Background: Mild hypothermia, i.e. maintenance of organ temperature by up to 8°C
lower than body temperature, is a critical strategy for exerting some functions of the cells and organs
normally, and is an useful therapy for recovering properly from some diseases, including myocardial
infarction, cardiac arrest, brain injury, and ischemic stroke. Nevertheless, there were no focusses
so far on organ temperature and potential responses of gene expression to organ temperature
in organs of homeothermic animals that survive under normal conditions.
Objective: The present study aimed to assess organ temperature in homeothermic animals and evaluate
the effect of their organ temperature on the expression of the cold shock protein RNA binding
motif protein 3 (RBM3), and to gain insights into the organ temperature-mediated regulation of RBM3
gene transcription via Nuclear factor β-light-chain-enhancer of activated B cells (NF-κB) p65,
which had been identified as a transcription factor that is activated by undergoing the Ser276 phosphorylation
and promotes the RBM3 gene expression during mild hypothermia.
Methods: We measured the temperature of several organs, where RBM3 expression was examined,
in female and male mice. Next, in male mice, we tested NF-κB p65 expression and its Ser276 phosphorylation
in organs that have their lower temperature than body temperature and compared them
with those in organs that have their temperature near body temperature.
Results: Organ temperature was around 32°C in the brain and reproductive organs, which is lower
than the body temperature, and around 37°C in the heart, liver, and kidney, which is comparable to
the body temperature. The expression of RBM3 was detected greatly in the brain and reproductive
organs with their organ temperature of around 32°C, and poorly in the heart, liver, and kidney with
their organ temperature of around 37°C. In accordance with the changes in the RBM3 expression,
the NF-κB p65 Ser276 phosphorylation was detected more greatly in the testis and brain with their
organ temperature of around 32°C, than in the heart, liver, and kidney with their organ temperature
of around 37°C, although the NF-κB p65 expression was unchanged among all the organs tested.
Discussion: Our data suggested that organ temperature lower than body temperature causes the expression
of RBM3 in the brain and reproductive organs of mice, and that lower organ temperature
causes the NF-κB p65 activation through the Ser276 phosphorylation, resulting in an increase in
the RBM3 gene transcription, in the brain and reproductive organs of mice.
Conclusion: The study may present the possibility that organ temperature-induced alterations in
gene expression are organ specific in homeotherms and the possibility that organ temperature-induced
alterations in gene expression are transcriptionally regulated in some organs of