DETERMINING THE ROLE FOR EXOSOMES DURING CELLULAR SENESCENCE AND AGEING
Lead Research Organisation:
Queen Mary University of London
Department Name: Blizard Institute of Cell and Molecular
Abstract
The number elderly population in the UK has dramatically increased in the last few decades. As a consequence, conditions associated with ageing, such as cancer, cardiovascular and neurodegenerative diseases, are having a huge impact on the public health system and the UK economy. It is therefore imperative to promote research that will improve our understanding of the mechanisms implicated in the maintenance of health across life. The primarily hallmark of ageing is the decline in the tissue homeostasis. However, the precise basic and cellular mechanisms implicated in the ageing process are not well established, hindering the advances in understanding how healthy ageing happens.
The organs and tissues in our body are formed by a vast number of cells, which altogether co-ordinate their actions for our body to function properly. However, a number of "abnormal" cells have been found in tissues derived from old patients. These particular cells suffer a growth arrest or lack of proliferation termed "senescence", which is thought to affect how the tissue functions. Senescent cells fail to proliferate, but they manage to communicate with their neighbour cells, mainly through the release of inflammatory proteins. In this application we will focus on a different way of intercellular communication during senescence, the release of small extracellular vesicles, called exosomes. Exosomes contain biological material in the form of proteins, RNA or small RNAs called microRNAs. Exosomes can release their inside content into particular cells, which as a consequence induce phenotypic changes in the target cells. Our preliminary data show that senescent cells secrete a high number of exosomes and, as a consequence, induce senescence in neighbouring cells. This application will explore the molecular mechanisms by which exosomes released from senescent cells induce senescence in neighbouring cells. We will also determine the inside content of these particular exosomes, in addition to the inside content of exosomes secreted by cells donated by elderly patients, to study similarities and differences between both models. Finally, we will focus on the functionality of exosomes using three-dimensional models of skin culture. During this application we will use a range of approaches, including human cell culture, high-resolution imaging techniques, state-of-the-art proteomics and genomics and an in vitro human skin model. Altogether, this project will help understand the mechanisms by which exosomes regulate normal ageing and it will allow to improve human health and wellbeing throughout life.
The organs and tissues in our body are formed by a vast number of cells, which altogether co-ordinate their actions for our body to function properly. However, a number of "abnormal" cells have been found in tissues derived from old patients. These particular cells suffer a growth arrest or lack of proliferation termed "senescence", which is thought to affect how the tissue functions. Senescent cells fail to proliferate, but they manage to communicate with their neighbour cells, mainly through the release of inflammatory proteins. In this application we will focus on a different way of intercellular communication during senescence, the release of small extracellular vesicles, called exosomes. Exosomes contain biological material in the form of proteins, RNA or small RNAs called microRNAs. Exosomes can release their inside content into particular cells, which as a consequence induce phenotypic changes in the target cells. Our preliminary data show that senescent cells secrete a high number of exosomes and, as a consequence, induce senescence in neighbouring cells. This application will explore the molecular mechanisms by which exosomes released from senescent cells induce senescence in neighbouring cells. We will also determine the inside content of these particular exosomes, in addition to the inside content of exosomes secreted by cells donated by elderly patients, to study similarities and differences between both models. Finally, we will focus on the functionality of exosomes using three-dimensional models of skin culture. During this application we will use a range of approaches, including human cell culture, high-resolution imaging techniques, state-of-the-art proteomics and genomics and an in vitro human skin model. Altogether, this project will help understand the mechanisms by which exosomes regulate normal ageing and it will allow to improve human health and wellbeing throughout life.
Technical Summary
The overall hypothesis of this project is that exosomes secreted by senescent and ageing cells play a key role in inducing senescence and ageing in a non-cell autonomous fashion. The secretion of inflammatory proteins, termed senescence-associated secretory phenotype or SASP, has been described as the main mechanism for senescent cells to communicate with their environment. However, most cells also signal through the release of extracellular vesicles (EV) termed exosomes, but little is known of their role during senescence or ageing. Exosomes contain a subset of proteins, lipids and nucleic acids that can change in composition depending on the parent cell. Our preliminary data show that senescent cells release a higher number of exosomes than proliferating cells. We show that exosomes from senescent cells express the cell adhesion protein integrin beta 3 and can induce senescence in other cells. This application proposes to study the mechanism(s) by which these exosomes induce senescence by studying the role of integrin beta 3 and investigating the role that other kinases play. We will also determine the cargo of exosomes from senescent and elderly patient cells and study their function using human skin organotypic models. Altogether, we propose a programme of research that aims to determine the role of exosomes secreted by senescent and old patient-derived cells in modulating the behaviour of cells in the surrounding environment. Data obtained from this proposal will give an extensive overview of the basic mechanisms for exosome function during ageing and senescence. In fact, it will advance our knowledge of the biology of normal ageing and will lead to approaches to improve healthy ageing.
