scholarly journals Impact of Endoplasmic Reticulum Stress in Otorhinolaryngologic Diseases

2020 ◽  
Vol 21 (11) ◽  
pp. 4121
Author(s):  
Su Young Jung ◽  
Sung Su Kim ◽  
Seung Geun Yeo
Keyword(s):  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Comprehensive Overview ◽  
Current State ◽  
Living Things ◽  
Obstructive Sleep ◽  
The Subject ◽  
Otorhinolaryngologic Diseases ◽  
The Relationship ◽  
Normal Cellular Function

The endoplasmic reticulum (ER) is an important organelle for normal cellular function and homeostasis in most living things. ER stress, which impairs ER function, occurs when the ER is overwhelmed by newly introduced immature proteins or when calcium in the ER is depleted. A number of diseases are associated with ER stress, including otorhinolaryngological diseases. The relationship between ER stress and otorhinolaryngologic conditions has been the subject of investigation over the last decade. Among otologic diseases associated with ER stress are otitis media and hearing loss. In rhinologic diseases, chronic rhinosinusitis, allergic rhinitis, and obstructive sleep apnea are also significantly associated with ER stress. In this review, we provide a comprehensive overview of the relationship between ER stress and otorhinolaryngological diseases, focusing on the current state of knowledge and mechanisms that link ER stress and otorhinolaryngologic diseases.

scholarly journals Expression, Distribution and Role of Aquaporins in Various Rhinologic Conditions

2020 ◽  
Vol 21 (16) ◽  
pp. 5853
Author(s):  
Su Young Jung ◽  
Dong Choon Park ◽  
Sung Su Kim ◽  
Seung Geun Yeo
Keyword(s):  
Inflammatory Diseases ◽  
Membrane Channel ◽  
Comprehensive Overview ◽  
Normal Tissues ◽  
Current State ◽  
The Subject ◽  
External Stimuli ◽  
The Relationship ◽  
Specific Membrane

Aquaporins (AQPs) are water-specific membrane channel proteins that regulate cellular and organismal water homeostasis. The nose, an organ with important respiratory and olfactory functions, is the first organ exposed to external stimuli. Nose-related topics such as allergic rhinitis (AR) and chronic rhinosinusitis (CRS) have been the subject of extensive research. These studies have reported that mechanisms that drive the development of multiple inflammatory diseases that occur in the nose and contribute to the process of olfactory recognition of compounds entering the nasal cavity involve the action of water channels such as AQPs. In this review, we provide a comprehensive overview of the relationship between AQPs and rhinologic conditions, focusing on the current state of knowledge and mechanisms that link AQPs and rhinologic conditions. Key conclusions include the following: (1) Various AQPs are expressed in both nasal mucosa and olfactory mucosa; (2) the expression of AQPs in these tissues is different in inflammatory diseases such as AR or CRS, as compared with that in normal tissues; (3) the expression of AQPs in CRS differs depending on the presence or absence of nasal polyps; and (4) the expression of AQPs in tissues associated with olfaction is different from that in the respiratory epithelium.

Apigetrin Promotes Cell Autophagy by Activating the Endoplasmic Reticulum Stress in Human Cervical Cancer Hela Cells

2021 ◽  
Vol 20 (1) ◽  
pp. 56-63
Author(s):  
Li Jiang ◽  
Zhi-Cheng Yao ◽  
Miao-Miao Liu ◽  
Run-Hui Ma ◽  
Kiran Thakur
Keyword(s):  
Cervical Cancer ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Hela Cells ◽  
Fruits And Vegetables ◽  
Radical Scavenging ◽  
Anticancer Activities ◽  
Treatment Results ◽  
Metastasis Rate ◽  
The Relationship

