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Aging (Aging-US)

Aging (Aging-US) published this trending research perspective in Volume 14, Issue 7, entitled, “Heterochronic parabiosis: a valuable tool to investigate cellular senescence and other hallmarks of aging” by researchers from the Institute on the Biology of Aging and Metabolism, University of Minnesota, Minneapolis, MN; Department of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota, Minneapolis, MN; Department of Molecular Pharmacology and Medicine, Albert Einstein College of Medicine, Bronx, NY; Institute for Aging Research, Albert Einstein College of Medicine, Bronx, NY.

DOI - https://doi.org/10.18632/aging.204015

Corresponding authors - Matthew J. Yousefzadeh - myousefz@umn.edu, and Derek M. Huffman - derek.huffman@einsteinmed.org

Abstract

Parabiosis is a well-established method to facilitate a shared blood supply between two conjoined animals. In particular, the pairing of mice of dissimilar ages, termed heterochronic parabiosis, has been used extensively for differentiating cell autonomous and non-autonomous mechanisms of aging. Analysis of heterochronic parabionts also has helped to identify individual circulating factors that may act as either pro- or anti-geronics. Heterochronic parabiosis also has proven to be a valuable experimental system to evaluate the effects of specific hallmarks of aging on the process of aging. For example, heterochronic parabiosis was used recently to examine whether cellular senescence was driven via cell autonomous and/or non-autonomous mechanisms. As anticipated, markers of cellular senescence were elevated in old isochronically-paired mice relative to young controls. However, compared to old isochronically paired mice, the senescent cell burden was reduced in multiple tissues of old parabionts joined with young mice. This suggests that the rejuvenation of cells and tissues in old mice by exposure to young blood could be mediated, in part, through suppression or immune clearance of senescent cells. Conversely, young heterochronic parabionts showed increased markers of cellular senescence, demonstrating that exposure to an old circulation is able to drive senescence through a cell non-autonomous mechanism(s), likely contributing to accelerated aging in the young mice. Thus, heterochronic parabiosis is still an important methodology that should continue to be leveraged for evaluating other hallmarks of aging and their mechanisms.

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Keywords - aging, cellular senescence, heterochronic parabiosis, geroscience

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

Please visit our website at http://www.Aging-US.com​​ and connect with us:

SoundCloud - https://soundcloud.com/Aging-Us
Facebook - https://www.facebook.com/AgingUS/
Twitter - https://twitter.com/AgingJrnl
Instagram - https://www.instagram.com/agingjrnl/
YouTube - https://www.youtube.com/agingus​
LinkedIn - https://www.linkedin.com/company/aging/
Pinterest - https://www.pinterest.com/AgingUS/

Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com​​

Media Contact
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MEDIA@IMPACTJOURNALS.COM

Trending With Impact: Heterochronic Parabiosis, Cellular Senescence and Aging

CD Genomics

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Aging (Aging-US) published this research paper as the cover for Volume 14, Issue 7, entitled, "Downregulation of IGFBP5 contributes to replicative senescence via ERK2 activation in mouse embryonic fibroblasts" by researchers from the Department of Pharmacology, Sapporo Medical University School of Medicine, Sapporo, Japan.

