Dr Diana Jurk
- Email: email@example.com
- Telephone: +44 (0) 191 208 1139
- Address: Institute for Ageing
Institute for Cell & Molecular Biosciences (ICaMB)
Campus for Ageing and Vitality
Newcastle upon Tyne, NE4 5PL, UK
- 2007-2012 PhD at the Faculty of Medical Science, Newcastle University “The role of cell senescence and inflammation in mouse ageing”
- 1997-2004 Degree in Natural Sciences (Diplom-Naturwissenschaftler) TU Bergakademie Freiberg, Germany
- March 2015 Faculty Fellow in the Institute for Cell & Molecular Biosciences (ICAMB) / Newcastle University Institute for Ageing (NUIA)
- 2012- 02/2015 Research Associate in the Newcastle University Institute for Ageing (NUIA) / Institute for Cell & Molecular Biosciences (ICAMB)
- 2007-2012 PhD at Newcastle University (UK) under the supervision of Professor T von Zglinicki
- 2009 Visiting scientist at the Max-Planck Institute on Stem Cell Ageing lead by Professor Lenhard Rudolph, Ulm University (Germany)
- Feb 2007-Aug 2007 Research Technician at the Centre for Integrated Systems Biology of Ageing and Nutrition (CISBAN), Newcastle University, UK
- 2005-2007 Research assistant at The Medical Center-University of Freiburg (Germany), Core facility Genomics lead by Dr. Dietmar Pfeifer
- 1997-2004 3 different work placements of 6 months each at Bayer AG (Wuppertal, Wuppertal-Elberfeld and Leverkusen, Germany)
Prizes and awards
- Travel bursary for 7th Annual Robert and Arlene Kogod Center on Aging Conference, Jacksonville (FL, US) 2016
- Travel bursary for 5th Annual Robert and Arlene Kogod Center on Aging Conference, Rochester, (MN, US) 2014 awarded by Mayo Clinic (Rochester, MN, US)
- Travel bursary for Cold Spring Harbor Asia Conference, Suzhou(China) 2013 awarded by IAH (Newcastle University)
- Travel bursary for 3rd Annual Robert and Arlene Kogod Center on Aging Conference, Rochester, (MN, US) 2012 awarded by Mayo Clinic (Rochester, MN, US)
- Awarded BSRA bursary for being UK representative at the American Aging Association Meeting in Phoenix, Arizona 2009
- Awarded best talk prize at the BSRA 2008 Annual scientific Meeting in Brighton (UK)
- International Cell Senescence Association (ICSA) Conference 2017, Paris (France)
- Molecules, Genes and Cells Club, Newcastle University, Newcastle (UK), 2016
- MIA-Summer School: Biology of Ageing, Alvor (Portugal), 2016
- 6th Annual Alliance for Healthy Aging Conference, Slaley Hall, Newcastle (UK), 2015
- CIMA Scientific Meeting, ‘Nutrition and Musculoskeletal Ageing, Newcastle (UK), 2014
- The Rank Prize Funds, Mini-symposium on Oxidative Stress, Grasmere (UK), 2014
- Cold Spring Harbor Asia Conference, Suzhou (China) 2013
- Ageing and Basic Bioscience Conference, Cambridge (UK), 2012
- Swedish Telomere and Telomerase Network Meeting, Fiskebäckskil (Sweden) 2010
- Gordon Research Seminar, Les Diablerets (Switzerland), 2010
- CISBAN Symposium, Newcastle University, 2009
- 38th Annual Meeting of the American Aging Association, Scottsdale (AZ, US) 2009
- BSRA, Annual Scientific Meeting, Brighton (UK), 2008
- 5th Alliance for Healthy Aging Symposium, Rochester (MN, US), 2014
- 4th Alliance for Healthy Aging Symposium, Groningen (Netherlands), 2013
- 3rd Alliance for Healthy Aging Symposium, Rochester (MN, USA) 2012
- Gordon Research Conference, Ventura (CA, US), 2012
- BSRA Annual Scientific Meeting, Brighton (UK), 2011
- Gordon Research Conference, Les Diablerets (Switzerland), 2010 BSRA Annual Scientific Meeting, Newcastle 2010 BSRA Annual Scientific Meeting, Manchester (UK), 2009
Cellular Senescence is most often induced as a response to persistent DNA damage and telomere dysfunction, leading to a massive cellular re-programming including hyper-production of reactive oxygen species (ROS) and secretion of bioactive peptides known as the senescence associated secretory phenotype (SASP). It occurs in vivo and contributes to age-related diseases.
