One protein, different cell fate: the differential outcome of depleting GRP75 during oxidative stress in neurons

Honrath, Birgit; Culmsee, Carsten; Dolga, Amalia M.

doi:10.1038/s41419-017-0148-7

Cited by 15 publications

(10 citation statements)

References 17 publications

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“…Failure to establish sufficient contacts in the MAM between ER and mitochondria resulting in reduced Ca 2+ transfer would negatively affect mitophagy and cell survival in the longer term. This is consistent with an essential role for GRP75 in maintaining contact between these organelles and facilitating the propagation of the Ca 2+ signal into mitochondria to regulate various mitochondrial functions (Phillips and Voeltz, 2016;Honrath et al, 2018). In addition, previous results have shown that contact sites between ER and mitochondria represent sites of autophagosome formation during starvation-induced autophagy and that autophagosome biogenesis is impaired in cells with defective ER-mitochondrial tethering (Hamasaki et al, 2013;Kishi-Itakura et al, 2014).…”

Section: Mitochondrial Function Is Defective In Glucose-deprived Atm-deficient Cells In Response To Nutrient Stresssupporting

confidence: 85%

Impaired endoplasmic reticulum-mitochondrial signaling in ataxia-telangiectasia

et al. 2021

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There is evidence that ATM mutated in ataxia-telangiectasia (A-T) plays a key role in protecting against mitochondrial dysfunction, the mechanism for which remains unresolved. We demonstrate here that ATM-deficient cells are exquisitely sensitive to nutrient deprivation, which can be explained by defective cross talk between the endoplasmic reticulum (ER) and the mitochondrion. Tethering between these two organelles in response to stress was reduced in cells lacking ATM, and consistent with this, Ca 2+ release and transfer between ER and mitochondria was reduced dramatically when compared with control cells. The impact of this on mitochondrial function was evident from an increase in oxygen consumption rates and a defect in mitophagy in ATM-deficient cells. Our findings reveal that ER-mitochondrial connectivity through IP3R1-GRP75-VDAC1, to maintain Ca 2+ homeostasis, as well as an abnormality in mitochondrial fusion defective in response to nutrient stress, can account for at least part of the mitochondrial dysfunction observed in A-T cells.

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Section: Mitochondrial Function Is Defective In Glucose-deprived Atm-deficient Cells In Response To Nutrient Stresssupporting

confidence: 85%

Impaired endoplasmic reticulum-mitochondrial signaling in ataxia-telangiectasia

et al. 2021

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“…Another novel and particularly important finding is that CL significantly induced protein expression of the mitochondrial transport/stress response protein GRP75, which we show to be upregulated across adipose tissue depots and in both sexes. GRP75 is vital for mitochondrial function in various cell types [ 62 , 63 , 64 ], and data collected in breast cancer cell lines have revealed that ERβ-associated increases in mitochondrial proteins [ 65 ] were dependent upon GRP75. We found that GRP75 expression coincided with indicators of WAT browning.…”

Section: Discussionmentioning

confidence: 99%

White Adipose Tissue Depots Respond to Chronic Beta-3 Adrenergic Receptor Activation in a Sexually Dimorphic and Depot Divergent Manner

Queathem

Welly

Clart

et al. 2021

Cells

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Beta-3 adrenergic receptor activation via exercise or CL316,243 (CL) induces white adipose tissue (WAT) browning, improves glucose tolerance, and reduces visceral adiposity. Our aim was to determine if sex or adipose tissue depot differences exist in response to CL. Daily CL injections were administered to diet-induced obese male and female mice for two weeks, creating four groups: male control, male CL, female control, and female CL. These groups were compared to determine the main and interaction effects of sex (S), CL treatment (T), and WAT depot (D). Glucose tolerance, body composition, and energy intake and expenditure were assessed, along with perigonadal (PGAT) and subcutaneous (SQAT) WAT gene and protein expression. CL consistently improved glucose tolerance and body composition. Female PGAT had greater protein expression of the mitochondrial uncoupling protein 1, while UCP1 (S, p < 0.001) was more responsive to CL in increasing UCP1 (S×T, p = 0.011) and the mitochondrial biogenesis induction protein, PPARγ coactivator 1α (PGC1α) (S×T, p = 0.026). Females also displayed greater mitochondrial OXPHOS (S, p < 0.05) and adiponectin protein content (S, p < 0.05). On the other hand, male SQAT was more responsive to CL in increasing protein levels of PGC1α (S×T, p = 0.046) and adiponectin (S, p < 0.05). In both depots and in both sexes, CL significantly increased estrogen receptor beta (ERβ) and glucose-related protein 75 (GRP75) protein content (T, p < 0.05). Thus, CL improves systemic and adipose tissue-specific metabolism in both sexes; however, sex differences exist in the WAT-specific effects of CL. Furthermore, across sexes and depots, CL affects estrogen signaling by upregulating ERβ.

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“…However, a more recent study using electron tomography demonstrated that the minimum distance is much less, 10 nm at the smooth ER and 25 nm at the rough ER ( Csordas et al, 2006 ). The physical cooperation between the ER and mitochondria offers pivotal roles in several aspects of cellular functions, including Ca 2+ signaling, lipid transport, energy metabolism, and cellular survival ( Honrath et al, 2018 ). However, in response to stress response, especially cardiac I/R injury, ER–mitochondria contact converts mitochondria and ER from ATP providers and protein factories that energize the cell to agents of cell death, respectively.…”

Section: Introductionmentioning

confidence: 99%

ER–Mitochondria Microdomains in Cardiac Ischemia–Reperfusion Injury: A Fresh Perspective

et al. 2018

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The mitochondrial and endoplasmic reticulum (ER) homeostasis is pivotal to the maintenance of an array of physiological processes. The physical contact and association between ER and mitochondria, known as the ER–mitochondria microdomains or mitochondria-associated ER membrane (MAM), temporally and spatially regulates the mitochondria/ER structure and function. More evidence suggests a role for MAMs in energy production, cellular contraction and mobility, and normal extracellular signal transmission. In pathological states, such as cardiac ischemia–reperfusion (I/R injury), this ER–mitochondria microdomains may act to participate in the cellular redox imbalance, ER stress, mitochondrial injury, energy deletion, and programmed cell death. From a therapeutic perspective, a better understanding of the cellular and molecular mechanisms of the pathogenic ER–mitochondria contact should help to identify potential therapeutic target for cardiac I/R injury and other cardiovascular diseases and also pave the road to new treatment modalities pertinent for the treatment of reperfusion damage in clinical practice. This review will mainly focus on the possible signaling pathways involved in the regulation of the ER–mitochondria contact. In particular, we will summarize the downstream signaling modalities influenced by ER–mitochondria microdomains, for example, mitochondrial fission, mitophagy, calcium balance, oxidative stress, and programmed cell death in details.

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One protein, different cell fate: the differential outcome of depleting GRP75 during oxidative stress in neurons

Cited by 15 publications

References 17 publications

Impaired endoplasmic reticulum-mitochondrial signaling in ataxia-telangiectasia

Impaired endoplasmic reticulum-mitochondrial signaling in ataxia-telangiectasia

White Adipose Tissue Depots Respond to Chronic Beta-3 Adrenergic Receptor Activation in a Sexually Dimorphic and Depot Divergent Manner

ER–Mitochondria Microdomains in Cardiac Ischemia–Reperfusion Injury: A Fresh Perspective

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