DOI - https://doi.org/10.18632/aging.203999

Corresponding author - Atsushi Kuno - kuno@sapmed.ac.jp

Abstract

Insulin-like growth factor (IGF)-binding proteins (IGFBPs) are secretory proteins that regulate IGF signaling. In this study, we investigated the role of IGFBP5 in replicative senescence in embryonic mouse fibroblasts (MEFs). During passages according to the 3T3 method, MEFs underwent senescence after the 5th passage (P5) based on cell growth arrest, an increase in the number of cells positive for senescence-associated β-galactosidase (SA-β-GAL) staining, and upregulation of p16 and p19. In P8 MEFs, IGFBP5 mRNA level was markedly reduced compared with that in P2 MEFs. Downregulation of IGFBP5 via siRNA in P2 MEFs increased the number of SA-β-GAL-positive cells, upregulated p16 and p19, and inhibited cell growth. Incubation of MEFs with IGFBP5 during serial passage increased the cumulative population doubling and decreased SA-β-GAL positivity compared with those in vehicle-treated cells. IGFBP5 knockdown in P2 MEFs increased phosphorylation levels of ERK1 and ERK2. Silencing of ERK2, but not that of ERK1, blocked the increase in the number of SA-β-GAL-positive cells in IGFBP5-knockdown cells. The reduction in the cell number and upregulation of p16 and p21 in IGFBP5-knockdown cells were attenuated by ERK2 knockdown. Our results suggest that downregulation of IGFBP5 during serial passage contributes to replicative senescence via ERK2 in MEFs.

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Keywords - aging, IGFBP5, replicative senescence, mouse embryonic fibroblasts, ERK2, ERK1

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

Please visit our website at http://www.Aging-US.com​​ and connect with us:

SoundCloud - https://soundcloud.com/Aging-Us
Facebook - https://www.facebook.com/AgingUS/
Twitter - https://twitter.com/AgingJrnl
Instagram - https://www.instagram.com/agingjrnl/
YouTube - https://www.youtube.com/agingus​
LinkedIn - https://www.linkedin.com/company/aging/
Pinterest - https://www.pinterest.com/AgingUS/

Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com​​

Media Contact
18009220957
MEDIA@IMPACTJOURNALS.COM

Paper Spotlight: Downregulated IGFBP5 Contributes to Replicative Senescence

Oncotarget

Oncotarget published this research paper on April 1, 2022 in Volume 13, entitled, "Role of the prorenin receptor in endometrial cancer cell growth" by researchers from the School of Biomedical Sciences and Pharmacy, Priority Research Centre for Reproductive Science, Mothers and Babies Research Centre, Hunter Medical Research Institute, University of Newcastle, Newcastle, New South Wales, Australia; School of Environmental and Life Sciences, Priority Research Centre for Reproductive Science, Hunter Medical Research Institute, University of Newcastle, Newcastle, New South Wales, Australia; School of Biomedical Sciences and Pharmacy, Priority Research Centre for Cancer Research, Innovation and Translation, Hunter Medical Research Institute, University of Newcastle, Newcastle, New South Wales, Australia; School of Life Sciences, Faculty of Science, University of Technology Sydney, Ultimo, New South Wales, Australia; Hudson Institute of Medical Research, Australia and Department of Molecular and Translational Sciences, Monash University, Clayton, Victoria, Australia; Department of Obstetrics and Gynaecology, Gynaecology Research Centre, The Women’s Hospital, University of Melbourne, Melbourne, Victoria, Australia.

DOI - https://doi.org/10.18632/oncotarget.28224

Correspondence to - Kirsty G. Pringle - kirsty.pringle@newcastle.edu.au

Abstract

Endometrial cancer is the most diagnosed gynecological malignancy. Despite numerous scientific advances, the incidence and mortality rate of endometrial cancer continues to rise. Emerging evidence suggests a putative role of the (pro)renin receptor ((P)RR), in the ontogenesis of endometrial cancer. The (P)RR is implicated in breast cancer and pancreatic carcinoma pathophysiology by virtue of its role in proliferation, angiogenesis, fibrosis, migration and invasion. Thus, we aimed to investigate the functional role of the (P)RR in human endometrial cancer.

We employed an siRNA-mediated knockdown approach to abrogate (P)RR expression in the endometrial epithelial cell lines; Ishikawa, AN3CA and HEC-1-A and examined cellular proliferation and viability. We also carried out a sophisticated proteomic screen to explore potential pathways via which the (P)RR is acting in endometrial cancer physiology.

These data confirmed that the (P)RR is critical for endometrial cancer development, contributing to both its proliferative capacity and in the maintenance of cell viability. This is likely mediated through proteins such as MGA, SLC4A7, SLC7A11 or DHRS2, which were reduced following (P)RR knockdown.

