A BDNF-TrkB autocrine loop enhances senescent cell viability
Cellular senescence is characterized by cell cycle arrest, resistance to apoptosis, and a senescence-associated secretory phenotype (SASP) whereby cells secrete pro-inflammatory and tissue-remodeling factors. Given that the SASP exacerbates age-associated pathologies, some aging interventions aim at...
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| Veröffentlicht in: | Nature communications Jg. 13; H. 1; S. 6228 - 17 |
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| Sprache: | Englisch |
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20.10.2022
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| Abstract | Cellular senescence is characterized by cell cycle arrest, resistance to apoptosis, and a senescence-associated secretory phenotype (SASP) whereby cells secrete pro-inflammatory and tissue-remodeling factors. Given that the SASP exacerbates age-associated pathologies, some aging interventions aim at selectively eliminating senescent cells. In this study, a drug library screen uncovered TrkB (NTRK2) inhibitors capable of triggering apoptosis of several senescent, but not proliferating, human cells. Senescent cells expressed high levels of TrkB, which supported senescent cell viability, and secreted the TrkB ligand BDNF. The reduced viability of senescent cells after ablating BDNF signaling suggested an autocrine function for TrkB and BDNF, which activated ERK5 and elevated BCL2L2 levels, favoring senescent cell survival. Treatment with TrkB inhibitors reduced the accumulation of senescent cells in aged mouse organs. We propose that the activation of TrkB by SASP factor BDNF promotes cell survival and could be exploited therapeutically to reduce the senescent-cell burden.
Selective elimination of senescent cells is an approach that has shown promise to ameliorate age-associated pathologies in preclinical models. Here the authors report that BDNF enhances senescent cell viability via TrkB in cultured cells, and that TrkB inhibition can reduce the accumulation of senescent cells in aged mouse organs. |
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| AbstractList | Cellular senescence is characterized by cell cycle arrest, resistance to apoptosis, and a senescence-associated secretory phenotype (SASP) whereby cells secrete pro-inflammatory and tissue-remodeling factors. Given that the SASP exacerbates age-associated pathologies, some aging interventions aim at selectively eliminating senescent cells. In this study, a drug library screen uncovered TrkB (NTRK2) inhibitors capable of triggering apoptosis of several senescent, but not proliferating, human cells. Senescent cells expressed high levels of TrkB, which supported senescent cell viability, and secreted the TrkB ligand BDNF. The reduced viability of senescent cells after ablating BDNF signaling suggested an autocrine function for TrkB and BDNF, which activated ERK5 and elevated BCL2L2 levels, favoring senescent cell survival. Treatment with TrkB inhibitors reduced the accumulation of senescent cells in aged mouse organs. We propose that the activation of TrkB by SASP factor BDNF promotes cell survival and could be exploited therapeutically to reduce the senescent-cell burden.Cellular senescence is characterized by cell cycle arrest, resistance to apoptosis, and a senescence-associated secretory phenotype (SASP) whereby cells secrete pro-inflammatory and tissue-remodeling factors. Given that the SASP exacerbates age-associated pathologies, some aging interventions aim at selectively eliminating senescent cells. In this study, a drug library screen uncovered TrkB (NTRK2) inhibitors capable of triggering apoptosis of several senescent, but not proliferating, human cells. Senescent cells expressed high levels of TrkB, which supported senescent cell viability, and secreted the TrkB ligand BDNF. The reduced viability of senescent cells after ablating BDNF signaling suggested an autocrine function for TrkB and BDNF, which activated ERK5 and elevated BCL2L2 levels, favoring senescent cell survival. Treatment with TrkB inhibitors reduced the accumulation of senescent cells in aged mouse organs. We propose that the activation of TrkB by SASP factor BDNF promotes cell survival and could be exploited therapeutically to reduce the senescent-cell burden. Cellular senescence is characterized by cell cycle arrest, resistance to apoptosis, and a senescence-associated secretory phenotype (SASP) whereby cells secrete pro-inflammatory and tissue-remodeling factors. Given that the SASP exacerbates age-associated pathologies, some aging interventions