Essay, Paper
Immunity & Ageing
Research
BioMed Central
Open Access
Cell autonomous expression of inflammatory genes in biologically aged fibroblasts associated with elevated NF-kappaB activity
Andres Kriete*1,2, Kelli L Mayo1,2, Nirupama Yalamanchili1, William Beggs2, Patrick Bender2, Csaba Kari3 and Ulrich Rodeck3
Address: 1School of Biomedical Engineering, Science and Health Systems, Drexel University, Bossone Research Center, 3141 Chestnut Street, Philadelphia, PA 19104, USA, 2Coriell Institute for Medical Research, 403 Haddon Avenue, Camden, NJ 08103, USA and 3Dept. of Dermatology and Cutaneous Biology, Thomas Jefferson University, 233 South 10th Street, Suite 326 BLSB, Philadelphia, PA 19107, USA Email: Andres Kriete* - ak3652@drexel.edu; Kelli L Mayo - mayokl@umdnj.edu; Nirupama Yalamanchili - ny29@drexel.edu; William Beggs - wgeggs@coriell.org; Patrick Bender - pbender@coriell.org; Csaba Kari - urodeck@mail.jci.tju.edu; Ulrich Rodeck - ulrich.rodeck@mail.jci.tju.edu * Corresponding author
Published: 16 July 2008 Immunity & Ageing 2008, 5:5 doi:10.1186/1742-4933-5-5
Received: 18 March 2008 Accepted: 16 July 2008
This article is available from: http://www.immunityageing.com/content/5/1/5 © 2008 Kriete et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Background: Chronic inflammation is a well-known corollary of the aging process and is believed to significantly contribute to morbidity and mortality of many age-associated chronic diseases. However, the mechanisms that cause age-associated inflammatory changes are not well understood. Particularly, the contribution of cell stress responses to age-associated inflammation in 'non-inflammatory' cells remains poorly defined. The present
Research
BioMed Central
Open Access
Cell autonomous expression of inflammatory genes in biologically aged fibroblasts associated with elevated NF-kappaB activity
Andres Kriete*1,2, Kelli L Mayo1,2, Nirupama Yalamanchili1, William Beggs2, Patrick Bender2, Csaba Kari3 and Ulrich Rodeck3
Address: 1School of Biomedical Engineering, Science and Health Systems, Drexel University, Bossone Research Center, 3141 Chestnut Street, Philadelphia, PA 19104, USA, 2Coriell Institute for Medical Research, 403 Haddon Avenue, Camden, NJ 08103, USA and 3Dept. of Dermatology and Cutaneous Biology, Thomas Jefferson University, 233 South 10th Street, Suite 326 BLSB, Philadelphia, PA 19107, USA Email: Andres Kriete* - ak3652@drexel.edu; Kelli L Mayo - mayokl@umdnj.edu; Nirupama Yalamanchili - ny29@drexel.edu; William Beggs - wgeggs@coriell.org; Patrick Bender - pbender@coriell.org; Csaba Kari - urodeck@mail.jci.tju.edu; Ulrich Rodeck - ulrich.rodeck@mail.jci.tju.edu * Corresponding author
Published: 16 July 2008 Immunity & Ageing 2008, 5:5 doi:10.1186/1742-4933-5-5
Received: 18 March 2008 Accepted: 16 July 2008
This article is available from: http://www.immunityageing.com/content/5/1/5 © 2008 Kriete et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Background: Chronic inflammation is a well-known corollary of the aging process and is believed to significantly contribute to morbidity and mortality of many age-associated chronic diseases. However, the mechanisms that cause age-associated inflammatory changes are not well understood. Particularly, the contribution of cell stress responses to age-associated inflammation in 'non-inflammatory' cells remains poorly defined. The present