Planned Impact
There are currently more than 10 million people in the UK over 65 years old, with an estimation for a significant increase within the next few years. The UK's ageing population has considerable consequences for public spending and the UK economy, due to the development of a number of age-associated diseases, such as cardiovascular, neurodegenerative and cancer. Consequently, there is an urgent need to promote research that will lead to a healthy lifespan across the entire life course.
The output of this piece of research will benefit a large number of sectors within the UK:
Academic and researcher peers will benefit from this proposal by providing new knowledge and basic scientific advancement of intercellular communication mechanisms during senescence and ageing. This will include not only peers within the immediate professional circle, but also professionals within other research areas such as cancer, immunobiology and fibrosis, where senescent cells have been identified in vivo.
Pharmaceutical companies will benefit from this project if we discover new kinases regulating exosome-induced senescence. We hypothesise that blocking the long-term accumulation of senescent cells induced by exosomes release and spread will improve healthy ageing in humans. In fact, the Van Deursen Lab has successfully demonstrated in animal models of premature ageing, that the elimination of senescence cells alleviates different ageing-related phenotypes.
The general public will also benefit from this research if it leads to the development of therapies improving healthy ageing and increasing the quality of life throughout our lifecourse. It will also benefit by increasing the public awareness and the scientific understanding of how healthy ageing occurs and by explaining how basic research impacts on the UK society and economy. In the event of finding very specific cargo contents in exosomes secreted by senescence cells and age-derived fibroblasts, future investigations will lead to the discovery of specific ageing biomarkers in a relatively short-term.
Our research will provide the UK Life sciences community with highly trained and exceedingly skilled scientists who will have received training in public engagement and have a clear emphasis on keeping the public informed about research discoveries in this field, as this is a QMUL number one priority. This is a benefit to the UK Life sciences sector by increasing UK Life sciences expertise, which will eventually help the UK science economy.
The UK Economy will also greatly benefit from the results obtained from this application. There are currently a large number of elderly people in the UK and, more than 65% of the Department for Work and Pensions benefits expenditure goes to this sector. This poses a huge burden on the UK economy and the NHS sector. Our research will lead to understanding the basic mechanism(s) for how normal and healthy ageing occurs and it will help promote healthy ageing and avoid the overuse of the NHS public spending.
The output of this piece of research will benefit a large number of sectors within the UK:
Academic and researcher peers will benefit from this proposal by providing new knowledge and basic scientific advancement of intercellular communication mechanisms during senescence and ageing. This will include not only peers within the immediate professional circle, but also professionals within other research areas such as cancer, immunobiology and fibrosis, where senescent cells have been identified in vivo.
Pharmaceutical companies will benefit from this project if we discover new kinases regulating exosome-induced senescence. We hypothesise that blocking the long-term accumulation of senescent cells induced by exosomes release and spread will improve healthy ageing in humans. In fact, the Van Deursen Lab has successfully demonstrated in animal models of premature ageing, that the elimination of senescence cells alleviates different ageing-related phenotypes.
The general public will also benefit from this research if it leads to the development of therapies improving healthy ageing and increasing the quality of life throughout our lifecourse. It will also benefit by increasing the public awareness and the scientific understanding of how healthy ageing occurs and by explaining how basic research impacts on the UK society and economy. In the event of finding very specific cargo contents in exosomes secreted by senescence cells and age-derived fibroblasts, future investigations will lead to the discovery of specific ageing biomarkers in a relatively short-term.
Our research will provide the UK Life sciences community with highly trained and exceedingly skilled scientists who will have received training in public engagement and have a clear emphasis on keeping the public informed about research discoveries in this field, as this is a QMUL number one priority. This is a benefit to the UK Life sciences sector by increasing UK Life sciences expertise, which will eventually help the UK science economy.