As part of my PhD, I have demonstrate that ageing mice neurons show multiple hallmarks of cell senescence. Moreover, I proved that this phenotype can be induced by telomere-dysfunction and is dependent on cyclin-kinase inhibitor p21. This was the first time that a senescent-like state was observed in post-mitotic neurons in vivo and has led to the recent proposal by several reputed researchers of a redefinition of senescence as a phenotype not exclusive to proliferation competent cells. Furthermore, I have shown how cellular senescence induced by genotoxic or oxidative stress depends on chronic DNA-damage signalling from irreparable damage to telomeres. This work showed that telomere-associated DNA damage foci (TAF) existed irrespectively of telomere length and presence of telomerase in a variety of mice tissues and that TAF are a sensitive and robust marker for senescence. More recently, I have demonstrated that nfkb1-/- mice develop chronic systemic inflammation which aggravates cell senescence in various tissues, inducing an accelerated ageing phenotype and decreasing lifespan. This paper establishes a link between chronic inflammation, cellular senescence and ageing.
My current research focuses on senescence during brain ageing and in neurodegenerative diseases like Alzheimer’s and Parkinson’s disease. Age is the single most relevant factor for developing neurodegenerative diseases which contribute to significant cognitive decline. I have demonstrated that cellular senescence occurs during brain ageing. However, it is still unknown how senescence in the brain impacts on its function during ageing. I aim to understand exactly how cellular senescence contributes to brain ageing and age-related cognitive decline.
Additionally, cellular senescence is a major contributor to age related tissue degeneration and has been shown to be involved in non-alcoholic fatty liver disease (NAFLD), but the mechanisms driving NAFLD are largely unknown. I aim to understand how cellular senescence might contribute to liver disease and if elimination of senescent cells could be used as a therapy to slow down, counteract NAFLD or prevent progression of NAFLD to HCC.
In the last 3 years I supervised two undergraduate students, 2 master students and I am supervising three PhD students (Mikolaj Ogrodnik, Edward Fielder, Melanie Weigand).
- Ogrodnik M, Jurk D. Senescence explains age- and obesity-related liver steatosis. Cell Stress 2017. In Press.
- Ogrodnik M, Miwa S, Tchkonia T, Tiniakos D, Wilson CL, Lahat A, Day CP, Burt A, Palmer A, Anstee QM, Nagaraja Grellscheid S, Hoeijmakers JHJ, Barnhoorn S, Mann DA, Bird TG, Vermeij WP, Kirkland JL, Passos JF, vonZglinicki T, Jurk D. Cellular senescence drives age-dependent hepatic steatosis. Nature Communications 2017, 8, 15691.
- Stout MB, Steyn F, Jurczak MJ, Camporez JG, Zhu Y, Hawse JR, Jurk D, Palmer AK, Xu M, Pirtskhalava T, Evans GL, deSouzaSantos R, Frank AP, White TA, Monroe DG, Singh RJ, Casaclang-Verzosa G, Miller JD, Clegg DJ, LeBrasseur NK, vonZglinicki T, Shulman GI, Tchkonia T, Kirkland JL. 17α-Estradiol Alleviates Age-related Metabolic and Inflammatory Dysfunction in Male Mice Without Inducing Feminization. Journals of Gerontology Series A: Biological Sciences & Medical Sciences 2017, 72(1), 3-15.
- Hewitt G, Carroll B, Sarallah R, Correia-Melo C, Ogrodnik M, Nelson G, Otten EG, Manni D, Antrobus R, Morgan BA, von Zglinicki T, Jurk D, Seluanov A, Gorbunova V, Johansen T, Passos JF, Korolchuk VI. SQSTM1/p62 mediates crosstalk between autophagy and the UPS in DNA repair. Autophagy 2016, 12(10), 1917-1930.
- Correia-Melo C, Marques FDM, Anderson R, Hewitt G, Hewitt R, Cole J, Carroll BM, Miwa S, Birch J, Merz A, Rushton MD, Charles M, Jurk D, Tait SWG, Czapiewski R, Greaves L, Nelson G, Bohlooly-Y M, Rodriguez-Cuenca S, Vidal-Puig A, Mann D, Saretzki G, Quarato G, Green DR, Adams PD, von Zglinicki T, Korolchuk VI, Passos JF. Mitochondria are required for pro-ageing features of the senescent phenotype. EMBO Journal 2016, 35(7), 724-742.
- Xu M, Bradley EW, Weivoda MW, Hwang SM, Pirtskhalava T, Decklever T, Curran GL, Ogrodnik M, Johnson KO, Lowe V, Jurk D, Tchkonia T, Westendorf JJ, Kirkland JL. Transplanted senescent cells induce an osteoarthritis-like condition in mice. Journal of Gerontology: Series A: Biological Sciences & Medical Sciences 2016, Epub ahead of print.
- Roos CM, Zhang B, Palmer AK, Ogrodnik MB, Pirtskhalava T, Thalji NM, Hagler M, Jurk D, Smith LA, Casaclang-Verzosa G, Zhu Y, Schafer MJ, Tchkonia T, Kirkland JL, Miller JD. Chronic senolytic treatment alleviates established vasomotor dysfunction in aged or atherosclerotic mice. Aging Cell 2016.
