Age-related trends in gene expression in the chemosensory-nasal mucosae of senescence-accelerated mice

Thomas V. Getchell; Xuejun Peng; Arnold J. Stromberg; Kuey Chu Chen; C. Paul Green; Nishikant K. Subhedar; Dharmen S. Shah; Mark P. Mattson; Marilyn L. Getchell

doi:10.1016/S1568-1637(02)00066-1

Age-related trends in gene expression in the chemosensory-nasal mucosae of senescence-accelerated mice

Thomas V. Getchell, Xuejun Peng, Arnold J. Stromberg, Kuey Chu Chen, C. Paul Green, Nishikant K. Subhedar, Dharmen S. Shah, Mark P. Mattson, Marilyn L. Getchell

Research output: Contribution to journal › Review article › peer-review

22 Scopus citations

Abstract

We have utilized high-density GeneChip oligonucleotide arrays to investigate the use of the senescence-accelerated mouse (SAM) as a biogerontological resource to identify patterns of gene expression in the chemosensory-nasal mucosa. Gene profiling in chronologically young and old mice of the senescence-resistant (SAMR) and senescence-prone (SAMP) strains revealed 133 known genes that were modulated by a three-fold or greater change either in one strain or the other or in both strains during aging. We also identified known genes in our study which based on their encoded proteins were identified as aging-related genes in the aging neocortex and cerebellum of mice as reported by Lee et al. (2000) [Nat. Genet. 25 (2000) 294]. Changes in gene profiles for chemosensory-related genes including olfactory and vomeronasal receptors, sensory transduction-associated proteins, and odor and pheromone transport molecules in the young SAMR and SAMP were compared with age-matched C57BL/6J mice. An analysis of known gene expression profiles suggests that changes in the expression of immune factor genes and genes associated with cell cycle progression and cell death were particularly prominent in the old SAM strains. A preliminary cellular validation study supported the dysregulation of cell cycle-related genes in the old SAM strains. The results of our initial study indicated that the use of the SAM models of aging could provide substantive information leading to a more fundamental understanding of the aging process in the chemosensory-nasal mucosa at the genomic, molecular, and cellular levels.

Original language	English
Pages (from-to)	211-243
Number of pages	33
Journal	Ageing Research Reviews
Volume	2
Issue number	2
DOIs	https://doi.org/10.1016/S1568-1637(02)00066-1
State	Published - Apr 2003

Bibliographical note

Funding Information:
The authors thank Professor Masanori Hosokawa, Secretary General of The Council for SAM Research, Kyoto University, for his guidance in the use of the SAM mice for research; Dr. Mark S. Kindy, University of Kentucky, for an early discussion that led to the identification of SAM breeding colonies in the USA; and Dr. Donald K. Ingram, Gerontology Research Center, National Institute on Aging, Baltimore, MD, for providing the SAM mice and the hospitality of his laboratory where the tissues were harvested. We also thank John M. Hengemihle, National Institute on Aging, and James V. Partin and Donna Wall, University of Kentucky, for their technical support. Supported by NIH-AG-016824-22 (TVG), Kentucky Biomedical Research Infrastructure Network grant NIH-1P20RR16481-01 and NSF-EPS-0132295 (AJS), the University of Kentucky Medical Research Fund, and the University of Kentucky Microarray Core Facility.

Keywords

Aging
DNA microarrays
Gene profiling
Olfactory receptor
Senescence-accelerated mouse
Vomeronasal receptor

ASJC Scopus subject areas

Biotechnology
Biochemistry
Aging
Molecular Biology
Neurology

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10.1016/S1568-1637(02)00066-1

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title = "Age-related trends in gene expression in the chemosensory-nasal mucosae of senescence-accelerated mice",

abstract = "We have utilized high-density GeneChip oligonucleotide arrays to investigate the use of the senescence-accelerated mouse (SAM) as a biogerontological resource to identify patterns of gene expression in the chemosensory-nasal mucosa. Gene profiling in chronologically young and old mice of the senescence-resistant (SAMR) and senescence-prone (SAMP) strains revealed 133 known genes that were modulated by a three-fold or greater change either in one strain or the other or in both strains during aging. We also identified known genes in our study which based on their encoded proteins were identified as aging-related genes in the aging neocortex and cerebellum of mice as reported by Lee et al. (2000) [Nat. Genet. 25 (2000) 294]. Changes in gene profiles for chemosensory-related genes including olfactory and vomeronasal receptors, sensory transduction-associated proteins, and odor and pheromone transport molecules in the young SAMR and SAMP were compared with age-matched C57BL/6J mice. An analysis of known gene expression profiles suggests that changes in the expression of immune factor genes and genes associated with cell cycle progression and cell death were particularly prominent in the old SAM strains. A preliminary cellular validation study supported the dysregulation of cell cycle-related genes in the old SAM strains. The results of our initial study indicated that the use of the SAM models of aging could provide substantive information leading to a more fundamental understanding of the aging process in the chemosensory-nasal mucosa at the genomic, molecular, and cellular levels.",

keywords = "Aging, DNA microarrays, Gene profiling, Olfactory receptor, Senescence-accelerated mouse, Vomeronasal receptor",

author = "Getchell, {Thomas V.} and Xuejun Peng and Stromberg, {Arnold J.} and Chen, {Kuey Chu} and Green, {C. Paul} and Subhedar, {Nishikant K.} and Shah, {Dharmen S.} and Mattson, {Mark P.} and Getchell, {Marilyn L.}",