The UK Economy will also greatly benefit from the results obtained from this application. There are currently a large number of elderly people in the UK and, more than 65% of the Department for Work and Pensions benefits expenditure goes to this sector. This poses a huge burden on the UK economy and the NHS sector. Our research will lead to understanding the basic mechanism(s) for how normal and healthy ageing occurs and it will help promote healthy ageing and avoid the overuse of the NHS public spending.
Organisations
- Queen Mary University of London (Lead Research Organisation)
- QUEEN MARY UNIVERSITY OF LONDON (Collaboration)
- Francis Crick Institute (Collaboration)
- Hospital Ramón y Cajal (Collaboration)
- Hebrew University of Jerusalem (Collaboration)
- Spanish National Cancer Research Center (Collaboration)
- UNIVERSITY OF CAMBRIDGE (Collaboration)
- Mount Sinai Hospital (USA) (Collaboration)
- KING'S COLLEGE LONDON (Collaboration)
People |
ORCID iD |
Ana O'Loghlen (Principal Investigator) |
Publications
Fafián-Labora JA
(2020)
Small Extracellular Vesicles Have GST Activity and Ameliorate Senescence-Related Tissue Damage.
in Cell metabolism
Fafián-Labora JA
(2020)
Classical and Nonclassical Intercellular Communication in Senescence and Ageing.
in Trends in cell biology
Fafián-Labora J
(2019)
FASN activity is important for the initial stages of the induction of senescence.
in Cell death & disease
Carpintero-Fernández P
(2022)
Genome wide CRISPR/Cas9 screen identifies the coagulation factor IX (F9) as a regulator of senescence.
in Cell death & disease
Carpintero-Fernández P
(2017)
Technical Advances to Study Extracellular Vesicles.
in Frontiers in molecular biosciences
Borghesan M
(2017)
Integrins in senescence and aging.
in Cell cycle (Georgetown, Tex.)
Description | Senescence is a cellular phenotype present in health and disease, characterized by a stable cell-cycle arrest and an inflammatory response termed senescence-associated secretory phenotype (SASP) 1-3. Although senescent cells can stay without proliferating for long periods of time, they are metabolically and transcriptionally active and communicate with their microenvironment through the release of inflammatory proteins. The SASP is important in influencing the behaviour of neighbouring cells and altering the microenvironment and tissue function; yet, this role has been mainly attributed to soluble factors. In this research project, we proposed an alternative way for senescent cells to communicate with other cells. We hypothesised that exosomes or small extracellular vesicles (sEV) released by senescent cells play a key role in inducing senescence and ageing in proliferating cells via a non-cell autonomous fashion 1. The strong preliminary data from our previous proposal confirmed our initial hypothesis. As proposed in Aim1, we demonstrated that sEV are capable of transmitting paracrine senescence to nearby cells named exosome-induced senescence, ExIS, herein 4. To address this, we isolated sEV using a variety of techniques and characterised the isolated sEV employing a diversity of methods as recommended by the International Society of Extracellular Vesicles guidelines -MISEV2018- to which we contributed 5,6. Confirmation of the senescent phenotype in proliferating cells treated with sEV from senescent cells was determined by transcriptomics analysis and validation. EV internalisation was determined following different techniques including but not limited to confocal microscopy. Importantly, we further confirmed a direct functional correlation between individual cell EV internalization and the establishment of the senescent phenotype using a Cre-loxP reporter system. The use of inhibitors and siRNA targeting neutral sphingomyelinase enzyme, which is important for the release of EV, prevented the transmission of paracrine senescence. As expected, the transmission of paracrine senescence mediated by sEV is dependent on the activation of classical senescence pathways such as p16INK4A and p21CIP. In addition, a MAPK screen to determined signalling pathways implicated in ExIS paracrine senescence identified the p38MAPK (mitogen-activated protein kinases), mTOR (mammalian target of rapamycin) and IKK (I?B kinase) pathways as important in ExIS. In fact, we found that the canonical NF-?B pathway plays a key role in ExIS transmission 7. "Omics" analysis of the sEV content described in Aim2 showed differential proteomics and transcriptomics expression between sEV isolated from proliferating and senescent cells. Importantly, bioinformatics analysis comparing mass spectrometry analyses of a previously published soluble fraction and the sEV fraction released by senescent cells in this project show little