Pathologic endoplasmic reticulum stress induced by glucotoxic insults inhibits adipocyte differentiation and induces an inflammatory phenotype.

@article{Longo2016PathologicER,
  title={Pathologic endoplasmic reticulum stress induced by glucotoxic insults inhibits adipocyte differentiation and induces an inflammatory phenotype.},
  author={Michele Longo and Rosa Spinelli and Vittoria D’Esposito and Federica Zatterale and Francesca Fiory and Cecilia Nigro and Gregory Alexander Raciti and Claudia Miele and Pietro Formisano and Francesco Beguinot and Bruno di Jeso},
  journal={Biochimica et biophysica acta},
  year={2016},
  volume={1863 6 Pt A},
  pages={
          1146-56
        }
}
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39 Citations
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39 Citations

Tetrahydrocannabivarin (THCV) Protects Adipose-Derived Mesenchymal Stem Cells (ASC) against Endoplasmic Reticulum Stress Development and Reduces Inflammation during Adipogenesis

The results show that pre-treatment with THCV prevents the subcellular alteration of cell components such as nuclei, F-actin, or mitochondria distribution, and restores cell migration, cell proliferation and colony-forming capacity upon ER stress, indicating the protective characteristics of this cannabinoid compound in the adipose tissue.

ER stress reliever enhances functionalities of in vitro cultured hepatocytes.

Glucosamine induces increased musclin gene expression through endoplasmic reticulum stress-induced unfolding protein response signaling pathways in mouse skeletal muscle cells.

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The Role of Endoplasmic Reticulum Stress in Differentiation of Cells of Mesenchymal Origin

Study of the role of UPR in the activation of cell differentiation is of both theoretical and practical interest, as it might result in the identification of molecular targets for selective regulation ofcell differentiation stages and as well as the potential to modulate the mechanisms involved in the development of various pathological states.

Activation of Endoplasmic Reticulum Stress in Granulosa Cells from Patients with Polycystic Ovary Syndrome Contributes to Ovarian Fibrosis

It is suggested that ER stress in granulosa cells of women with PCOS contributes to the induction of pro-fibrotic growth factors during ovarian fibrosis, and that ER Stress may serve as a therapeutic target in PCOS.

The Pervasive Effects of ER Stress on a Typical Endocrine Cell: Dedifferentiation, Mesenchymal Shift and Antioxidant Response in the Thyrocyte

Together, data indicate that ER stress in thyroid cells induces dedifferentiation, loss of epithelial organization, shift towards a mesenchymal phenotype, and activation of the antioxidant response, highlighting a new and wide strategy to achieve survival following ER stress.

ER stress and inflammation crosstalk in obesity

Key mechanisms of ER stress‐induced inflammation in the context of obesity are elucidated and potential therapeutic strategies in the management of obesity through maneuvering ER stress and ER stress-associated inflammation are summarized.

Effects of diacylglycerol O-acyltransferase 1 (DGAT1) on endoplasmic reticulum stress and inflammatory responses in adipose tissue of ketotic dairy cows.

Data indicated that activation of DGAT1 may act as an adaptive mechanism to dampen metabolic dysregulation in adipose tissue, which contributes to relief from ER stress and inflammatory responses.

Epigenetic modifications of the Zfp/ZNF423 gene control murine adipogenic commitment and are dysregulated in human hypertrophic obesity

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60 References

The chemical chaperone 4-phenylbutyrate inhibits adipogenesis by modulating the unfolded protein response[S]

It is suggested that UPR activation contributes to adipogenesis and that blocking its activation with 4-PBA prevents adipocyte differentiation and weight gain in mice.

Investigating the involvement of the ATF6α pathway of the unfolded protein response in adipogenesis

This study investigates the importance of ATF6α during adipogenesis using stable knockdown of this protein in the model adipogenic cell line, C3H10T1/2, and indicates that all three arms of the UPR must be intact to permit adipogenesis to occur.

ER stress signalling through eIF2α and CHOP, but not IRE1α, attenuates adipogenesis in mice

These results demonstrate that eIF2α–CHOP suppresses adipogenesis and limits expansion of fat mass in vivo in mice, rendering this pathway a potential therapeutic target.

Glucosamine-induced endoplasmic reticulum stress affects GLUT4 expression via activating transcription factor 6 in rat and human skeletal muscle cells

It is shown that glucosamine-induced ER stress causes insulin resistance in both human and rat myotubes and impairs GLUT4 production and insulin-induced glucose uptake via an ATF6-dependent decrease of theGLUT4 regulators MEF2A and PGC1α.

The physiological unfolded protein response in the thyroid epithelial cells.

Increased hexosamine biosynthetic pathway flux dedifferentiates INS-1E cells and murine islets by an extracellular signal-regulated kinase (ERK)1/2-mediated signal transmission pathway

Glucotoxic ER stress dedifferentiates beta cells, in the absence of apoptosis, through a transcriptional response, and these effects are mediated by the activation of ERK1/2.

ER stress is associated with dedifferentiation and an epithelial-to-mesenchymal transition-like phenotype in PC Cl3 thyroid cells

The data indicate that ER stress induces dedifferentiation and an EMT-like phenotype in thyroid cells through a Src-mediated signaling pathway.

T-Cell Accumulation and Regulated on Activation, Normal T Cell Expressed and Secreted Upregulation in Adipose Tissue in Obesity

Obesity is associated with increased accumulation of T cells and macrophages in AT, which may play important roles in obesity-related disease by influencing preadipocytes/adipocyte functions.

Grp78 Heterozygosity Promotes Adaptive Unfolded Protein Response and Attenuates Diet-Induced Obesity and Insulin Resistance

HFD-induced obesity and type 2 diabetes are improved in Grp78+/− mice, and Adaptive UPR in WAT could contribute to this improvement, linking ER homeostasis to energy balance and glucose metabolism.

Glucosamine-Induced Endoplasmic Reticulum Stress Promotes ApoB100 Degradation: Evidence for Grp78-Mediated Targeting to Proteasomal Degradation

Findings suggest that binding and retention by Grp78 may play a critical role in proteasomal targeting and the ER quality-control of misfolded apoB.
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