note = "Funding Information: The authors thank Professor Masanori Hosokawa, Secretary General of The Council for SAM Research, Kyoto University, for his guidance in the use of the SAM mice for research; Dr. Mark S. Kindy, University of Kentucky, for an early discussion that led to the identification of SAM breeding colonies in the USA; and Dr. Donald K. Ingram, Gerontology Research Center, National Institute on Aging, Baltimore, MD, for providing the SAM mice and the hospitality of his laboratory where the tissues were harvested. We also thank John M. Hengemihle, National Institute on Aging, and James V. Partin and Donna Wall, University of Kentucky, for their technical support. Supported by NIH-AG-016824-22 (TVG), Kentucky Biomedical Research Infrastructure Network grant NIH-1P20RR16481-01 and NSF-EPS-0132295 (AJS), the University of Kentucky Medical Research Fund, and the University of Kentucky Microarray Core Facility.",

year = "2003",

month = apr,

doi = "10.1016/S1568-1637(02)00066-1",

language = "English",

volume = "2",

pages = "211--243",

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AU - Getchell, Thomas V.

AU - Peng, Xuejun

AU - Stromberg, Arnold J.

AU - Chen, Kuey Chu

AU - Green, C. Paul

AU - Subhedar, Nishikant K.

AU - Shah, Dharmen S.

AU - Mattson, Mark P.

AU - Getchell, Marilyn L.

N1 - Funding Information: The authors thank Professor Masanori Hosokawa, Secretary General of The Council for SAM Research, Kyoto University, for his guidance in the use of the SAM mice for research; Dr. Mark S. Kindy, University of Kentucky, for an early discussion that led to the identification of SAM breeding colonies in the USA; and Dr. Donald K. Ingram, Gerontology Research Center, National Institute on Aging, Baltimore, MD, for providing the SAM mice and the hospitality of his laboratory where the tissues were harvested. We also thank John M. Hengemihle, National Institute on Aging, and James V. Partin and Donna Wall, University of Kentucky, for their technical support. Supported by NIH-AG-016824-22 (TVG), Kentucky Biomedical Research Infrastructure Network grant NIH-1P20RR16481-01 and NSF-EPS-0132295 (AJS), the University of Kentucky Medical Research Fund, and the University of Kentucky Microarray Core Facility.

PY - 2003/4

Y1 - 2003/4

N2 - We have utilized high-density GeneChip oligonucleotide arrays to investigate the use of the senescence-accelerated mouse (SAM) as a biogerontological resource to identify patterns of gene expression in the chemosensory-nasal mucosa. Gene profiling in chronologically young and old mice of the senescence-resistant (SAMR) and senescence-prone (SAMP) strains revealed 133 known genes that were modulated by a three-fold or greater change either in one strain or the other or in both strains during aging. We also identified known genes in our study which based on their encoded proteins were identified as aging-related genes in the aging neocortex and cerebellum of mice as reported by Lee et al. (2000) [Nat. Genet. 25 (2000) 294]. Changes in gene profiles for chemosensory-related genes including olfactory and vomeronasal receptors, sensory transduction-associated proteins, and odor and pheromone transport molecules in the young SAMR and SAMP were compared with age-matched C57BL/6J mice. An analysis of known gene expression profiles suggests that changes in the expression of immune factor genes and genes associated with cell cycle progression and cell death were particularly prominent in the old SAM strains. A preliminary cellular validation study supported the dysregulation of cell cycle-related genes in the old SAM strains. The results of our initial study indicated that the use of the SAM models of aging could provide substantive information leading to a more fundamental understanding of the aging process in the chemosensory-nasal mucosa at the genomic, molecular, and cellular levels.

AB - We have utilized high-density GeneChip oligonucleotide arrays to investigate the use of the senescence-accelerated mouse (SAM) as a biogerontological resource to identify patterns of gene expression in the chemosensory-nasal mucosa. Gene profiling in chronologically young and old mice of the senescence-resistant (SAMR) and senescence-prone (SAMP) strains revealed 133 known genes that were modulated by a three-fold or greater change either in one strain or the other or in both strains during aging. We also identified known genes in our study which based on their encoded proteins were identified as aging-related genes in the aging neocortex and cerebellum of mice as reported by Lee et al. (2000) [Nat. Genet. 25 (2000) 294]. Changes in gene profiles for chemosensory-related genes including olfactory and vomeronasal receptors, sensory transduction-associated proteins, and odor and pheromone transport molecules in the young SAMR and SAMP were compared with age-matched C57BL/6J mice. An analysis of known gene expression profiles suggests that changes in the expression of immune factor genes and genes associated with cell cycle progression and cell death were particularly prominent in the old SAM strains. A preliminary cellular validation study supported the dysregulation of cell cycle-related genes in the old SAM strains. The results of our initial study indicated that the use of the SAM models of aging could provide substantive information leading to a more fundamental understanding of the aging process in the chemosensory-nasal mucosa at the genomic, molecular, and cellular levels.

KW - Aging

KW - DNA microarrays

KW - Gene profiling

KW - Olfactory receptor

KW - Senescence-accelerated mouse

KW - Vomeronasal receptor

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Age-related trends in gene expression in the chemosensory-nasal mucosae of senescence-accelerated mice

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

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