Abstract
Embryonic stem cells (ESCs) are metabolically distinct from their differentiated counterparts. ESC mitochondria are less complex and fewer in number than their differentiated progeny. However, few studies have examined the proteins responsible for differences in mitochondrial structure and function between ESCs and somatic cells. Therefore, in this study, we aimed to investigate the differences between mitochondrial proteins in these two cell types. We demonstrate that HSP60 is more abundant in mouse ESC mitochondria than in mouse embryonic fibroblasts. Depletion of HSP60 inhibited mouse ESC proliferation and self-renewal, characterized by decreased OCT4 expression. HSP60 depletion also enhanced apoptosis during mouse ESC differentiation into embryoid bodies. Our results suggest that HSP60 expression has an essential role in ESC self-renewal and survival of differentiated cells from ESCs.
Highlights
Embryonic stem cells (ESCs) have the remarkable capacity to proliferate indefinitely and generate any type of cell in the body.[1]
We found that 5,5′,6,6′-tetrachloro-1,1′ 3,3′-tetraethyl-benzamidazol carboncyanine and 10-nonyl bromide fluorescence levels were decreased in mESCs compared with mouse embryonic fibroblasts (MEFs) (Figures 1a and b), indicating that mitochondrial function and mass were reduced in mESCs compared with MEFs
Increased expression of HSP60 in mESCs compared with MEFs To determine whether the expression levels of proteins other than the electron transfer complexes differed between MEFs and mESCs, we performed two-dimensional electrophoresis analysis
Summary
Embryonic stem cells (ESCs) have the remarkable capacity to proliferate indefinitely and generate any type of cell in the body.[1] ESCs are thought to hold great promise for tissue repair and regeneration, and to provide a powerful tool for modeling human disease and understanding biological development.[2,3] to take advantage of the full potential of ESCs, it is critical to understand the mechanisms underlying the regulation of ESC self-renewal and differentiation. ESC metabolism is distinct from that of their differentiated counterparts and has an important role in the maintenance of ESC identity.[4] ESCs have immature mitochondria with poorly developed cristae; upon differentiation, these immature mitochondria mature into mitochondria with dense matrix and complex cristae.[5,6] Consistent with these observations, ESCs rely on high rates of glycolysis, even when cultured in vitro. Few studies have examined which proteins are responsible for differences in mitochondrial structure and function between ESCs and somatic cells
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