aim at selectively eliminating senescent cells. In this study, a drug library screen uncovered TrkB (NTRK2) inhibitors capable of triggering apoptosis of several senescent, but not proliferating, human cells. Senescent cells expressed high levels of TrkB, which supported senescent cell viability, and secreted the TrkB ligand BDNF. The reduced viability of senescent cells after ablating BDNF signaling suggested an autocrine function for TrkB and BDNF, which activated ERK5 and elevated BCL2L2 levels, favoring senescent cell survival. Treatment with TrkB inhibitors reduced the accumulation of senescent cells in aged mouse organs. We propose that the activation of TrkB by SASP factor BDNF promotes cell survival and could be exploited therapeutically to reduce the senescent-cell burden. Selective elimination of senescent cells is an approach that has shown promise to ameliorate age-associated pathologies in preclinical models. Here the authors report that BDNF enhances senescent cell viability via TrkB in cultured cells, and that TrkB inhibition can reduce the accumulation of senescent cells in aged mouse organs. Cellular senescence is characterized by cell cycle arrest, resistance to apoptosis, and a senescence-associated secretory phenotype (SASP) whereby cells secrete pro-inflammatory and tissue-remodeling factors. Given that the SASP exacerbates age-associated pathologies, some aging interventions aim at selectively eliminating senescent cells. In this study, a drug library screen uncovered TrkB (NTRK2) inhibitors capable of triggering apoptosis of several senescent, but not proliferating, human cells. Senescent cells expressed high levels of TrkB, which supported senescent cell viability, and secreted the TrkB ligand BDNF. The reduced viability of senescent cells after ablating BDNF signaling suggested an autocrine function for TrkB and BDNF, which activated ERK5 and elevated BCL2L2 levels, favoring senescent cell survival. Treatment with TrkB inhibitors reduced the accumulation of senescent cells in aged mouse organs. We propose that the activation of TrkB by SASP factor BDNF promotes cell survival and could be exploited therapeutically to reduce the senescent-cell burden.Selective elimination of senescent cells is an approach that has shown promise to ameliorate age-associated pathologies in preclinical models. Here the authors report that BDNF enhances senescent cell viability via TrkB in cultured cells, and that TrkB inhibition can reduce the accumulation of senescent cells in aged mouse organs. Cellular senescence is characterized by cell cycle arrest, resistance to apoptosis, and a senescence-associated secretory phenotype (SASP) whereby cells secrete pro-inflammatory and tissue-remodeling factors. Given that the SASP exacerbates age-associated pathologies, some aging interventions aim at selectively eliminating senescent cells. In this study, a drug library screen uncovered TrkB (NTRK2) inhibitors capable of triggering apoptosis of several senescent, but not proliferating, human cells. Senescent cells expressed high levels of TrkB, which supported senescent cell viability, and secreted the TrkB ligand BDNF. The reduced viability of senescent cells after ablating BDNF signaling suggested an autocrine function for TrkB and BDNF, which activated ERK5 and elevated BCL2L2 levels, favoring senescent cell survival. Treatment with TrkB inhibitors reduced the accumulation of senescent cells in aged mouse organs. We propose that the activation of TrkB by SASP factor BDNF promotes cell survival and could be exploited therapeutically to reduce the senescent-cell burden. Selective elimination of senescent cells is an approach that has shown promise to ameliorate age-associated pathologies in preclinical models. Here the authors report that BDNF enhances senescent cell viability via TrkB in cultured cells, and that TrkB inhibition can reduce the accumulation of senescent cells in aged mouse organs. |
| ArticleNumber | 6228 |
| Author | Fan, Jinshui Cui, Chang-Yi Herman, Allison B. Payea, Matthew J. Mazan-Mamczarz, Krystyna Gorospe, Myriam Lam, Kwan-Wood Gabriel Rossi, Martina De, Supriyo Anerillas, Carlos Piao, Yulan Garrido, Amanda Abdelmohsen, Kotb de Cabo, Rafael Martindale, Jennifer L. Tsitsipatis, Dimitrios Munk, Rachel |