These putative protein interactions/pathways, which rely on the presence of the (P)RR, are likely to contribute to endometrial cancer progression and could therefore, represent several novel therapeutic targets for endometrial cancer.

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Keywords - (P)RR; ATP6AP2, endometrial cancer, cellular viability, cellular proliferation

About Oncotarget

Oncotarget is a peer-reviewed, open access biomedical journal covering research on all aspects of oncology.

To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us:

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Oncotarget is published by Impact Journals, LLC: https://www.ImpactJournals.com

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Paper Spotlight: The Prorenin Receptor in Endometrial Cancer

feiyuebio Agnes

Wuhan Feiyue Biotechnology Co., LTD., Focusing on the research and development, production, sales and import and export of biological research reagents and primary and secondary medical devices. 

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Aging (Aging-US) published this research paper in Volume 13, Issue 18, entitled, "SARS-CoV-2 causes senescence in human cells and exacerbates the senescence-associated secretory phenotype through TLR-3" by researchers from the Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN; Institute of Molecular Virology, Ulm University Medical Center, Ulm, Germany; Department of Physiology and Bioengineering, Mayo Clinic, Rochester, MN; Institute for Medical Microbiology and Hygiene, Ulm University Medical Center, Ulm, Germany; Institute on the Biology of Aging and Metabolism, Department of Biochemistry, Molecular Biology and Biophysics, University of Minnesota, Minneapolis, MN; Department of Epidemiology and Biostatistics, School of Public Health, Indiana University-Bloomington, Bloomington, IN; Division of General Internal Medicine, Department of Medicine, Mayo Clinic, Rochester, MN.

DOI - https://doi.org/10.18632/aging.203560

Corresponding authors - Tamar Tchkonia - tchkonia.tamar@mayo.edu, and James L. Kirkland - kirkland.james@mayo.edu

Abstract

Senescent cells, which arise due to damage-associated signals, are apoptosis-resistant and can express a pro-inflammatory, tissue-destructive senescence-associated secretory phenotype (SASP). We recently reported that a component of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) surface protein, S1, can amplify the SASP of senescent cultured human cells and that a related mouse β-coronavirus, mouse hepatitis virus (MHV), increases SASP factors and senescent cell burden in infected mice. Here, we show that SARS-CoV-2 induces senescence in human non-senescent cells and exacerbates the SASP in human senescent cells through Toll-like receptor-3 (TLR-3). TLR-3, which senses viral RNA, was increased in human senescent compared to non-senescent cells. Notably, genetically or pharmacologically inhibiting TLR-3 prevented senescence induction and SASP amplification by SARS-CoV-2 or Spike pseudotyped virus. While an artificial TLR-3 agonist alone was not sufficient to induce senescence, it amplified the SASP in senescent human cells. Consistent with these findings, lung p16INK4a+ senescent cell burden was higher in patients who died from acute SARS-CoV-2 infection than other causes. Our results suggest that induction of cellular senescence and SASP amplification through TLR-3 contribute to SARS-CoV-2 morbidity, indicating that clinical trials of senolytics and/or SASP/TLR-3 inhibitors for alleviating acute and long-term SARS-CoV-2 sequelae are warranted.

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Keywords - aging, SARS-COV-2, senescence, toll like receptor 3, COVID-19

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

Please visit our website at http://www.Aging-US.com​​ and connect with us:

SoundCloud - https://soundcloud.com/Aging-Us
Facebook - https://www.facebook.com/AgingUS/
Twitter - https://twitter.com/AgingJrnl
Instagram - https://www.instagram.com/agingjrnl/
YouTube - https://www.youtube.com/agingus​
LinkedIn - https://www.linkedin.com/company/aging/
Pinterest - https://www.pinterest.com/AgingUS/

Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com​​

Media Contact
18009220957
MEDIA@IMPACTJOURNALS.COM

Paper Spotlight: COVID Induces Cell Senescence and SASP via TLR-3

Don Whitley Scientific

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