correlation suggesting that a particular sEV-specific secretome might exist 4,8. These findings have been further confirmed by a recent independent report 9. The top proteins and microRNA found to be enriched in sEV from senescent cells have been further validated. In addition, by combining functional assays manipulating the sEV protein content with functional siRNA screens we identified two proteins implicated in the interferon pathway (IFITM3 and MX1) as being partially responsible for the transmission of paracrine senescence to proliferating cells 4. Regarding the physiological relevance of sEV in senescence and ageing described in Aim3 we have shown an increase in the number of sEV released in the plasma of healthy old human donors (?80 years) in comparison with young donors (?33 years) 4. Interestingly, we found an increase in the protein expression levels of IFITM3 in these sEV isolated from the old human donors versus sEV from young donors 4. We have also confirmed that sEV isolated from human primary fibroblasts cultures derived from elderly donors (?80 years) transmit paracrine senescence to human primary fibroblasts cultures derived from young donors (?2 years) suggesting that sEV could play a role in the transmission of ageing 7. Objectives achieved beyond the described aims We found an increase in the number of multivesicular bodies (MVB) within senescent cells by electron microscopy in a pancreatic mouse model of senescence in collaboration with the University of Jerusalem and King's College. Importantly, we established a new collaboration with the University of Cambridge where we found that the cells staining positive for senescence-associated-?-galactosidase (SA-?? -Gal), a biomarker for senescence, by immunohistochemistry in lung fibrotic lesions from human patients co-stained with CD63, a tetraspan biomarker for EV 4. In addition, as an increase in the release of sEV during senescence independent of the trigger occurs, we further hypothesised that the lipid biosynthesis pathway could be altered during senescence. In fact, we found that a main regulator of lipid synthesis, the fatty acid synthase enzyme (FASN) was an important regulator of senescence. Thus, blocking FASN activity not only prevented senescence via p53 activation but also blocked the release of sEV 10. We have also unveiled a role for sEV in delaying ageing both in aged human cell cultures and naturally aged mice 11,12. Thus, sEV have the potential to be considered as rejuvenation therapy 11,13. Aged human cell cultures and mice tissue contain a mixed population of both proliferative and senescent cells. While we have previously unveiled the effect that sEV from senescent cell have on proliferating cells 4, here we have found that sEV from proliferative cells also influence senescent cells. We have found that sEV from proliferative cells contain a glutathione-S-transferase enzyme (GST) conferring sEV with GST activity. As a consequence, sEV from proliferative cells confer GST activity to human aged cell cultures and mice aged tissues such as liver, kidney, adipose tissue and serum. These changes in the glutathione metabolism pathway influence the oxidation of lipids and induce cellular and tissue rejuvenation 12. REFERENCES 1 O'Loghlen, A. Role for extracellular vesicles in the tumour microenvironment. Philos Trans R Soc Lond B Biol Sci 373, doi:10.1098/rstb.2016.0488 (2018). 2 Fafian-Labora, J. A. & O'Loghlen, A. Classical and Nonclassical Intercellular Communication in Senescence and Ageing. Trends Cell Biol 30, 628-639, doi:10.1016/j.tcb.2020.05.003 (2020). 3 Prasanna, P. G. et al. Therapy-Induced Senescence: Opportunities to Improve Anticancer Therapy. J Natl Cancer Inst 113, 1285-1298, doi:10.1093/jnci/djab064 (2021). 4 Borghesan, M. et al. Small Extracellular Vesicles Are Key Regulators of Non-cell Autonomous Intercellular Communication in Senescence via the Interferon Protein IFITM3. Cell Rep 27, 3956-3971 e3956, doi:10.1016/j.celrep.2019.05.095 (2019). 5 Carpintero-Fernandez, P., Fafian-Labora, J. & O'Loghlen, A. Technical Advances to Study Extracellular Vesicles. Front Mol Biosci 4, 79, doi:10.3389/fmolb.2017.00079 (2017). 6 Thery, C. et al. Minimal information for studies of extracellular vesicles 2018 (MISEV2018): a position statement of the International Society for Extracellular Vesicles and update of the MISEV2014 guidelines. J Extracell Vesicles 7, 1535750, doi:10.1080/20013078.2018.1535750 (2018). 7 Fafian-Labora, J. A. & O'Loghlen, A. NF-kappaB/IKK activation by small extracellular vesicles within the SASP. Aging cell 20, e13426, doi:10.1111/acel.13426 (2021). 8 Acosta, J. C. et al. A complex secretory program orchestrated by the inflammasome controls paracrine senescence. Nat Cell Biol 15, 978-990, doi:10.1038/ncb2784 (2013). 