicki, Thomas, LeBrasseur, Nathan K, Campisi, Judith, Tchkonia, Tamar, and Kirkland, James L

Subjects
Medical Physiology, Biomedical and Clinical Sciences, Nutrition, Obesity, Prevention, Diabetes, 2.1 Biological and endogenous factors, Aetiology, Cardiovascular, Metabolic and endocrine, Adipocytes, Adipogenesis, Adipose Tissue, Aging, Animals, Cell Death, Cell Line, Cellular Senescence, Cyclin-Dependent Kinase Inhibitor p16, Dasatinib, Female, Ganciclovir, Glucose, Humans, Inflammation, Insulin Resistance, Macrophages, Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Quercetin, adipogenesis, aging, cellular senescence, dasatinib, quercetin, senolytics, type 2 diabetes, Biological Sciences, Medical and Health Sciences, Developmental Biology, Biological sciences, Biomedical and clinical sciences
Abstract

Adipose tissue inflammation and dysfunction are associated with obesity-related insulin resistance and diabetes, but mechanisms underlying this relationship are unclear. Although senescent cells accumulate in adipose tissue of obese humans and rodents, a direct pathogenic role for these cells in the development of diabetes remains to be demonstrated. Here, we show that reducing senescent cell burden in obese mice, either by activating drug-inducible "suicide" genes driven by the p16Ink4a promoter or by treatment with senolytic agents, alleviates metabolic and adipose tissue dysfunction. These senolytic interventions improved glucose tolerance, enhanced insulin sensitivity, lowered circulating inflammatory mediators, and promoted adipogenesis in obese mice. Elimination of senescent cells also prevented the migration of transplanted monocytes into intra-abdominal adipose tissue and reduced the number of macrophages in this tissue. In addition, microalbuminuria, renal podocyte function, and cardiac diastolic function improved with senolytic therapy. Our results implicate cellular senescence as a causal factor in obesity-related inflammation and metabolic derangements and show that emerging senolytic agents hold promise for treating obesity-related metabolic dysfunction and its complications.

Published
2019

4. Rejuvenation of the aged brain immune cell landscape in mice through p16-positive senescent cell clearance

Author

Zhang, Xu, Pearsall, Vesselina M., Carver, Chase M., Atkinson, Elizabeth J., Clarkson, Benjamin D. S., Grund, Ethan M., Baez-Faria, Michelle, Pavelko, Kevin D., Kachergus, Jennifer M., White, Thomas A., Johnson, Renee K., Malo, Courtney S., Gonzalez-Suarez, Alan M., Ayasoufi, Katayoun, Johnson, Kurt O., Tritz, Zachariah P., Fain, Cori E., Khadka, Roman H., Ogrodnik, Mikolaj, Jurk, Diana, Zhu, Yi, Tchkonia, Tamara, Revzin, Alexander, Kirkland, James L., Johnson, Aaron J., Howe, Charles L., Thompson, E. Aubrey, LeBrasseur, Nathan K., and Schafer, Marissa J.

Published
2022
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5. Orally-active, clinically-translatable senolytics restore α-Klotho in mice and humans

Author

Zhu, Yi, Prata, Larissa G.P. Langhi, Gerdes, Erin O. Wissler, Netto, Jair Machado Espindola, Pirtskhalava, Tamar, Giorgadze, Nino, Tripathi, Utkarsh, Inman, Christina L., Johnson, Kurt O., Xue, Ailing, Palmer, Allyson K., Chen, Tingjun, Schaefer, Kalli, Justice, Jamie N., Nambiar, Anoop M., Musi, Nicolas, Kritchevsky, Stephen B., Chen, Jun, Khosla, Sundeep, Jurk, Diana, Schafer, Marissa J., Tchkonia, Tamar, and Kirkland, James L.

Published
2022
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7. Disease drivers of aging.

