Principal Investigator, Linus Pauling Institute
Associate Professor, Department of Biochemistry and Biophysics
Office: 351 Linus Pauling Science Center
Email Address: email@example.com
Mailing/Express Delivery Address:
Viviana Pérez, Ph.D.
Linus Pauling Institute
Oregon State University
307 Linus Pauling Science Center
Corvallis, OR 97331
My primary research focus is investigation of the role of protein homeostasis in aging. Studies in mice, Drosophila and C. elegans suggest that activities associated with protein homeostasis decrease during aging. Previously in our laboratory, we found that the proteomes of long-lived species (i.e., little brown bat and naked mole rat) are more resistant to both urea-induced and heat-induced unfolding than that of shorter-lived bats or mice. Using a comparative biology approach, we recently showed that not all proteostasis mechanisms are enhanced in all long-lived species, i.e., while long-lived rodents (naked mole rat) and marsupials (sugar glider), show increased autophagy, proteasome, and heat shock proteins, long-lived bats only show upregulation of autophagy and heat shock proteins, suggesting that different long-lived species may use different proteostasis mechanisms to protect their proteome. The improvement in proteostasis pathways observed in long-lived mammals suggests that they might have an improved ability to deal with aggregation-prone proteins. Our preliminary data indicate that skin fibroblasts from naked mole rats (a long-lived species) are able to respond better to poly-Q proteotoxicity than fibroblasts from mice (a short-lived species from the same clade). Therefore, the research goal of my laboratory is to determine the mechanism(s) by which long-lived species are more resistance to proteotoxicity.
My second area of interest includes studies on cellular senescence and rapamycin. It is well known that senescent cells contribute to age-related pathology and loss of function, and their selective removal improves function and longevity. Rapamycin, an inhibitor of mTOR, inhibits cell senescence in vitro and increases longevity in several species. Our preliminary data using wild type fibroblasts indicates that rapamycin increases the levels of Nrf-2, and this correlates with activation of autophagy and a reduction in the induction of senescent cells, as measured by β-gal staining and p16 and p21 molecular markers. Therefore, my laboratory is investigating whether Nrf2 is involved in the mechanism by which rapamycin delays cell senescence.
|2004-2011||Postdoc, Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio|
|2004||Ph.D., University of Chile|
|1997||Pharmaceutical Chemist (with Maximal Distinction), Pharmacy School, University of Chile|
|1994||Licensed in Pharmaceutical Chemistry (with Distinction), Pharmacy School, University of Chile|
|2017-present||Associate Professor, Department of Biochemistry and Biophysics, Oregon State University
Principal Investigator, Linus Pauling Institute, Oregon State University
|2011-2017||Assistant Professor, Department of Biochemistry and Biophysics, Oregon State University
Principal Investigator, Linus Pauling Institute, Oregon State University
|2010-2011||Assistant Professor/Research, Barshop Institute for Longevity and Aging Studies, Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio|
|2010||Ellison Medical Foundation New Scholar in Aging Award|
|2009||Travel award sponsored by AFAR's Dorothy Dillon Eweson Lecture Series on Advances in Aging Research for the 2009 Gordon Research Conference on Oxidative Stress and Disease, Lucca (Barga) Italy|
|2009||Selected for a short talk in Gordon Research Conference on Oxidative Stress and Disease, Lucca (Barga), Italy|
|2008||Ellison Medical Foundation/AFAR Senior Postdoctoral Award|
|2008||Barbara H Bowman Postdoctoral Research Award|
|2007||Paul E. Glenn Award for postdoctoral research from American Aging Association, 36th Annual Meeting, San Antonio, TX|
|2007||Travel award from American Aging Association - 36th Annual Meeting, San Antonio, TX|
|2007||Invited as a Faculty/Instructor in Molecular Biology on Aging Course, Marine Biology Laboratory, Woods Hole, MA|
|2006||Accepted for Fourteenth Annual Summer Training Course in Experimental Aging Research, Buck Institute, Novato, CA|
|2006||Accepted for participation in Postdoctoral Career Workshop, The University of Texas Health Science Center at San Antonio, TX|
|2005||Accepted for participation in Molecular Biology on Aging Course, Marine Biology Laboratory, Woods Hole, MA|
|2001-2003||FONDECYT grant for Ph.D. dissertation (Chilean Ph.D. grant)|
|2000-2003||CONICYT Fellowship (Chilean fellowship for graduate student)|
Free Radical Biology and Medicine
American Aging Association
American Federation for Aging Studies
Gerontological Society of America
Zhang Y, Liu Y, Walsh M, Bokov A, Ikeno Y, Jang YC, Pérez VI, Van Remmen H, Richardson A. (2016). Liver specific expression of Cu/ZnSOD extends the lifespan of Sod1 null mice. Mechanisms of ageing and development 154:1-8.
