LEF1 isoforms regulate cellular senescence and aging
The study of aging and its mechanisms, such as cellular senescence, has provided valuable insights into age‐related pathologies, thus contributing to their prevention and treatment. The current abundance of high‐throughput data combined with the surge of robust analysis algorithms has facilitated no...
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| Published in | Aging cell Vol. 22; no. 12; pp. e14024 - n/a |
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| Main Authors | , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
John Wiley & Sons, Inc
01.12.2023
John Wiley and Sons Inc |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1474-9718 1474-9726 1474-9726 |
| DOI | 10.1111/acel.14024 |
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| Abstract | The study of aging and its mechanisms, such as cellular senescence, has provided valuable insights into age‐related pathologies, thus contributing to their prevention and treatment. The current abundance of high‐throughput data combined with the surge of robust analysis algorithms has facilitated novel ways of identifying underlying pathways that may drive these pathologies. For the purpose of identifying key regulators of lung aging, we performed comparative analyses of transcriptional profiles of aged versus young human subjects and mice, focusing on the common age‐related changes in the transcriptional regulation in lung macrophages, T cells, and B immune cells. Importantly, we validated our findings in cell culture assays and human lung samples. Our analysis identified lymphoid enhancer binding factor 1 (LEF1) as an important age‐associated regulator of gene expression in all three cell types across different tissues and species. Follow‐up experiments showed that the differential expression of long and short LEF1 isoforms is a key regulatory mechanism of cellular senescence. Further examination of lung tissue from patients with idiopathic pulmonary fibrosis, an age‐related disease with strong ties to cellular senescence, revealed a stark dysregulation of LEF1. Collectively, our results suggest that LEF1 is a key factor of aging, and its differential regulation is associated with human and murine cellular senescence.
Lymphoid enhancer‐binding factor 1 (LEF1) regulon is a common mechanism of aging in human and murine lungs and in human blood. Experimental evidence supports a direct functional role of the long LEF1 isoform in partially reversing cellular senescence through a possible new regulatory mechanism. LEF1 expression and regulon activity in IPF suggest a diverse mode of action during the early and late stages of the disease. |
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| AbstractList | The study of aging and its mechanisms, such as cellular senescence, has provided valuable insights into age‐related pathologies, thus contributing to their prevention and treatment. The current abundance of high‐throughput data combined with the surge of robust analysis algorithms has facilitated novel ways of identifying underlying pathways that may drive these pathologies. For the purpose of identifying key regulators of lung aging, we performed comparative analyses of transcriptional profiles of aged versus young human subjects and mice, focusing on the common age‐related changes in the transcriptional regulation in lung macrophages, T cells, and B immune cells. Importantly, we validated our findings in cell culture assays and human lung samples. Our analysis identified lymphoid enhancer binding factor 1 (LEF1) as an important age‐associated regulator of gene expression in all three cell types across different tissues and species. Follow‐up experiments showed that the differential expression of long and short LEF1 isoforms is a key regulatory mechanism of cellular senescence. Further examination of lung tissue from patients with idiopathic pulmonary fibrosis, an age‐related disease with strong ties to cellular senescence, revealed a stark dysregulation of LEF1. Collectively, our results suggest that LEF1 is a key factor of aging, and its differential regulation is associated with human and murine cellular senescence.