Author

Hodes, Richard J, Sierra, Felipe, Austad, Steven N, Epel, Elissa, Neigh, Gretchen N, Erlandson, Kristine M, Schafer, Marissa J, LeBrasseur, Nathan K, Wiley, Christopher, Campisi, Judith, Sehl, Mary E, Scalia, Rosario, Eguchi, Satoru, Kasinath, Balakuntalam S, Halter, Jeffrey B, Cohen, Harvey Jay, Demark-Wahnefried, Wendy, Ahles, Tim A, Barzilai, Nir, Hurria, Arti, and Hunt, Peter W

Subjects
Humans, Acquired Immunodeficiency Syndrome, Neoplasms, Diabetes Mellitus, Chronic Disease, Aging, HIV, age-related, aging, cancer, chronic, diabetes, disease, pathology, prevention, HIV/AIDS, Aetiology, 2.1 Biological and endogenous factors, General Science & Technology
Abstract

It has long been known that aging, at both the cellular and organismal levels, contributes to the development and progression of the pathology of many chronic diseases. However, much less research has examined the inverse relationship-the contribution of chronic diseases and their treatments to the progression of aging-related phenotypes. Here, we discuss the impact of three chronic diseases (cancer, HIV/AIDS, and diabetes) and their treatments on aging, putative mechanisms by which these effects are mediated, and the open questions and future research directions required to understand the relationships between these diseases and aging.

Published
2016

12. Exercise reduces circulating biomarkers of cellular senescence in humans

Author

Englund, Davis A., primary, Sakamoto, Ayumi E., additional, Fritsche, Chad M., additional, Heeren, Amanda A., additional, Zhang, Xu, additional, Kotajarvi, Brian R., additional, Lecy, Denise R., additional, Yousefzadeh, Matthew J., additional, Schafer, Marissa J., additional, White, Thomas A., additional, Atkinson, Elizabeth J., additional, and LeBrasseur, Nathan K., additional

Published
2021
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13. Whole‐body senescent cell clearance alleviates age‐related brain inflammation and cognitive impairment in mice

Author

Ogrodnik, Mikolaj, primary, Evans, Shane A., additional, Fielder, Edward, additional, Victorelli, Stella, additional, Kruger, Patrick, additional, Salmonowicz, Hanna, additional, Weigand, Bettina M., additional, Patel, Ayush D., additional, Pirtskhalava, Tamar, additional, Inman, Christine L., additional, Johnson, Kurt O., additional, Dickinson, Stephanie L., additional, Rocha, Azucena, additional, Schafer, Marissa J., additional, Zhu, Yi, additional, Allison, David B., additional, Zglinicki, Thomas, additional, LeBrasseur, Nathan K., additional, Tchkonia, Tamar, additional, Neretti, Nicola, additional, Passos, João F., additional, Kirkland, James L., additional, and Jurk, Diana, additional

Published
2021
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16. The senescence-associated secretome as an indicator of age and medical risk

Author

Schafer, Marissa J., primary, Zhang, Xu, additional, Kumar, Amanika, additional, Atkinson, Elizabeth J., additional, Zhu, Yi, additional, Jachim, Sarah, additional, Mazula, Daniel L., additional, Brown, Ashley K., additional, Berning, Michelle, additional, Aversa, Zaira, additional, Kotajarvi, Brian, additional, Bruce, Charles J., additional, Greason, Kevin L., additional, Suri, Rakesh M., additional, Tracy, Russell P., additional, Cummings, Steven R., additional, White, Thomas A., additional, and LeBrasseur, Nathan K., additional

Published
2020
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17. Late‐life time‐restricted feeding and exercise differentially alter healthspan in obesity

Author

Schafer, Marissa J., primary, Mazula, Daniel L., additional, Brown, Ashley K., additional, White, Thomas A., additional, Atkinson, Elizabeth, additional, Pearsall, Vesselina M., additional, Aversa, Zaira, additional, Verzosa, Grace C., additional, Smith, Leslie A., additional, Matveyenko, Aleksey, additional, Miller, Jordan D., additional, and LeBrasseur, Nathan K., additional

Published
2019
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18. Length‐independent telomere damage drives post‐mitotic cardiomyocyte senescence

Author

Anderson, Rhys, primary, Lagnado, Anthony, additional, Maggiorani, Damien, additional, Walaszczyk, Anna, additional, Dookun, Emily, additional, Chapman, James, additional, Birch, Jodie, additional, Salmonowicz, Hanna, additional, Ogrodnik, Mikolaj, additional, Jurk, Diana, additional, Proctor, Carole, additional, Correia‐Melo, Clara, additional, Victorelli, Stella, additional, Fielder, Edward, additional, Berlinguer‐Palmini, Rolando, additional, Owens, Andrew, additional, Greaves, Laura C, additional, Kolsky, Kathy L, additional, Parini, Angelo, additional, Douin‐Echinard, Victorine, additional, LeBrasseur, Nathan K, additional, Arthur, Helen M, additional, Tual‐Chalot, Simon, additional, Schafer, Marissa J, additional, Roos, Carolyn M, additional, Miller, Jordan D, additional, Robertson, Neil, additional, Mann, Jelena, additional, Adams, Peter D, additional, Tchkonia, Tamara, additional, Kirkland, James L, additional, Mialet‐Perez, Jeanne, additional, Richardson, Gavin D, additional, and Passos, João F, additional

