Association of heat shock proteins with all-cause mortality

Experimental mild heat shock is widely known as an intervention that results in extended longevity in various models along the evolutionary lineage. Heat shock proteins (HSPs) are highly upregulated immediately after a heat shock. The elevation in HSP levels was shown to inhibit stress-mediated cell...

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Main Authors: Broer, L., Demerath, E. W., Garcia, M. E., Homuth, G., Kaplan, R. C., Lunetta, K. L., Tanaka, T., Tranah, G. J., Walter, S., Arnold, A. M., Atzmon, G., Harris, T. B., Hoffmann, W., Karasik, D., Kiel, D. P., Kocher, T., Launer, L. J., Lohman, K. K., Rotter, J. I., Tiemeier, H., Uitterlinden, A. G., Wallaschofski, H., Bandinelli, S., Dörr, M., Ferrucci, L., Franceschini, N., Gudnason, V., Hofman, A., Liu, Y., Murabito, J. M., Newman, A. B., Oostra, B. A., Psaty, B. M., Smith, A. V., van Duijn, C. M.
Format: Online
Language:English
Published: Springer Netherlands 2012
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3705092/
id pubmed-3705092
recordtype oai_dc
spelling pubmed-37050922013-07-11 Association of heat shock proteins with all-cause mortality Broer, L. Demerath, E. W. Garcia, M. E. Homuth, G. Kaplan, R. C. Lunetta, K. L. Tanaka, T. Tranah, G. J. Walter, S. Arnold, A. M. Atzmon, G. Harris, T. B. Hoffmann, W. Karasik, D. Kiel, D. P. Kocher, T. Launer, L. J. Lohman, K. K. Rotter, J. I. Tiemeier, H. Uitterlinden, A. G. Wallaschofski, H. Bandinelli, S. Dörr, M. Ferrucci, L. Franceschini, N. Gudnason, V. Hofman, A. Liu, Y. Murabito, J. M. Newman, A. B. Oostra, B. A. Psaty, B. M. Smith, A. V. van Duijn, C. M. Article Experimental mild heat shock is widely known as an intervention that results in extended longevity in various models along the evolutionary lineage. Heat shock proteins (HSPs) are highly upregulated immediately after a heat shock. The elevation in HSP levels was shown to inhibit stress-mediated cell death, and recent experiments indicate a highly versatile role for these proteins as inhibitors of programmed cell death. In this study, we examined common genetic variations in 31 genes encoding all members of the HSP70, small HSP, and heat shock factor (HSF) families for their association with all-cause mortality. Our discovery cohort was the Rotterdam study (RS1) containing 5,974 participants aged 55 years and older (3,174 deaths). We assessed 4,430 single nucleotide polymorphisms (SNPs) using the HumanHap550K Genotyping BeadChip from Illumina. After adjusting for multiple testing by permutation analysis, three SNPs showed evidence for association with all-cause mortality in RS1. These findings were followed in eight independent population-based cohorts, leading to a total of 25,007 participants (8,444 deaths). In the replication phase, only HSF2 (rs1416733) remained significantly associated with all-cause mortality. Rs1416733 is a known cis-eQTL for HSF2. Our findings suggest a role of HSF2 in all-cause mortality. Springer Netherlands 2012-05-04 2013-08 /pmc/articles/PMC3705092/ /pubmed/22555621 http://dx.doi.org/10.1007/s11357-012-9417-7 Text en © The Author(s) 2012
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Broer, L.
Demerath, E. W.
Garcia, M. E.
Homuth, G.
Kaplan, R. C.
Lunetta, K. L.
Tanaka, T.
Tranah, G. J.
Walter, S.
Arnold, A. M.
Atzmon, G.
Harris, T. B.
Hoffmann, W.
Karasik, D.
Kiel, D. P.
Kocher, T.
Launer, L. J.
Lohman, K. K.
Rotter, J. I.
Tiemeier, H.
Uitterlinden, A. G.
Wallaschofski, H.
Bandinelli, S.
Dörr, M.
Ferrucci, L.
Franceschini, N.
Gudnason, V.
Hofman, A.
Liu, Y.
Murabito, J. M.
Newman, A. B.
Oostra, B. A.
Psaty, B. M.
Smith, A. V.
van Duijn, C. M.
spellingShingle Broer, L.
Demerath, E. W.
Garcia, M. E.
Homuth, G.
Kaplan, R. C.
Lunetta, K. L.
Tanaka, T.
Tranah, G. J.
Walter, S.
Arnold, A. M.
Atzmon, G.
Harris, T. B.
Hoffmann, W.
Karasik, D.
Kiel, D. P.
Kocher, T.
Launer, L. J.
Lohman, K. K.
Rotter, J. I.
Tiemeier, H.
Uitterlinden, A. G.
Wallaschofski, H.
Bandinelli, S.
Dörr, M.
Ferrucci, L.
Franceschini, N.
Gudnason, V.
Hofman, A.
Liu, Y.
Murabito, J. M.
Newman, A. B.
Oostra, B. A.
Psaty, B. M.
Smith, A. V.
van Duijn, C. M.
Association of heat shock proteins with all-cause mortality
author_facet Broer, L.
Demerath, E. W.
Garcia, M. E.
Homuth, G.
Kaplan, R. C.
Lunetta, K. L.
Tanaka, T.
Tranah, G. J.
Walter, S.
Arnold, A. M.
Atzmon, G.
Harris, T. B.
Hoffmann, W.
Karasik, D.
Kiel, D. P.
Kocher, T.
Launer, L. J.
Lohman, K. K.
Rotter, J. I.
Tiemeier, H.
Uitterlinden, A. G.
Wallaschofski, H.
Bandinelli, S.
Dörr, M.
Ferrucci, L.
Franceschini, N.
Gudnason, V.
Hofman, A.
Liu, Y.
Murabito, J. M.
Newman, A. B.
Oostra, B. A.
Psaty, B. M.
Smith, A. V.
van Duijn, C. M.
author_sort Broer, L.
title Association of heat shock proteins with all-cause mortality
title_short Association of heat shock proteins with all-cause mortality
title_full Association of heat shock proteins with all-cause mortality
title_fullStr Association of heat shock proteins with all-cause mortality
title_full_unstemmed Association of heat shock proteins with all-cause mortality
title_sort association of heat shock proteins with all-cause mortality
description Experimental mild heat shock is widely known as an intervention that results in extended longevity in various models along the evolutionary lineage. Heat shock proteins (HSPs) are highly upregulated immediately after a heat shock. The elevation in HSP levels was shown to inhibit stress-mediated cell death, and recent experiments indicate a highly versatile role for these proteins as inhibitors of programmed cell death. In this study, we examined common genetic variations in 31 genes encoding all members of the HSP70, small HSP, and heat shock factor (HSF) families for their association with all-cause mortality. Our discovery cohort was the Rotterdam study (RS1) containing 5,974 participants aged 55 years and older (3,174 deaths). We assessed 4,430 single nucleotide polymorphisms (SNPs) using the HumanHap550K Genotyping BeadChip from Illumina. After adjusting for multiple testing by permutation analysis, three SNPs showed evidence for association with all-cause mortality in RS1. These findings were followed in eight independent population-based cohorts, leading to a total of 25,007 participants (8,444 deaths). In the replication phase, only HSF2 (rs1416733) remained significantly associated with all-cause mortality. Rs1416733 is a known cis-eQTL for HSF2. Our findings suggest a role of HSF2 in all-cause mortality.
publisher Springer Netherlands
publishDate 2012
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3705092/
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