Hypoxia‐stimulated membrane trafficking requires T‐plastin

Wottawa, Marieke; Naas, S.; Böttger, J.; Belle, Gijsbert J. van; Möbius, Wiebke; Revelo, Natalia H.; Heidenreich, Doris; Ahlen, Melanie von; Zieseniß, Anke; Kröhnert, Katharina; Lutz, Susanne; Lenz, Christof; Urlaub, Henning; Rizzoli, Silvio O.; Katschinski, Doerthe M.

doi:10.1111/apha.12859

Cited by 16 publications

(21 citation statements)

References 39 publications

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“…In HeLa and several other cancer cells, acute hypoxia led to a HIF1‐independent decrease in global protein internalization, but an increase in clathrin‐mediated internalization of transferrin . In contrast, in MDA‐MB‐231 breast cancer cells and MEFs, hypoxia decreased clathrin‐dependent transferrin endocytosis yet increased membrane internalization in a HIF1‐independent manner . Hypoxia also induces changes in endocytic traffic in breast cancer cells and cultured cortical neurons …”

Section: Regulation Of Endocytic Traffic By Hypoxiamentioning

confidence: 98%

Energetic adaptations: Metabolic control of endocytic membrane traffic

Rahmani

Defferrari

Wakarchuk

et al. 2019

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Endocytic membrane traffic controls the access of myriad cell surface proteins to the extracellular milieu, and thus gates nutrient uptake, ion homeostasis, signaling, adhesion and migration. Coordination of the regulation of endocytic membrane traffic with a cell's metabolic needs represents an important facet of maintenance of homeostasis under variable conditions of nutrient availability and metabolic demand. Many studies have revealed intimate regulation of endocytic membrane traffic by metabolic cues, from the specific control of certain receptors or transporters, to broader adaptation or remodeling of the endocytic membrane network. We examine how metabolic sensors such as AMP‐activated protein kinase, mechanistic target of rapamycin complex 1 and hypoxia inducible factor 1 determine sufficiency of various metabolites, and in turn modulate cellular functions that includes control of endocytic membrane traffic. We also examine how certain metabolites can directly control endocytic traffic proteins, such as the regulation of specific protein glycosylation by limiting levels of uridine diphosphate N‐acetylglucosamine (UDP‐GlcNAc) produced by the hexosamine biosynthetic pathway. From these ideas emerge a growing appreciation that endocytic membrane traffic is orchestrated by many intrinsic signals derived from cell metabolism, allowing alignment of the functions of cell surface proteins with cellular metabolic requirements. Endocytic membrane traffic determines how cells interact with their environment, thus defining many aspects of nutrient uptake and energy consumption. We examine how intrinsic signals that reflect metabolic status of a cell regulate endocytic traffic of specific proteins, and, in some cases, exert broad control of endocytic membrane traffic phenomena. Hence, endocytic traffic is versatile and adaptable and can be modulated to meet the changing metabolic requirements of a cell.

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Section: Regulation Of Endocytic Traffic By Hypoxiamentioning

confidence: 98%

Energetic adaptations: Metabolic control of endocytic membrane traffic

Rahmani

Defferrari

Wakarchuk

et al. 2019

Traffic

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show abstract

“…Even if insufficient oxygen supply in general is harmful for the embryo and foetus, it might have positive effects in some cases of extreme prematurity or low oxygen supply, for example, for a tailored increase in angiogenesis . As the influence of HIFs and hypoxia on the diverse functions of the human body is still incompletely understood, the long‐term and potentially unfavourable effects of Roxadustat are unknown yet. It is also unexplored how it might influence the generation of reactive oxygen species causing oxidative stress in patients .…”

Section: Is There a Risk Of Roxadustat Abuse?mentioning

confidence: 99%

ExActa HIF prolyl hydroxylase inhibitors—The new lifestyle drug?

Sciesielski

Kirschner

2019

Acta Physiologica

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“…In a study of Wottawa et al the authors were able to describe the hypoxia-raised increase of membrane trafficking as a HIF-independent effect which is quickly reversible upon reoxygenation. 14 In addition they identified the actin-bundling protein T-plastin as a major mediator of hypoxia-induced membrane trafficking. Hypoxic conditions in solid tumours are a result of an extracellular acidosis.…”

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confidence: 99%