Cervical cancer has always been the top malignant cancer among female cancers in the world. Due to its recurrence, metastasis rate, and drug resistance, the treatment results of cervical cancer have been unsatisfactory. Apigetrin is present in a variety of fruits and vegetables and has been reported to have antioxidant, free radical scavenging, anti-inflammatory, and anticancer activities. Therefore, this study focuses on the effect of apigetrin on the autophagy of cervical cancer HeLa cells based on the previous research. The results showed that apigetrin can enhance the autophagy fluorescence of light chain 3B (LC3B), and further combined with quantitative real-time PCR (qPCR) and Western blotting found that the expression of autophagy-related genes and proteins p-mTOR, Beclin1, and LC3B increased, while the expression of AMPK, ULK1, and p62 decreased. In addition, apigetrin also promoted the release of Ca2+, the PERK/eIF2α/ATF4/chop, and IRE1α pathways activate endoplasmic reticulum (ER) stress. The addition of 4PBA proved that ER stress promoted autophagy in HeLa cells. Finally, the addition of the 3-MA indicates the relationship between autophagy and apoptosis in HeLa cells. Our results indicate that apigetrin has a certain anticancer potential and can be used as a drug adjuvant and food additive for the prevention and treatment of cervical cancer.

scholarly journals Chemotherapy Resistance Explained through Endoplasmic Reticulum Stress-Dependent Signaling

Cancers ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 338 ◽  
Author(s):  
Entaz Bahar ◽  
Ji-Ye Kim ◽  
Hyonok Yoon
Keyword(s):  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Molecular Mechanism ◽  
Molecular Mechanisms ◽  
Cellular Proliferation ◽  
Protein Quality ◽  
Chemotherapy Resistance ◽  
Persistent Problem ◽  
Stress Dependent ◽  
The Relationship

Cancers cells have the ability to develop chemotherapy resistance, which is a persistent problem during cancer treatment. Chemotherapy resistance develops through different molecular mechanisms, which lead to modification of the cancer cells signals needed for cellular proliferation or for stimulating an immune response. The endoplasmic reticulum (ER) is an important organelle involved in protein quality control, by promoting the correct folding of protein and ER-mediated degradation of unfolded or misfolded protein, namely, ER-associated degradation. Disturbances of the normal ER functions causes an accumulation of unfolded or misfolded proteins in the ER lumen, resulting in a condition called “ER stress (ERS).” ERS triggers the unfolded protein response (UPR)—also called the ERS response (ERSR)—to restore homeostasis or activate cell death. Although the ERSR is one emerging potential target for chemotherapeutics to treat cancer, it is also critical for chemotherapeutics resistance, as well. However, the detailed molecular mechanism of the relationship between the ERSR and tumor survival or drug resistance remains to be fully understood. In this review, we aim to describe the most vital molecular mechanism of the relationship between the ERSR and chemotherapy resistance. Moreover, the review also discusses the molecular mechanism of ER stress-mediated apoptosis on cancer treatments.

scholarly journals Endoplasmic Reticulum Stress and Unfolded Protein Response in Breast Cancer: The Balance between Apoptosis and Autophagy and Its Role in Drug Resistance

2019 ◽  
Vol 20 (4) ◽  
pp. 857 ◽  
Author(s):  
Lorenza Sisinni ◽  
Michele Pietrafesa ◽  
Silvia Lepore ◽  
Francesca Maddalena ◽  
Valentina Condelli ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Unfolded Protein Response ◽  
Inflammatory Diseases ◽  
Unfolded Protein ◽  
Chronic Activation ◽  
The Unfolded Protein Response ◽  
Protein Response ◽  
The Relationship

The unfolded protein response (UPR) is a stress response activated by the accumulation of unfolded or misfolded proteins in the lumen of the endoplasmic reticulum (ER) and its uncontrolled activation is mechanistically responsible for several human pathologies, including metabolic, neurodegenerative, and inflammatory diseases, and cancer. Indeed, ER stress and the downstream UPR activation lead to changes in the levels and activities of key regulators of cell survival and autophagy and this is physiologically finalized to restore metabolic homeostasis with the integration of pro-death or/and pro-survival signals. By contrast, the chronic activation of UPR in cancer cells is widely considered a mechanism of tumor progression. In this review, we focus on the relationship between ER stress, apoptosis, and autophagy in human breast cancer and the interplay between the activation of UPR and resistance to anticancer therapies with the aim to disclose novel therapeutic scenarios. The hypothesis that autophagy and UPR may provide novel molecular targets in human malignancies is discussed.