Lymphoid enhancer‐binding factor 1 (LEF1) regulon is a common mechanism of aging in human and murine lungs and in human blood. Experimental evidence supports a direct functional role of the long LEF1 isoform in partially reversing cellular senescence through a possible new regulatory mechanism. LEF1 expression and regulon activity in IPF suggest a diverse mode of action during the early and late stages of the disease. The study of aging and its mechanisms, such as cellular senescence, has provided valuable insights into age‐related pathologies, thus contributing to their prevention and treatment. The current abundance of high‐throughput data combined with the surge of robust analysis algorithms has facilitated novel ways of identifying underlying pathways that may drive these pathologies. For the purpose of identifying key regulators of lung aging, we performed comparative analyses of transcriptional profiles of aged versus young human subjects and mice, focusing on the common age‐related changes in the transcriptional regulation in lung macrophages, T cells, and B immune cells. Importantly, we validated our findings in cell culture assays and human lung samples. Our analysis identified lymphoid enhancer binding factor 1 (LEF1) as an important age‐associated regulator of gene expression in all three cell types across different tissues and species. Follow‐up experiments showed that the differential expression of long and short LEF1 isoforms is a key regulatory mechanism of cellular senescence. Further examination of lung tissue from patients with idiopathic pulmonary fibrosis, an age‐related disease with strong ties to cellular senescence, revealed a stark dysregulation of LEF1. Collectively, our results suggest that LEF1 is a key factor of aging, and its differential regulation is associated with human and murine cellular senescence. The study of aging and its mechanisms, such as cellular senescence, has provided valuable insights into age-related pathologies, thus contributing to their prevention and treatment. The current abundance of high-throughput data combined with the surge of robust analysis algorithms has facilitated novel ways of identifying underlying pathways that may drive these pathologies. For the purpose of identifying key regulators of lung aging, we performed comparative analyses of transcriptional profiles of aged versus young human subjects and mice, focusing on the common age-related changes in the transcriptional regulation in lung macrophages, T cells, and B immune cells. Importantly, we validated our findings in cell culture assays and human lung samples. Our analysis identified lymphoid enhancer binding factor 1 (LEF1) as an important age-associated regulator of gene expression in all three cell types across different tissues and species. Follow-up experiments showed that the differential expression of long and short LEF1 isoforms is a key regulatory mechanism of cellular senescence. Further examination of lung tissue from patients with idiopathic pulmonary fibrosis, an age-related disease with strong ties to cellular senescence, revealed a stark dysregulation of LEF1. Collectively, our results suggest that LEF1 is a key factor of aging, and its differential regulation is associated with human and murine cellular senescence.The study of aging and its mechanisms, such as cellular senescence, has provided valuable insights into age-related pathologies, thus contributing to their prevention and treatment. The current abundance of high-throughput data combined with the surge of robust analysis algorithms has facilitated novel ways of identifying underlying pathways that may drive these pathologies. For the purpose of identifying key regulators of lung aging, we performed comparative analyses of transcriptional profiles of aged versus young human subjects and mice, focusing on the common age-related changes in the transcriptional regulation in lung macrophages, T cells, and B immune cells. Importantly, we validated our findings in cell culture assays and human lung samples. Our analysis identified lymphoid enhancer binding factor 1 (LEF1) as an important age-associated regulator of gene expression in all three cell types across different tissues and species. Follow-up experiments showed that the differential expression of long and short LEF1 isoforms is a key regulatory mechanism of cellular senescence. Further examination of lung tissue from patients with idiopathic pulmonary fibrosis, an age-related disease with strong ties to cellular senescence, revealed a stark dysregulation of LEF1. Collectively, our results suggest that LEF1 is a key factor of aging, and its differential regulation is associated with human and murine cellular senescence. |
