Abstract
Background/Objectives: The first camelized mouse model (Nrapc.255ins78) was developed to investigate the mechanisms underlying camels’ adaptation to extreme environments. Previous studies demonstrated that these mice exhibit a cold-resistant phenotype, characterized by increased expression of inflammatory cytokine-related genes in the heart under cold stress. Nebulin-related anchoring protein (NRAP) plays a critical role in organizing myofibrils during cardiomyocyte development. This study builds on prior research by analyzing the heart transcriptomes of Nrapc.255ins78 mice under non-stress conditions to explore the origins of inflammatory cytokine responses during cold exposure. Methods: RNA sequencing was performed on the hearts of 12-week-old male and female Nrapc.255ins78 and wild-type control mice. Results: Differential expression analysis identified 25 genes, including 12 associated with cell cycle and division, all consistently downregulated in Nrapc.255ins78. Notably, the calcium and integrin-binding protein gene (Cib3) was significantly upregulated (FDR < 0.05; p < 0.001). Conclusions: These differentially expressed genes suggest altered calcium dynamics in cardiomyocytes and mechanisms for maintaining homeostasis, supporting the hypothesis that inflammatory cytokines during cold exposure may represent an adaptive response. These findings provide valuable insights into the genetic mechanisms of temperature adaptation in camels and highlight potential pathways for enhancing stress resistance in other mammals.
Published Version
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