scholarly journals Endoplasmic reticulum stress-related neuroinflammation and neural stem cells decrease in mice exposure to paraquat

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Zhengli Yang ◽  
Yiming Shao ◽  
Yifan Zhao ◽  
Qian Li ◽  
Rui Li ◽  
...  
Keyword(s):  
Stem Cells ◽  
Endoplasmic Reticulum ◽  
Stem Cell ◽  
Endoplasmic Reticulum Stress ◽  
Er Stress ◽  
Subventricular Zone ◽  
Vehicle Control ◽  
Unknown Mechanism ◽  
The Relationship

Abstract Paraquat (PQ), a widely used herbicide, could cause neurodegenerative diseases, yet the mechanism remains incompletely understood. This study aimed to investigate the direct effect of PQ on NSC in vivo and its possible mechanism. Adult C57BL/6 mice were subcutaneously injected with 2 mg/kg PQ, 20 mg/kg PQ or vehicle control once a week for 2 weeks, and sacrificed 1 week after the last PQ injection. Furthermore, extra experiments with Tauroursodeoxycholic Acid (TUDCA) intervention were performed to observe the relationship between ER stress, neuroinflammation and the neural stem cell (NSC) impairment. The results showed that 20 mg/kg PQ caused the NSC number decrease in both subgranular zones (SGZ) and subventricular zone (SVZ). Further analysis indicated that the 20 mg/kg PQ suppressed the proliferation of NSC, without affecting the apoptosis. Moreover, 20 mg/kg PQ also induced ER stress in microglia and caused neuroinflammation in SGZ and SVZ. Interestingly, the ER stress inhibitor could simultaneously ameliorate the neuroinflammation and NSC reduction. These data suggested that increased ER stress in microglia might be a possible pathway for PQ-induced neuroinflammation and NSC impairment. That is a previously unknown mechanism for PQ neurotoxicity.

scholarly journals Chemokines – role in inflammatory and cancer diseases

2019 ◽  
Vol 73 ◽  
pp. 372-386
Author(s):  
Sylwia Cisoń-Jurek ◽  
Paulina Czajka-Francuz ◽  
Tomasz Francuz ◽  
Jerzy Wojnar
Keyword(s):  
Chemokine Receptors ◽  
Bacterial Infections ◽  
Current State ◽  
The Family ◽  
The Subject ◽  
And Migration ◽  
And Function ◽  
Human Chemokines ◽  
The Relationship

Over 50 human chemokines are known at present; the number of the newly discovered compounds from this group still grows. These proteins of low molecular weight, belonging to the family of cytokines with chemotactic properties. Chemokines participate in the physiological and pathological processes of the organism. Recent papers show their role in the processes of embryogenesis, organogenesis, allergies, wound healing, angiogenesis and apoptosis, the course of viral and bacterial infections, autoimmune diseases and cancerogenesis. Chemokines play crucial role in activation and migration of immune cells. Being a key player in chronic inflammation, chemokines may interfere the processes of cellular differentiation and contribute to loss of control over proliferation. Coexistence of inflammatory and cancerogenesis processes, impact of chemokines on cells associated with the tumor and stromal cells, mechanisms of immunological escape is considered to be a current scientific issue. Newly discovered functions of chemokines may reveal their new roles and create the new therapeutic perspectives. It is important to understand the relationship between the structure and function of chemokine receptors, the regulation of their signaling pathways and the genetic and epigenetic mechanisms that regulate the expression of chemokines and their receptors. This article presents the current state of knowledge regarding the construction and classification of chemokines and summarizes the most prominent roles of chemokines. Chemokines are still the subject of many scientific studies, new functions are being discovered. It gives an opportunity to limit the development of many dangerous diseases.

