ER Stress Responses: An Emerging Modulator for Innate Immunity

Conza, Giusy Di; Ho, Ping‐Chih

doi:10.3390/cells9030695

Cited by 153 publications

(130 citation statements)

References 70 publications

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“…Prolonged UPR has been shown to be proinflammatory [32,33].Therefore, we next sought to determine if leukocyte adhesion to AngII exposed VSMCs could be mitigated by the ER chaperone treatment. THP-1 monocyte recruitment assay with VSMCs was utilized to simulate vascular inflammation [34].…”

Section: Angii-induced Proinflammatory Phenotype Is Mitigated By Grp78mentioning

confidence: 99%

78 kDa Glucose-Regulated Protein Attenuates Protein Aggregation and Monocyte Adhesion Induced by Angiotensin II in Vascular Cells

Cicalese

Okuno

Elliott

et al. 2020

IJMS

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Investigations of vascular smooth muscle cell (VSMC) phenotypic modulation due to angiotensin II (AngII) stimulation are important for understanding molecular mechanisms contributing to hypertension and associated vascular pathology. AngII induces endoplasmic reticulum (ER) stress in VSMCs, which has been implicated in hypertensive vascular remodeling. Under ER stress, 78 kDa glucose-regulated protein (GRP78) acts as an endogenous chaperone, as well as a master controller of unfolded protein response (UPR) to maintain protein quality control. However, the potential downstream consequences of ER stress induced by AngII on protein quality control and pro-inflammatory phenotype in VSMCs remain elusive. This study aims to identify protein aggregation as evidence of the disruption of protein quality control in VSMCs, and to test the hypothesis that preservation of proteostasis by overexpression of GRP78 can attenuate the AngII-induced pro-inflammatory phenotype in VSMCs. Increases in protein aggregation and enhanced UPR were observed in VSMCs exposed to AngII, which were mitigated by overexpression of GRP78. Moreover, GRP78 overexpression attenuated enhanced monocyte adhesion to VSMCs induced by AngII. Our results thus indicate that the prevention of protein aggregation can potentially mitigate an inflammatory phenotype in VSMCs, which may suggest an alternative therapy for the treatment of AngII-associated vascular disorders.

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Section: Angii-induced Proinflammatory Phenotype Is Mitigated By Grp78mentioning

confidence: 99%

78 kDa Glucose-Regulated Protein Attenuates Protein Aggregation and Monocyte Adhesion Induced by Angiotensin II in Vascular Cells

Cicalese

Okuno

Elliott

et al. 2020

IJMS

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“…Accumulating studies have shown that cellular ERS promotes the expression of pro-inflammatory cytokines (such as IFN-γ and TNF-α) and then participates in the regulation of innate and adaptive immunity [33,34]. Both IFN-γ and TNF-α belong to the Th1-type cytokines and play significant roles in the regulation of cellular immune responses to intracellular microbial infections [58,59].…”

Section: Discussionmentioning

confidence: 99%

“…Increasing evidence have revealed that many stressorsinduced cellular ERS can promote the expression of inflammatory cytokines and then participate in the regulation of innate immunity [33,34]. Many proinflammatory cytokines, such as interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α), can promote induction of autophagy [35,36].…”

Section: The Perk and Ire1 Pathways Are Associated With Transcriptionmentioning

confidence: 99%

Classical swine fever virus employs the PERK- and IRE1-dependent autophagy for viral replication in cultured cells.

Zhu

Chen

et al. 2020

Virulence

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“…Macrophage activation occurs through the DAMP (damage-associated molecular patterns) and PAMP (pathogen-associated molecular patterns) interaction with TLR [ 95 ]. TLR activation leads to the IRE1α/XBP1 signaling pathway (UPR activation) induction and subsequent production of the pro-inflammatory cytokines IL6, CCL2, and TNF-α.…”

Section: Relationship Between Cholesterol Accumulation Er Stressmentioning

confidence: 99%

Endoplasmic Reticulum Stress in Macrophages: The Vicious Circle of Lipid Accumulation and Pro-Inflammatory Response

et al. 2020

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The endoplasmic reticulum (ER) stress is an important event in the pathogenesis of different human disorders, including atherosclerosis. ER stress leads to disturbance of cellular homeostasis, apoptosis, and in the case of macrophages, to foam cell formation and pro-inflammatory cytokines production. In atherosclerosis, several cell types can be affected by ER stress, including endothelial cells, vascular smooth muscular cells, and macrophages. Modified low-density lipoproteins (LDL) and cytokines, in turn, can provoke ER stress through different processes. The signaling cascades involved in ER stress initiation are complex and linked to other cellular processes, such as lysosomal biogenesis and functioning, autophagy, mitochondrial homeostasis, and energy production. In this review, we discuss the underlying mechanisms of ER stress formation and the interplay of lipid accumulation and pro-inflammatory response. We will specifically focus on macrophages, which are the key players in maintaining chronic inflammatory milieu in atherosclerotic lesions, and also a major source of lipid-accumulating foam cells.

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ER Stress Responses: An Emerging Modulator for Innate Immunity

Cited by 153 publications

References 70 publications

78 kDa Glucose-Regulated Protein Attenuates Protein Aggregation and Monocyte Adhesion Induced by Angiotensin II in Vascular Cells

78 kDa Glucose-Regulated Protein Attenuates Protein Aggregation and Monocyte Adhesion Induced by Angiotensin II in Vascular Cells

Classical swine fever virus employs the PERK- and IRE1-dependent autophagy for viral replication in cultured cells.

Endoplasmic Reticulum Stress in Macrophages: The Vicious Circle of Lipid Accumulation and Pro-Inflammatory Response

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