Reduced telomerase activity in human T lymphocytes exposed to cortisol

Accelerated telomere shortening in lymphocytes has been associated with a variety of human pathologies, including HIV disease, Down syndrome, and cardiovascular disease. Recent findings indicate that reduced telomere length is also associated with chronic psychological stress and mood disorders. Tel...

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Vydané v:	Brain, behavior, and immunity Ročník 22; číslo 4; s. 600 - 605
Hlavní autori:	Choi, Jenny, Fauce, Steven R., Effros, Rita B.
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	Netherlands Elsevier Inc 01.05.2008
Predmet:	Adult Allergy and Immunology Anti-Inflammatory Agents - pharmacology CD4-Positive T-Lymphocytes - drug effects CD4-Positive T-Lymphocytes - enzymology CD8-Positive T-Lymphocytes - drug effects CD8-Positive T-Lymphocytes - enzymology Cells, Cultured Cortisol Enzyme Activation - drug effects Enzyme Activation - immunology Female Human Human immunodeficiency virus Humans Hydrocortisone - pharmacology Male Middle Aged Protein Subunits - genetics Protein Subunits - metabolism Psychiatry RNA, Messenger - metabolism Stress T lymphocytes Telomerase Telomerase - genetics Telomerase - metabolism Telomeres T lymphocytes Human Telomeres Cortisol Telomerase Stress
ISSN:	0889-1591, 1090-2139, 1090-2139
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Abstract	Accelerated telomere shortening in lymphocytes has been associated with a variety of human pathologies, including HIV disease, Down syndrome, and cardiovascular disease. Recent findings indicate that reduced telomere length is also associated with chronic psychological stress and mood disorders. Telomerase, which prevents telomere shortening, can be upregulated in T lymphocytes in concert with activation, thereby retarding telomere shortening. Here, we demonstrate that exposure of human T lymphocytes to cortisol is associated with a significant reduction in telomerase activity both during primary stimulation of resting cells and secondary stimulation of previously activated cells. The effect is observed in both CD4 and CD8 T lymphocytes, and is associated with reduced transcription of hTERT, the telomerase catalytic component. These findings provide a potential mechanism for stress-associated telomere length attrition, and suggest that strategies to enhance T lymphocyte telomerase activity may provide beneficial effects on immune function in situations of chronic emotional stress.
AbstractList	Accelerated telomere shortening in lymphocytes has been associated with a variety of human pathologies, including HIV disease, Down syndrome, and cardiovascular disease. Recent findings indicate that reduced telomere length is also associated with chronic psychological stress and mood disorders. Telomerase, which prevents telomere shortening, can be upregulated in T lymphocytes in concert with activation, thereby retarding telomere shortening. Here, we demonstrate that exposure of human T lymphocytes to cortisol is associated with a significant reduction in telomerase activity both during primary stimulation of resting cells and secondary stimulation of previously activated cells. The effect is observed in both CD4 and CD8 T lymphocytes, and is associated with reduced transcription of hTERT, the telomerase catalytic component. These findings provide a potential mechanism for stress-associated telomere length attrition, and suggest that strategies to enhance T lymphocyte telomerase activity may provide beneficial effects on immune function in situations of chronic emotional stress. Abstract Accelerated telomere shortening in lymphocytes has been associated with a variety of human pathologies, including HIV disease, Down syndrome, and cardiovascular disease. Recent findings indicate that reduced telomere length is also associated with chronic psychological stress and mood disorders. Telomerase, which prevents telomere shortening, can be upregulated in T lymphocytes in concert with activation, thereby retarding telomere shortening. Here, we demonstrate that exposure of human T lymphocytes to cortisol is associated with a significant reduction in telomerase activity both during primary stimulation of resting cells and secondary stimulation of previously activated cells. The effect is observed in both CD4 and CD8 T lymphocytes, and is associated with reduced transcription of hTERT, the telomerase catalytic component. These findings provide a potential mechanism for stress-associated telomere length attrition, and suggest that strategies to enhance T lymphocyte telomerase activity may provide beneficial effects on immune function in situations of chronic emotional stress. Accelerated telomere shortening in lymphocytes has been associated with a variety of human pathologies, including HIV disease, Down syndrome, and cardiovascular disease. Recent findings indicate that reduced telomere length is also associated with chronic psychological stress and mood disorders. Telomerase, which prevents telomere shortening, can be upregulated in T lymphocytes in concert with activation, thereby retarding telomere shortening. Here, we demonstrate that exposure of human T lymphocytes to cortisol is associated with a significant reduction in telomerase activity both during primary stimulation of resting cells and secondary stimulation of previously activated cells. The effect is observed in both CD4 and CD8 T lymphocytes, and is associated with reduced transcription of hTERT, the telomerase catalytic component. These findings provide a potential mechanism for stress-associated telomere length attrition, and suggest that strategies to enhance T lymphocyte telomerase activity may provide beneficial effects on immune function in situations of chronic emotional stress.Accelerated telomere shortening in lymphocytes has been associated with a variety of human pathologies, including HIV disease, Down syndrome, and cardiovascular disease. Recent findings indicate that reduced telomere length is also associated with chronic psychological stress and mood disorders. Telomerase, which prevents telomere shortening, can be upregulated in T lymphocytes in concert with activation, thereby retarding telomere shortening. Here, we demonstrate that exposure of human T lymphocytes to cortisol is associated with a significant reduction in telomerase activity both during primary stimulation of resting cells and secondary stimulation of previously activated cells. The effect is observed in both CD4 and CD8 T lymphocytes, and is associated with reduced transcription of hTERT, the telomerase catalytic component. These findings provide a potential mechanism for stress-associated telomere length attrition, and suggest that strategies to enhance T lymphocyte telomerase activity may provide beneficial effects on immune function in situations of chronic emotional stress.
Author	Choi, Jenny Fauce, Steven R. Effros, Rita B.
Author_xml	– sequence: 1 givenname: Jenny surname: Choi fullname: Choi, Jenny – sequence: 2 givenname: Steven R. surname: Fauce fullname: Fauce, Steven R. – sequence: 3 givenname: Rita B. surname: Effros fullname: Effros, Rita B. email: reffros@mednet.ucla.edu
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/18222063$$D View this record in MEDLINE/PubMed
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Snippet	Accelerated telomere shortening in lymphocytes has been associated with a variety of human pathologies, including HIV disease, Down syndrome, and... Abstract Accelerated telomere shortening in lymphocytes has been associated with a variety of human pathologies, including HIV disease, Down syndrome, and...
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SubjectTerms	Adult Allergy and Immunology Anti-Inflammatory Agents - pharmacology CD4-Positive T-Lymphocytes - drug effects CD4-Positive T-Lymphocytes - enzymology CD8-Positive T-Lymphocytes - drug effects CD8-Positive T-Lymphocytes - enzymology Cells, Cultured Cortisol Enzyme Activation - drug effects Enzyme Activation - immunology Female Human Human immunodeficiency virus Humans Hydrocortisone - pharmacology Male Middle Aged Protein Subunits - genetics Protein Subunits - metabolism Psychiatry RNA, Messenger - metabolism Stress T lymphocytes Telomerase Telomerase - genetics Telomerase - metabolism Telomeres
Title	Reduced telomerase activity in human T lymphocytes exposed to cortisol
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