Abstract
The core proteomes of human and rat pancreatic beta cells were compared by label-free LC-MS/MS: this resulted in quantification of relative molar abundances of 707 proteins belonging to functional pathways of intermediary metabolism, protein synthesis, and cytoskeleton. Relative molar abundances were conserved both within and between pathways enabling the selection of a housekeeping network for geometric normalization and the analysis of potentially relevant differential expressions. Human beta cells differed from rat beta cells in their lower level of enzymes involved in glucose sensing (MDH1, PC, and ACLY) and upregulation of lysosomal enzymes. Human cells also expressed more heat shock proteins and radical scavenging systems: apart from SOD2, they expressed high levels of H2O2-scavenger peroxiredoxin 3 (PRDX3), confirmed by microarray, Western blotting, and microscopy. Besides conferring lower susceptibility to oxidative stress to human cells PRDX3 might also play a role in physiological redox regulation as, in rat, its expression was restricted to a beta cell subset with higher metabolic glucose responsiveness. In conclusion, although their core proteomic architecture is conserved, human and rat beta cells differ in their molar expression of key enzymes involved in glucose sensing and redox control.
Highlights
Most of our current understanding of the physiology of pancreatic beta cells comes from studies in rodents
The core proteomes of human and rat pancreatic beta cells were compared by label-free LC-MS/MS: this resulted in quantification of relative molar abundances of 707 proteins belonging to functional pathways of intermediary metabolism, protein synthesis, and cytoskeleton
Human beta cells differed from rat beta cells in their lower level of enzymes involved in glucose sensing (MDH1, pyruvate carboxylase (PC), and ATP-citrate lyase (ACLY)) and upregulation of lysosomal enzymes
Summary
Most of our current understanding of the physiology of pancreatic beta cells comes from studies in rodents. Previous studies indicated that human beta cells display a higher glucose responsiveness than rodent beta cells [1] and a higher resistance to reactive oxygen species (ROS) and, unlike rodent beta cells [3], they are considered long-lived and postmitotic in adults [4, 5]. These functional differences are reflected by adaptations in their gene/protein expression patterns, for example, by a higher expression of heat shock protein 70 (HSP70) and some ROS scavenging enzymes (heme oxygenase 1, catalase, and superoxide dismutase 2) [6,7,8]. I found that the expression levels of core functional pathways (intermediary metabolism, protein synthesis, Journal of Diabetes Research signaling, and cytoskeleton) were well conserved and discovered interesting differences, in enzymes of nutrient metabolism and antioxidant defenses
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