Watson GW, Wickramasekara S, Fang Y, Maier CS, Williams DE, Dashwood RH, Pérez VI, Ho E. (2015) HDAC6 activity is not required for basal autophagic flux in metastatic prostate cancer cells. Exp Biol Med (Maywood), Epub ahead of print.
Watson GW, Wickramasekara S, Fang Y, Palomera-Sanchez Z, Maier CS, Williams DE, Dashwood RH, Pérez VI, Ho E. (2015) Analysis of autophagic flux in response to sulforaphane in metastatic prostate cancer cells. Mol Nutr Food Res 59:1954-1961.
Yu Z, Sunchu B, Fok WC, Alshaikh N, Pérez VI. (2015) Gene expression in the liver of female, but not male mice treated with rapamycin resembles changes observed under dietary restriction. Springerplus 4:174.
Pride H, Yu Z, Sunchu B, Mochnick J, Coles A, Zhang Y, Buffenstein R, Hormsby PJ, Austad SN, Pérez VI. (2015) Long-lived species have improvoed proteostasis compared to phylogenetically-related shorter-lived species. Biochem Biophys Res Comm 457:669-675.
Fok WC, Livi C, Bokov A, Yu Z, Chen Y, Richardson A, Pérez VI. (2014) Short-term rapamycin treatment in mice has few effects on the transcriptome of white adipose tissue compared to dietary restriction. Mech Ageing Dev 140:23-29.
Yu Z, Wang R, Fok WC, Coles A, Salmon AB, Pérez VI. (2014) Rapamycin and dietary restriction induce metabolically distinctive changes in mouse liver. J Gerontol A Biol Sci Med Sci 70:410-420.
Fok WC, Chen Y, Bokov A, Zhang Y, Salmon AB, Diaz V, Javors M, Wood WH 3rd, Zhang Y, Becker KG, Pérez VI, Richardson A. (2014) Mice fed rapamycin have an increase in lifespan associated with major changes in the liver transcriptome. PLoS One 9:e83988.
Triana-Martínez F, López-Diazguerrero NE, Maciel-Barón LA, Morales-Rosales SL, Galván-Arzate S, Fernandez-Perrino FJ, Zentella A, Pérez VI, Gomez-Quiroz LE, Königsberg M. (2014) Cell proliferation arrest and redox state status as part of different stages during senescence establishment in mouse fibroblasts. Biogerontology 15:165-176.
Fok WC, Bokov A, Gelfond J, Yu Z, Zhang Y, Doderer M, Chen Y, Javors M, Wood WH 3rd, Zhang Y, Becker KG, Richardson A, Pérez VI. (2014) Combined treatment of rapamycin and dietary restriction has a larger effect on the transcriptome and metabolome of liver. Aging Cell 13:311-319.
Fok WC, Zhang Y, Salmon AB, Bhattacharya A, Gunda R, Jones D, Ward W, Fisher K, Richardson A, Pérez VI. (2012) Short-term treatment with rapamycin and dietary restriction have overlapping and distinctive effects in young mice. J Gerontol A Biol Sci Med Sci 68:108-116.