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Hypoxia-stimulated membrane trafficking requires T-plastin
M Wottawa1, S Naas1, J Böttger1
1Institute of Cardiovascular Physiology, University Medical Center Göttingen (UMG), Göttingen, Germany.
Acta Physiologica (Oxford, England)
|February 21, 2017
Summary
Cellular adaptation to low oxygen (hypoxia) involves dynamic changes in plasma membrane trafficking. This process, mediated by T-plastin, is rapidly reversible upon reoxygenation and crucial for cell homeostasis.
Area of Science:
- Cell Biology
- Molecular Biology
- Physiology
Background:
- Membrane trafficking is vital for eukaryotic cell homeostasis, balancing the secretory and endocytic pathways.
- Cells must adapt to environmental changes like reduced oxygen (hypoxia), but its impact on membrane trafficking is not fully understood.
Purpose of the Study:
- To investigate the dynamic changes in plasma membrane trafficking under normoxia, hypoxia, and reoxygenation.
- To identify molecular mechanisms underlying hypoxia-induced alterations in membrane trafficking.
Main Methods:
- Utilized bulk endocytosis markers (FM 1-43, mCLING), wheat germ agglutinin, and cholera toxin subunit B.
- Employed Stable Isotope Labeling by Amino acids in Cell culture (SILAC) for unbiased proteomic analysis.
- Assessed membrane protein uptake and actin density via electron microscopy.
Main Results:
- Hypoxia significantly increased membrane trafficking, which rapidly reversed upon reoxygenation, independent of the hypoxia-inducible factor (HIF) system.
- Identified T-plastin as a key protein recruited to the plasma membrane during hypoxia.
- T-plastin knockdown cells exhibited reduced hypoxia-induced membrane trafficking and actin density.
Conclusions:
- Hypoxia induces dynamic and reversible changes in membrane trafficking, essential for cellular adaptation.
- T-plastin plays a critical role in mediating hypoxia-induced membrane trafficking and actin remodeling.
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