Published
2019
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19. Loss of Ovarian Hormones and Accelerated Somatic and Mental Aging

Author

Rocca, Walter A., primary, Gazzuola Rocca, Liliana, additional, Smith, Carin Y., additional, Grossardt, Brandon R., additional, Faubion, Stephanie S., additional, Shuster, Lynne T., additional, Kirkland, James L., additional, LeBrasseur, Nathan K., additional, Schafer, Marissa J., additional, Mielke, Michelle M., additional, Kantarci, Kejal, additional, Stewart, Elizabeth A., additional, and Miller, Virginia M., additional

Published
2018
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20. Disease drivers of aging

Author

Hodes, Richard J., Sierra, Felipe, Austad, Steven N., Epel, Elissa, Neigh, Gretchen N., Erlandson, Kristine M., Schafer, Marissa J., LeBrasseur, Nathan K., Wiley, Christopher, Campisi, Judith, Sehl, Mary E., Scalia, Rosario, Eguchi, Satoru, Kasinath, Balakuntalam S., Halter, Jeffrey B., Cohen, Harvey Jay, Demark-Wahnefried, Wendy, Ahles, Tim A., Barzilai, Nir, Hurria, Arti, and Hunt, Peter W.

Subjects
Acquired Immunodeficiency Syndrome, Aging, disease, diabetes, General Science & Technology, HIV, age-related, Article, chronic, prevention, Neoplasms, Chronic Disease, Diabetes Mellitus, Humans, cancer, HIV/AIDS, 2.1 Biological and endogenous factors, pathology, Aetiology
Abstract

© 2016 New York Academy of Sciences. It has long been known that aging, at both the cellular and organismal levels, contributes to the development and progression of the pathology of many chronic diseases. However, much less research has examined the inverse relationship—the contribution of chronic diseases and their treatments to the progression of aging-related phenotypes. Here, we discuss the impact of three chronic diseases (cancer, HIV/AIDS, and diabetes) and their treatments on aging, putative mechanisms by which these effects are mediated, and the open questions and future research directions required to understand the relationships between these diseases and aging.

Published
2016

22. Circulating levels of monocyte chemoattractant protein‐1 as a potential measure of biological age in mice and frailty in humans

Author

Yousefzadeh, Matthew J., primary, Schafer, Marissa J., additional, Noren Hooten, Nicole, additional, Atkinson, Elizabeth J., additional, Evans, Michele K., additional, Baker, Darren J., additional, Quarles, Ellen K., additional, Robbins, Paul D., additional, Ladiges, Warren C., additional, LeBrasseur, Nathan K., additional, and Niedernhofer, Laura J., additional

Published
2017
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23. Cellular senescence mediates fibrotic pulmonary disease

Author

Schafer, Marissa J., primary, White, Thomas A., additional, Iijima, Koji, additional, Haak, Andrew J., additional, Ligresti, Giovanni, additional, Atkinson, Elizabeth J., additional, Oberg, Ann L., additional, Birch, Jodie, additional, Salmonowicz, Hanna, additional, Zhu, Yi, additional, Mazula, Daniel L., additional, Brooks, Robert W., additional, Fuhrmann-Stroissnigg, Heike, additional, Pirtskhalava, Tamar, additional, Prakash, Y. S., additional, Tchkonia, Tamara, additional, Robbins, Paul D., additional, Aubry, Marie Christine, additional, Passos, João F., additional, Kirkland, James L., additional, Tschumperlin, Daniel J., additional, Kita, Hirohito, additional, and LeBrasseur, Nathan K., additional

Published
2017
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25. Chronic senolytic treatment alleviates established vasomotor dysfunction in aged or atherosclerotic mice