9 Basisty, N. et al. A proteomic atlas of senescence-associated secretomes for aging biomarker development. PLoS Biol 18, e3000599, doi:10.1371/journal.pbio.3000599 (2020). 10 Fafian-Labora, J. et al. FASN activity is important for the initial stages of the induction of senescence. Cell Death Dis 10, 318, doi:10.1038/s41419-019-1550-0 (2019). 11 Rodriguez-Navarro, J. A. et al. Extracellular vesicles as potential tools for regenerative therapy. Mol Cell Oncol 7, 1809958, doi:10.1080/23723556.2020.1809958 (2020). 12 Fafian-Labora, J. A., Rodriguez-Navarro, J. A. & O'Loghlen, A. Small Extracellular Vesicles Have GST Activity and Ameliorate Senescence-Related Tissue Damage. Cell Metab 32, 71-86 e75, doi:10.1016/j.cmet.2020.06.004 (2020). 13 O'Loghlen, A. The potential of aging rejuvenation. Cell Cycle, 1-6, doi:10.1080/15384101.2021.2013612 (2022). |
Exploitation Route | We believe, the identification of a role for small extracellular vesicles during cellular senescence, ageing and age-related diseases has opened new lines of research into the files in addition to the opportunity to take the results of this project to pharmaceutical companies. |
Sectors | Pharmaceuticals and Medical Biotechnology |
URL | https://sites.google.com/view/theologhlenlab |
Description | MISEV guidelines |
Geographic Reach | Multiple continents/international |
Policy Influence Type | Influenced training of practitioners or researchers |
Description | Becas postdoctorales |
Amount | € 120,000 (EUR) |
Organisation | Government of Galicia |
Sector | Public |
Country | Spain |
Start | 06/2017 |
End | 06/2020 |
Description | Collaboration with an industrial partner |
Amount | £84,000 (GBP) |
Organisation | Reneuron |
Sector | Private |
Country | United Kingdom |
Start | 01/2017 |
End | 01/2018 |
Description | DMM Conference Travel Grant - CTG-DMM181175 - 20th International AEK Cancer Congress |
Amount | £600 (GBP) |
Funding ID | CTG-DMM181175 |
Organisation | Company of Biologists |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start | 02/2019 |
End | 03/2019 |
Description | Extracellular vesicles rejuvenation potential in ageing |
Amount | £38,000 (GBP) |
Funding ID | MGU0497 |
Organisation | Barts Charity |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start | 02/2020 |
End | 01/2021 |
Description | Life Science Initiative - Centre for Genomics and Child Health |
Amount | £5,000 (GBP) |
Organisation | Queen Mary University of London |
Sector | Academic/University |
Country | United Kingdom |
Start | 06/2018 |
End | 12/2018 |
Description | Papel de la autofagia glial en neurodegeneracio´n y envejecimiento |
Amount | € 150,000 (EUR) |
Organisation | Ministry of Economy, Industry and Competitivity, Spain |
Sector | Public |
Country | Spain |
Start |
Description | Royal Society of London |
Amount | £15,000 (GBP) |
Funding ID | RG170399 |
Organisation | The Royal Society |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start | 03/2018 |
End | 04/2019 |
Description | The potential of extracellular vesicles as a therapeutic approach to prevent ageing |
Amount | £282,000 (GBP) |
Funding ID | G-002158 |
Organisation | Barts Charity |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start | 01/2022 |
End | 12/2025 |
Title | Proteomics for exos from senescent cells |
Description | Proteomic analyses of exosomes derived from cell undergoing senescence induce by different triggers. |
Type Of Material | Database/Collection of data |
Year Produced | 2018 |
Provided To Others? | No |
Impact | Not yet as it hasn't beed released to the public |
Title | RNA seq of exoPS |
Description | Database on RNA seq of exosome-induced senescence |
Type Of Material | Database/Collection of data |
Year Produced | 2019 |
Provided To Others? | No |
Impact | No impact yet as it has not been released |
Description | Amaia Lujambio collaboration |
Organisation | Mount Sinai Hospital (USA) |
Country | United States |
Sector | Hospitals |
PI Contribution | We provided intelectual input on a project and the publication of a manuscript. |
Collaborator Contribution | Provided a novel experimental approach for the publication of a paper and contacts to obtain a particular cell line. |
Impact | 10.1016/j.celrep.2017.02.012 |
Start Year | 2016 |
Description | Anna Vossenkamper |
Organisation | Queen Mary University of London |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | Experimentla design |
Collaborator Contribution | Provided samples and performed experiments |
Impact | Manuscript in preparation |
Start Year | 2018 |
Description | CNIO proteomics unit - Javier Munoz |
Organisation | Spanish National Cancer Research Center |
Country | Spain |
Sector | Public |
