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pmid:31969994

Thermotolerance and plasticity of camel somatic cells exposed to acute and chronic heat stress.

Islam M Saadeldin · Ayman Abdel-Aziz Swelum · Mona Elsafadi · Amer Mahmood · Aya Osama · Hassan Shikshaky · Musaad Alfayez · Abdullah N Alowaimer · Sameh Magdeldin

Journal of advanced research · 2020 doi:10.1016/j.jare.2019.11.009

Paper

complete

Experiment

complete

Data

partial

Analysis

complete

Execution

absent

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Thermotolerance and plasticity of camel somatic cells exposed to acute and chronic heat stress.
doi
10.1016/j.jare.2019.11.009
pmid
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[0]
Islam M Saadeldin
[1]
Ayman Abdel-Aziz Swelum
[2]
Mona Elsafadi
[3]
Amer Mahmood
[4]
Aya Osama
[5]
Hassan Shikshaky
[6]
Musaad Alfayez
[7]
Abdullah N Alowaimer
[8]
Sameh Magdeldin
journal
Journal of advanced research
year
2020
abstract
The Arabian camel is the largest known mammal that can survive in severe hot climatic conditions. We provide the molecular explanation for the thermotolerance of camel granulosa somatic cells after exposure to 45 °C for 2 (acute heat shock) or 20 h (chronic heat shock). The common features of the cellular responses to acute heat stress were the increase of heat shock proteins and DNA repair enzymes expression. Actin polymerization and Rho signaling were critically activated as a cellular defense against heat shock. Cells exposed to chronic heat shock showed altered cell architecture with a decrease in total detected proteins, metabolic enzymes, and cytoskeletal protein expression. Treatment with transforming growth factor beta (TGFβ) pathway inhibitor SB-431542 suppressed the morphological alterations of cells exposed to chronic heat shock. Moreover, during the recovery stage at 38 °C for 24 h, proteomic changes were partially restored with an exponential increase in HSP70 expression, and the cells restored their normal cellular morphology on the 9th day of recovery. Full proteomics data are available via ProteomeXchange with identifier PXD012159. The strategies of cellular defense and tolerance to both thermal conditions reflect the flexible adaptability of camel somatic cells to conserve life under extremely hot conditions.
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thermotolerance of camel cells
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Levels of malondialdehyde (MDA) and reduced glutathione (GSH) in the response to acute and chronic heat shock.
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Impact of heat shock on oxidative stress, anti-oxidative defense, apoptosis and cell viability
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ary video 8Time-lapse imaging of camel cells cultured in 45 °C for 20 h and gradually decreased to 38
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ication of time-lapse imaging of camel cells cultured in 45 °C for 20 h and gradually decreased to 38
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ime-lapse imaging of porcine granulosa cells cultured in 45 °C for 20 h and gradually decreased to 38
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We provide the molecular explanation for the thermotolerance of camel granulosa somatic cells after exposure to 45 °C for 2 (acute heat shock) or 20 h (chronic heat shock). The common features of the cellular responses to acute heat stress were the increase of heat shock proteins and DNA repair enzymes expression. Actin polymerization and Rho signaling were critically activated as a cellular defense against heat shock. Cells exposed to chronic heat shock showed altered cell architecture with a decrease in total detected proteins, metabolic enzymes, and cytoskeletal protein expression. Treatment with transforming growth factor beta (TGFβ) pathway inhibitor SB-431542 suppressed the morphological alterations of cells exposed to chronic heat shock. Moreover, during the recovery stage at 38 °C for 24 h, proteomic changes were partially restored with an exponential increase in HSP70 expression, and the cells restored their normal cellular morphology on the 9th day of recovery. 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