Author

Roos, Carolyn M., primary, Zhang, Bin, additional, Palmer, Allyson K., additional, Ogrodnik, Mikolaj B., additional, Pirtskhalava, Tamar, additional, Thalji, Nassir M., additional, Hagler, Michael, additional, Jurk, Diana, additional, Smith, Leslie A., additional, Casaclang‐Verzosa, Grace, additional, Zhu, Yi, additional, Schafer, Marissa J., additional, Tchkonia, Tamara, additional, Kirkland, James L., additional, and Miller, Jordan D., additional

Published
2016
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26. Exercise Prevents Diet-Induced Cellular Senescence in Adipose Tissue

Author

Schafer, Marissa J., primary, White, Thomas A., additional, Evans, Glenda, additional, Tonne, Jason M., additional, Verzosa, Grace C., additional, Stout, Michael B., additional, Mazula, Daniel L., additional, Palmer, Allyson K., additional, Baker, Darren J., additional, Jensen, Michael D., additional, Torbenson, Michael S., additional, Miller, Jordan D., additional, Ikeda, Yasuhiro, additional, Tchkonia, Tamara, additional, van Deursen, Jan M., additional, Kirkland, James L., additional, and LeBrasseur, Nathan K., additional

Published
2016
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27. Circulating levels of monocyte chemoattractant protein‐1 as a potential measure of biological age in mice and frailty in humans.

Author

Yousefzadeh, Matthew J., Schafer, Marissa J., Noren Hooten, Nicole, Atkinson, Elizabeth J., Evans, Michele K., Baker, Darren J., Quarles, Ellen K., Robbins, Paul D., Ladiges, Warren C., LeBrasseur, Nathan K., and Niedernhofer, Laura J.

Subjects
*BIOMARKERS, *DISEASE risk factors, *CLINICAL trials, *MONOCYTES, *CHEMOKINES
Abstract

Summary: A serum biomarker of biological versus chronological age would have significant impact on clinical care. It could be used to identify individuals at risk of early‐onset frailty or the multimorbidities associated with old age. It may also serve as a surrogate endpoint in clinical trials targeting mechanisms of aging. Here, we identified MCP‐1/CCL2, a chemokine responsible for recruiting monocytes, as a potential biomarker of biological age. Circulating monocyte chemoattractant protein‐1 (MCP‐1) levels increased in an age‐dependent manner in wild‐type (WT) mice. That age‐dependent increase was accelerated in Ercc1−/Δ and Bubr1H/H mouse models of progeria. Genetic and pharmacologic interventions that slow aging of Ercc1−/Δ and WT mice lowered serum MCP‐1 levels significantly. Finally, in elderly humans with aortic stenosis, MCP‐1 levels were significantly higher in frail individuals compared to nonfrail. These data support the conclusion that MCP‐1 can be used as a measure of mammalian biological age that is responsive to interventions that extend healthy aging. [ABSTRACT FROM AUTHOR]

Published
2018
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30. Length‐independent telomere damage drives post‐mitotic cardiomyocyte senescence

Author

Anderson, Rhys, Lagnado, Anthony, Maggiorani, Damien, Walaszczyk, Anna, Dookun, Emily, Chapman, James, Birch, Jodie, Salmonowicz, Hanna, Ogrodnik, Mikolaj, Jurk, Diana, Proctor, Carole, Correia‐Melo, Clara, Victorelli, Stella, Fielder, Edward, Berlinguer‐Palmini, Rolando, Owens, Andrew, Greaves, Laura C, Kolsky, Kathy L, Parini, Angelo, Douin‐Echinard, Victorine, LeBrasseur, Nathan K, Arthur, Helen M, Tual‐Chalot, Simon, Schafer, Marissa J, Roos, Carolyn M, Miller, Jordan D, Robertson, Neil, Mann, Jelena, Adams, Peter D, Tchkonia, Tamara, Kirkland, James L, Mialet‐Perez, Jeanne, Richardson, Gavin D, Passos, João F, Ageing Research Laboratories [Newcastle upon Tyne, UK] (Institute for Ageing), Newcastle University [Newcastle], Institute for Cell and Molecular Biosciences, Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), Cardiovascular Research Centre [Newcastle upon Tyne, UK] (Institute for Genetic Medicine), The Bio-Imaging Unit [Newcastle upon Tyne, UK], Wellcome Trust Centre for Mitochondrial Research [Newcastle upon Tyne, UK] (Institute of Genetic Medicine), Newcastle University [Newcastle]-International Centre for Life, Robert and Arlene Kogod Center on Aging [Rochester, MN, USA], Mayo Clinic, Institut de médecine moléculaire de Rangueil (I2MR), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées- Institut Fédératif de Recherche Bio-médicale Institution (IFR150)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institute of Cancer Sciences [Glasgow, UK] (CR-UK Beatson Institute), University of Glasgow, This work was funded by BBSRC grants BB/H022384/1 and BB/K017314/1 to JFP, BHF project grant PG/15/85/31744 to GR and JFP, NIH grant AG013925 and funding from the Connor Group and Noaber Foundation to JLK, and grant from Région Occitanie, France and a grant from foundation Cariplo 2014-0672, to JMP, DM and VDE. CJP and JFP were funded by the MRCArthritis Research UK Centre for Integrated research into Musculoskeletal Ageing (CIMA) grant MR/K0063121/1., Mialet-Perez, Jeanne, and Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-IFR150-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
DNA Replication, senescence, [SDV]Life Sciences [q-bio], DNA Replication, Repair & Recombination, cardiomyocytes, Articles, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, Telomere, telomeres, Article, telomeres Subject Categories Ageing, [SDV] Life Sciences [q-bio], Metabolism, ageing, senolytics, Myocytes, Cardiac, Repair & Recombination, Telomerase, [SDV.BC] Life Sciences [q-bio]/Cellular Biology, Cellular Senescence
Abstract

