Rainbow trout (Oncorhynchus mykiss) shift the age composition of circulating red blood cells towards a younger cohort when exposed to thermal stress

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• 作者：Johanne M. Lewis (1)
  Georgia Klein (3)
  Patrick J. Walsh (2) pwalsh@uottawa.ca
  Suzanne Currie (3)
• 关键词：Heat stress &#8211 ; Teleost &#8211 ; Red blood cells &#8211 ; Apoptosis &#8211 ; Heat shock proteins
• 刊名：Journal of Comparative Physiology B: Biochemical, Systemic, and Environmental Physiology
• 出版年：2012
• 出版时间：July 2012
• 年：2012
• 卷：182
• 期：5
• 页码：663-671
• 全文大小：506.4 KB
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• 作者单位：1. Department of Biology, Georgia Southern University, 69 Georgia Avenue, Statesboro, GA 30458, USA2. Department of Biology, University of Ottawa, 30 Marie Curie, Ottawa, ON K1N 6N5, Canada3. Department of Biology, Mount Allison University, 63B York Street, Sackville, NB E4L 1G7, Canada
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Life Sciences
  Biochemistry
  Biomedicine
  Human Physiology
  Zoology
  Animal Physiology
  
• 出版者：Springer Berlin / Heidelberg
• ISSN：1432-136X

文摘

Freshwater fish, such as the rainbow trout, are commonly exposed to temperature fluctuations in their aquatic environment. Exposure to increased temperatures places fish under respiratory stress and increases the likelihood of protein misfolding and degradation that could eventually lead to cell death. Previously, we showed that genes associated with the cellular stress response, apoptosis and hematopoiesis are upregulated in the red blood cells (RBCs) of rainbow trout post-thermal stress, leading to the hypothesis that a tightly regulated interaction between cell repair and cell death is occurring after heat stress. To test this hypothesis, we tracked changes in age class composition and markers of apoptosis in circulating RBCs within individual trout during exposure to and recovery from acute thermal stress. RBCs did not show any indication of apoptosis or necrosis following acute heat stress; however, we observed significant increases in numbers of early, juvenile and dividing RBCs. We also observed a shift in the composition of the circulating RBCs towards a younger cohort following heat shock through release of stored cells from the spleen and an increase in the maturation rate of early RBCs. These results suggest that the genes activated by increased temperature provided sufficient protection against thermal stress in the RBC, subsequently preventing the triggering of the cell death cascade.