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Metabolic Reprogramming in Response to Cell Mechanics
Journal article   Open access   Peer reviewed

Metabolic Reprogramming in Response to Cell Mechanics

Rebecca L Splitt and Kris A DeMali
Biology of the cell, Vol.115(5), e202200108
02/18/2023
DOI: 10.1111/boc.202200108
PMCID: PMC10192020
PMID: 36807920
Appears in  UI Libraries Support Open Access
url
https://doi.org/10.1111/boc.202200108View
Published (Version of record) Open Access

Abstract

Autophagy is a conserved process that functions as a cytoprotective mechanism; it may function as a cell death process called programmed cell death type II. There is considerable evidence for the presence of autophagic cell death during oocyte elimination in prepubertal rats. However, the mechanisms involved in this process have not been deciphered. Our observations revealed autophagic cell death in oocytes with increased labeling of the autophagic proteins Beclin 1, light chain 3 A (LC3 A), and lysosomal-associated membrane protein 1 (Lamp1). Furthermore, mTOR and phosphorylated (p)-mTOR (S2448) proteins were significantly decreased in oocytes with increased levels of autophagic proteins, indicating autophagic activation. Moreover, phosphorylated protein kinase B (p-AKT) was not expressed by oocytes, but mitogen-activated protein kinase/extracellular signalregulated kinase (MAPK/ERK) signaling was observed. Additionally, selective and elevated mitochondrial degradation was identified in altered oocytes. All these results suggest that mTOR downregulation, which promotes autophagy, could be mediated by low energy levels and sustained starvation involving the phosphoinositide 3-kinase (PI3K)/AKT/mTOR and MAPK/ERK pathways. In this work, we analyzed the manner in which autophagy is carried out in oocytes undergoing autophagic cell death by studying the behavior of proteins involved in different steps of the autophagic pathway.
 Metabolism UIOWA OA Agreement actin cell adhesion

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