| Author_xml | – sequence: 1 givenname: Carlos orcidid: 0000-0003-4424-7913 surname: Anerillas fullname: Anerillas, Carlos email: carlos.anerillasaljama@nih.gov organization: Laboratory of Genetics and Genomics, National Institute on Aging Intramural Research Program, National Institutes of Health – sequence: 2 givenname: Allison B. surname: Herman fullname: Herman, Allison B. organization: Laboratory of Genetics and Genomics, National Institute on Aging Intramural Research Program, National Institutes of Health – sequence: 3 givenname: Rachel surname: Munk fullname: Munk, Rachel organization: Laboratory of Genetics and Genomics, National Institute on Aging Intramural Research Program, National Institutes of Health – sequence: 4 givenname: Amanda orcidid: 0000-0003-3140-3251 surname: Garrido fullname: Garrido, Amanda organization: Translational Gerontology Branch, National Institute on Aging Intramural Research Program, National Institutes of Health – sequence: 5 givenname: Kwan-Wood Gabriel orcidid: 0000-0003-2527-9186 surname: Lam fullname: Lam, Kwan-Wood Gabriel organization: Laboratory of Genetics and Genomics, National Institute on Aging Intramural Research Program, National Institutes of Health – sequence: 6 givenname: Matthew J. surname: Payea fullname: Payea, Matthew J. organization: Laboratory of Genetics and Genomics, National Institute on Aging Intramural Research Program, National Institutes of Health – sequence: 7 givenname: Martina orcidid: 0000-0001-7738-9841 surname: Rossi fullname: Rossi, Martina organization: Laboratory of Genetics and Genomics, National Institute on Aging Intramural Research Program, National Institutes of Health – sequence: 8 givenname: Dimitrios surname: Tsitsipatis fullname: Tsitsipatis, Dimitrios organization: Laboratory of Genetics and Genomics, National Institute on Aging Intramural Research Program, National Institutes of Health – sequence: 9 givenname: Jennifer L. orcidid: 0000-0002-3234-6861 surname: Martindale fullname: Martindale, Jennifer L. organization: Laboratory of Genetics and Genomics, National Institute on Aging Intramural Research Program, National Institutes of Health – sequence: 10 givenname: Yulan surname: Piao fullname: Piao, Yulan organization: Laboratory of Genetics and Genomics, National Institute on Aging Intramural Research Program, National Institutes of Health – sequence: 11 givenname: Krystyna surname: Mazan-Mamczarz fullname: Mazan-Mamczarz, Krystyna organization: Laboratory of Genetics and Genomics, National Institute on Aging Intramural Research Program, National Institutes of Health – sequence: 12 givenname: Jinshui surname: Fan fullname: Fan, Jinshui organization: Laboratory of Genetics and Genomics, National Institute on Aging Intramural Research Program, National Institutes of Health – sequence: 13 givenname: Chang-Yi surname: Cui fullname: Cui, Chang-Yi organization: Laboratory of Genetics and Genomics, National Institute on Aging Intramural Research Program, National Institutes of Health – sequence: 14 givenname: Supriyo surname: De fullname: De, Supriyo organization: Laboratory of Genetics and Genomics, National Institute on Aging Intramural Research Program, National Institutes of Health – sequence: 15 givenname: Kotb orcidid: 0000-0001-6240-5810 surname: Abdelmohsen fullname: Abdelmohsen, Kotb organization: Laboratory of Genetics and Genomics, National Institute on Aging Intramural Research Program, National Institutes of Health – sequence: 16 givenname: Rafael orcidid: 0000-0002-3354-2442 surname: de Cabo fullname: de Cabo, Rafael organization: Translational Gerontology Branch, National Institute on Aging Intramural Research Program, National Institutes of Health – sequence: 17 givenname: Myriam orcidid: 0000-0001-5439-3434 surname: Gorospe fullname: Gorospe, Myriam email: myriam-gorospe@nih.gov organization: Laboratory of Genetics and Genomics, National Institute on Aging Intramural Research Program, National Institutes of Health |
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| Snippet | Cellular senescence is characterized by cell cycle arrest, resistance to apoptosis, and a senescence-associated secretory phenotype (SASP) whereby cells... Selective elimination of senescent cells is an approach that has shown promise to ameliorate age-associated pathologies in preclinical models. Here the authors... |
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| SubjectTerms | 13/106 38/89 631/337/1427/2566 631/443/7 631/80/509 Ablation Accumulation Aging Animals Apoptosis Autocrine signalling Brain-Derived Neurotrophic Factor Cell cycle Cell Survival Cell viability Cellular Senescence - genetics Humanities and Social Sciences Humans Inflammation Ligands Mice multidisciplinary Organs Phenotypes Science Science (multidisciplinary) Senescence Survival TrkB receptors |
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| Title | A BDNF-TrkB autocrine loop enhances senescent cell viability |
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