- Wilson CL, Jurk D, Fullard N, Banks P, Page A, Luli S, Elsharkawy AM, Gieling RG, Bagchi-Chakraborty J, Fox C, Richardson C, Callaghan K, Blair GE, Fox N, Lagnado A, Passos JF, Moore AJ, Smith GR, Tiniakos DG, Mann J, Oakley F, Mann DA. NFkB1 is a suppressor of neutrophil-driven hepatocellular carcinoma. Nature Communications 2015, 6, 6818.
- Birch J, Anderson RK, Correia-Melo C, Jurk D, Hewitt G, Marques FM, Green NJ, Moisey E, Birrell MA, Belvisi MG, Black F, Taylor JJ, Fisher AJ, De Soyza A, Passos JF. DNA damage response at telomeres contributes to lung aging and chronic obstructive pulmonary disease. American Journal of Physiology: Lung Cellular and Molecular Physiology 2015, 309(10), L1124-L1137.
- Jurk D, Wilson C, Passos J, Oakley F, Correia-Melo C, Greaves L, Saretzki G, Fox C, Lawless C, Anderson R, Hewitt G, Pender SLF, Fullard N, Nelson G, Mann J, van de Sluis B, Mann DA, von Zglinicki T. Chronic inflammation induces telomere dysfunction and accelerates ageing in mice. Nature Communications 2014, 2, 4172.
- Jurk D, Wang C, Miwa S, Maddick M, Korolchuk V, Tsolou A, Gonos ES, Thrasivoulou C, Saffrey JM, Cameron K, von Zglinicki T. Postmitotic neurons develop a p21-dependent senescence-like phenotype driven by a DNA damage response. Aging Cell 2012, 11(6), 996-1004.
- Hewitt G, Jurk D, Marques FDM, Correia-Melo C, Hardy T, Gackowska A, Anderson R, Taschuk M, Mann J, Passos JF. Telomeres are favoured targets of a persistent DNA damage response in ageing and stress-induced senescence. Nature Communications 2012, 3(2), 708.
- Speakman JR, Blount JD, Bronikowski AM, Buffenstein R, Isaksson C, Kirkwood TB, Monaghan P, Ozanne SE, Beaulieu M, Briga M, Carr SK, Christensen LL, Cochemé HM, Cram DL, Dantzer B, Harper JM, Jurk D, King A, Noguera JC, Salin K, Sild E, Simons MJ, Smith S, Stier A, Tobler M, Vitikainen E, Peaker M, Selman C. Oxidative stress and life histories: unresolved issues and current needs. Ecology and Evolution 2015, 5(24), 5745-5757.
- Correia-Melo C, Jurk D, Passos JF. Robust Multiparametric Assessment of Cellular Senescence. In: Cellular Senescence. Humana Press, 2013, pp.409-419.
- Nelson G, Wordsworth J, Wang CF, Jurk D, Lawless C, Martin-Ruiz C, von Zglinicki T. A senescent cell bystander effect: senescence-induced senescence. Aging Cell 2012, 11(2), 345-349.
- Lawless C, Jurk D, Gillespie CS, Shanley D, Saretzki G, von Zglinicki T, Passos JF. A Stochastic Step Model of Replicative Senescence Explains ROS Production Rate in Ageing Cell Populations. PLoS One 2012, 7(2), e32117.
- Verma S, Tachtatzis P, Penrhyn-Lowe S, Scarpini C, Jurk D, von Zglinicki T, Coleman N, Alexander GJ. Sustained telomere length in hepatocytes and cholangiocytes with increasing age in normal liver. Hepatology 2012, 56(4), 1510-1520.
- Wang CF, Maddick M, Miwa S, Jurk D, Czapiewski R, Saretzki G, Langie SAS, Godschalk RWL, Cameron K, von Zglinicki T. Adult-onset, short-term dietary restriction reduces cell senescence in mice. Aging 2010, 2(9), 555-566.
- Lawless C, Wang CF, Jurk D, Merz A, von Zglinicki T, Passos JF. Quantitative assessment of markers for cell senescence. Experimental Gerontology 2010, 45(10), 772-778.
- Wang CF, Jurk D, Maddick M, Nelson G, Martin-Ruiz C, von Zglinicki T. DNA damage response and cellular senescence in tissues of aging mice. Aging Cell 2009, 8(3), 311-323.
- Gieling RG, Rajasekaran V, Jurk D, Elsharkawy AM, Burt AD, Oakley F, Mann DA. The Anti-Inflammatory and Anti-Proliferative Properties of the NFKB1 (P50) Gene Protect Against Hepatocellular Carcinoma. In: Hepatology: 60th Annual Meeting of the American Association for the Study of Liver Diseases. 2009, Boston, Massachusetts, USA: John Wiley & Sons, Inc.