| Author | Zhu, Bokai Dion, William Irfan, Saad Kapetanaki, Maria G. Sayed, Khaled Valenzi, Eleanor Rojas, Mauricio Jia, Minxue Mora, Ana L. Rosas, Lorena Benos, Panayiotis V. Lafyatis, Robert A. |
| AuthorAffiliation | 2 Joint Carnegie Mellon University‐University of Pittsburgh Ph.D. Program in Computational Biology Pittsburgh Pennsylvania USA 4 Department of Epidemiology University of Florida Gainesville Florida USA 1 Department of Computational and Systems Biology University of Pittsburgh Pittsburgh Pennsylvania USA 6 Division of Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine The Ohio State University Columbus Ohio USA 8 Department of Medicine University of Pittsburgh Pittsburgh Pennsylvania USA 9 Pittsburgh Liver Research Center University of Pittsburgh Pittsburgh Pennsylvania USA 7 Department of Rheumatology University of Pittsburgh Pittsburgh Pennsylvania USA 5 Aging Institute of UPMC University of Pittsburgh Pittsburgh Pennsylvania USA 3 Department of Electrical & Computer Engineering and Computer Science University of New Haven West Haven Connecticut USA |
| AuthorAffiliation_xml | – name: 6 Division of Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine The Ohio State University Columbus Ohio USA – name: 7 Department of Rheumatology University of Pittsburgh Pittsburgh Pennsylvania USA – name: 1 Department of Computational and Systems Biology University of Pittsburgh Pittsburgh Pennsylvania USA – name: 5 Aging Institute of UPMC University of Pittsburgh Pittsburgh Pennsylvania USA – name: 8 Department of Medicine University of Pittsburgh Pittsburgh Pennsylvania USA – name: 9 Pittsburgh Liver Research Center University of Pittsburgh Pittsburgh Pennsylvania USA – name: 2 Joint Carnegie Mellon University‐University of Pittsburgh Ph.D. Program in Computational Biology Pittsburgh Pennsylvania USA – name: 4 Department of Epidemiology University of Florida Gainesville Florida USA – name: 3 Department of Electrical & Computer Engineering and Computer Science University of New Haven West Haven Connecticut USA |
| Author_xml | – sequence: 1 givenname: Minxue orcidid: 0000-0001-9305-1218 surname: Jia fullname: Jia, Minxue organization: Joint Carnegie Mellon University‐University of Pittsburgh Ph.D. Program in Computational Biology – sequence: 2 givenname: Khaled surname: Sayed fullname: Sayed, Khaled organization: University of New Haven – sequence: 3 givenname: Maria G. surname: Kapetanaki fullname: Kapetanaki, Maria G. organization: University of Florida – sequence: 4 givenname: William surname: Dion fullname: Dion, William organization: University of Pittsburgh – sequence: 5 givenname: Lorena surname: Rosas fullname: Rosas, Lorena organization: The Ohio State University – sequence: 6 givenname: Saad surname: Irfan fullname: Irfan, Saad organization: University of Pittsburgh – sequence: 7 givenname: Eleanor surname: Valenzi fullname: Valenzi, Eleanor organization: University of Pittsburgh – sequence: 8 givenname: Ana L. surname: Mora fullname: Mora, Ana L. organization: The Ohio State University – sequence: 9 givenname: Robert A. surname: Lafyatis fullname: Lafyatis, Robert A. organization: University of Pittsburgh – sequence: 10 givenname: Mauricio surname: Rojas fullname: Rojas, Mauricio organization: The Ohio State University – sequence: 11 givenname: Bokai orcidid: 0000-0003-0827-5757 surname: Zhu fullname: Zhu, Bokai organization: University of Pittsburgh – sequence: 12 givenname: Panayiotis V. orcidid: 0000-0003-3172-3132 surname: Benos fullname: Benos, Panayiotis V. email: pbenos@ufl.edu organization: University of Florida |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/37961030$$D View this record in MEDLINE/PubMed |
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| Keywords | lung cellular senescence aging IPF LEF1 |
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| SubjectTerms | Age Aged Aging Aging - genetics Animals Automation Cell culture Cells cellular senescence Cellular Senescence - genetics Comparative analysis Datasets Fibrosis Gene expression Gene regulation Histopathology Humans IPF Isoforms LEF1 lung Lung - pathology Lung diseases Lungs Lymphocytes T Lymphoid Enhancer-Binding Factor 1 - genetics Lymphoid Enhancer-Binding Factor 1 - metabolism Macrophages Mice Protein Isoforms - genetics Senescence |
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| Title | LEF1 isoforms regulate cellular senescence and aging |
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