PI Contribution | Expertise and intelectual contribution |
Collaborator Contribution | Expertise in mass spectometry analysis and intelectual input in data analysis |
Impact | Exosomes are key regulators of non-cell autonomous intercellular communication in senescence (submitted manuscript) |
Start Year | 2017 |
Description | Daniel Munoz-Espin |
Organisation | University of Cambridge |
Department | Department of Oncology |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | Intellectual input onthe experimental design |
Collaborator Contribution | This collaboration provided access to human samples and technical help by staining and analysing the samples. |
Impact | A joint publication is currently under preparation |
Start Year | 2018 |
Description | Genomics Centre Bart Cancer Institute |
Organisation | Queen Mary University of London |
Department | Barts Cancer Institute |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | Intellectual input in the design of the experiments |
Collaborator Contribution | Collaboration finding a transcriptional profile in primary cells treated with the exosomes derived from a variety of control and senescent-derived exosomes |
Impact | Identification of a new trigger of senescence involving non-cell autonomous signaling. |
Start Year | 2017 |
Description | Hector Peinado |
Organisation | Spanish National Cancer Research Center |
Country | Spain |
Sector | Public |
PI Contribution | Provided intellectual input into novel findings regarding exosome biogenesis |
Collaborator Contribution | Intellectual contribution into exosome biogenesis |
Impact | We currently have a manuscript in preparation |
Start Year | 2017 |
Description | Ittai Ben-Porath |
Organisation | Hebrew University of Jerusalem |
Country | Israel |
Sector | Academic/University |
PI Contribution | Intellectual input and helped perform, analyse and take electron microscopy images. |
Collaborator Contribution | Provided pancreatic mouse tissue and contributed to discuss the data obtained |
Impact | We currently have a publication under preparation. |
Start Year | 2017 |
Description | Jose Antonio Rodriguez Navarro |
Organisation | Hospital Ramón y Cajal |
Country | Spain |
Sector | Hospitals |
PI Contribution | I provided staff and expertise in cellular senescence |
Collaborator Contribution | Expertise in determining ageing in vivo |
Impact | Publication under preparation Patent under-revision |
Start Year | 2022 |
Description | Proteomics Francis Crick London |
Organisation | Francis Crick Institute |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | Intelectual input that led to a publication |
Collaborator Contribution | Provided expertise in mass spectometry and data analysis |
Impact | 10.1016/j.celrep.2017.02.012 |
Start Year | 2013 |
Description | Rob Lowe |
Organisation | Queen Mary University of London |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | Provided RNA seq data and samples |
Collaborator Contribution | Provided data from RNA sequencing samples and experimental design |
Impact | Manuscript in preparation |
Start Year | 2018 |
Description | Roland Fleck - KCL |
Organisation | King's College London |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | Provided samples for analyses and contributed to the staining of samples |
Collaborator Contribution | Performed, in collaboration with members of my group, staining of samples and helped with the imaging of the samples |
Impact | Manuscript in preparation |
Start Year | 2017 |
Description | Centre of the Cell |
Form Of Engagement Activity | Participation in an open day or visit at my research institution |
Part Of Official Scheme? | No |
Geographic Reach | Local |
Primary Audience | Schools |
Results and Impact | Discussion aboutn my line of work with Sedondary School pupils |
Year(s) Of Engagement Activity | 2018,2019,2020 |
Description | Interview for MedicalResearch.com |
Form Of Engagement Activity | A press release, press conference or response to a media enquiry/interview |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Public/other audiences |
Results and Impact | Interview by Medical Research.com |
Year(s) Of Engagement Activity | 2017 |
URL | https://medicalresearch.com/author-interviews/why-cells-fall-apart-protein-regulates-cell-aging/3270... |
Description | Interview for the New Channel CCN |
Form Of Engagement Activity | A press release, press conference or response to a media enquiry/interview |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Public/other audiences |
Results and Impact | Interview by the television news channel CCN |
Year(s) Of Engagement Activity | 2017 |
URL | http://en.cncnews.cn/news/v_show/63929_Study_makes_Anti-ageing_breakthrough.shtml |