International audience; Ageing is the biggest risk factor for cardiovascular health and is associated with increased incidence of cardiovascular disease. Cellular senescence, a process driven in part by telomere shortening, has been implicated in age-related tissue dysfunction. Here, we address the question of how senescence is induced in rarely dividing/post-mitotic cardiomyocytes and investigate if clearance of senescent cells attenuates age related cardiac dysfunction. During ageing, human and murine cardiomyocytes acquire a senescent-like phenotype characterised by persistent DNA damage at telomere regions that can be driven by mitochondrial dysfunction, and crucially can occur independently of cell-division and telomere length. Length-independent telomere damage in cardiomyocytes activates the classical senescence-inducing pathways, p21 CIP and p16 INK4a and results in a non-canonical senescence-associated secretory phenotype. Pharmacological or genetic clearance of senescent cells in mice alleviates myocardial hypertrophy and fibrosis, detrimental features 2 of cardiac ageing, and promotes cardiomyocyte regeneration. Our data describes a mechanism by which senescence can occur and contribute to ageing in post-mitotic tissues.

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31. Pim-1 kinase is a positive feedback regulator of the senescent lung fibroblast inflammatory secretome.

Author

Gao AY, Diaz Espinosa AM, Gianì F, Pham TX, Carver CM, Aravamudhan A, Bartman CM, Ligresti G, Caporarello N, Schafer MJ, and Haak AJ

Subjects
Humans, Proto-Oncogene Proteins c-pim-1 metabolism, Proto-Oncogene Proteins c-pim-1 pharmacology, NF-kappa B metabolism, Fibroblasts metabolism, Cellular Senescence, Lung metabolism, Cytokines metabolism, Idiopathic Pulmonary Fibrosis metabolism, Pneumonia metabolism
Abstract

Cellular senescence is emerging as a driver of idiopathic pulmonary fibrosis (IPF), a progressive and fatal disease with limited effective therapies. The senescence-associated secretory phenotype (SASP), involving the release of inflammatory cytokines and profibrotic growth factors by senescent cells, is thought to be a product of multiple cell types in IPF, including lung fibroblasts. NF-κB is a master regulator of the SASP, and its activity depends on the phosphorylation of p65/RelA. The purpose of this study was to assess the role of Pim-1 kinase as a driver of NF-κB-induced production of inflammatory cytokines from low-passage IPF fibroblast cultures displaying markers of senescence. Our results demonstrate that Pim-1 kinase phosphorylates p65/RelA, activating NF-κB activity and enhancing IL-6 production, which in turn amplifies the expression of PIM1 , generating a positive feedback loop. In addition, targeting Pim-1 kinase with a small molecule inhibitor dramatically inhibited the expression of a broad array of cytokines and chemokines in IPF-derived fibroblasts. Furthermore, we provide evidence that Pim-1 overexpression in low-passage human lung fibroblasts is sufficient to drive premature senescence, in vitro. These findings highlight the therapeutic potential of targeting Pim-1 kinase to reprogram the secretome of senescent fibroblasts and halt IPF progression.

Published
2022
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