scholarly journals Sevoflurane Post-Conditioning Alleviated Hypoxic-Ischemic Brain Injury in Neonatal Rats by Inhibiting Endoplasmic Reticulum Stress-Mediated Autophagy via IRE1 Signalings

2021 ◽  
Author(s):  
Jiayuan Niu ◽  
Ziyi Wu ◽  
Hang Xue ◽  
Yahan Zhang ◽  
Qiushi Gao ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Brain Injury ◽  
Er Stress ◽  
Signaling Pathway ◽  
Ischemic Brain Injury ◽  
Neonatal Rats ◽  
Artery Ligation ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury ◽  
The Relationship

Abstract Post-conditioning with sevoflurane, a volatile anesthetic, has been proved to be neuroprotective against hypoxic-ischemic brain injury (HIBI). Our previous research showed that autophagy is over-activated in a rat model of neonatal HIBI, and inhibition of autophagy confers neuroprotection. There is increasing recognition that autophagy can be triggered by activating endoplasmic reticulum (ER) stress. This study aimed to explore: i) the relationship between ER stress and autophagy in the setting of neonatal HIBI; and ii) the possible roles of ER stress-mediated autophagy and IRE1 signalings in the neuroprotection of sevoflurane post-conditioning against neonatal HIBI. Seven-day-old rats underwent left common artery ligation followed by 2 h hypoxia (8% O2 / 92% N2). The relationship between ER stress and autophagy was examined by ER stress inducer (tunicamycin), ER stress inhibitor (4-PBA), or autophagy inhibitor (3-MA). Rats in the sevoflurane post-conditioning groups were treated with 2.4% sevoflurane for 30 min after HIBI induction. The roles of ER stress-mediated autophagy and the IRE1/JNK/beclin1 signaling pathway in the neuroprotection afforded by sevoflurane were examined by ER stress inducer (tunicamycin) and the IRE1 inhibitor (STF-083010). HIBI over‑activated ER stress and autophagy in neonatal rats. HIBI-induced autophagy was significantly aggravated by tunicamycin but blocked by 4-PBA; however, HIBI-induced ER stress was not affected by 3-MA. Sevoflurane post-conditioning significantly alleviated ER stress, autophagy, cell apoptosis, and cognitive impairments, which were remarkably abolished by tunicamycin. Also, tunicamycin blocked sevoflurane-induced downregulation of IRE1/JNK/beclin1 signaling pathway. Whereas, IRE1 inhibitor could reverse the effects of tunicamycin. ER stress contributes to autophagy induced by HIBI. Furthermore, sevoflurane post-conditioning significantly protects against HIBI in neonatal rats by inhibiting ER stress-mediated autophagy via IRE1/JNK/beclin1 signaling pathway.

History of Philosophy as a Memory

2019 ◽  
Vol 1 ◽  
pp. 129-142
Author(s):  
Stanisław Buda
Keyword(s):  
Special Property ◽  
The Third ◽  
The Core ◽  
Current State ◽  
History Of ◽  
The Subject ◽  
The Relationship ◽  
Philosophical Progress ◽  
New System ◽  
The Way

In the first part I focus on the issue of progress, in particular progress in philosophy. Philosophical progress has a special property that it shares with the process of becoming a better person. It is constantly finding yourself “on the way”. This path is not only anchored in the Absolutely Perfect but it conditions and stimulates the reflection towards the truth about the relationship between Him and us. We can assume that the core of this reflection is philosophy. The second part is devoted to the paradoxical nature of the most generally understood memory. I assume that the condition of awareness of a certain content is its outdatedness, that is, its transfer to the sphere of memory. Memory is a constantly updated and constantly re-ordered picture of everything that the subject has ever relegated from being, so that it can be replaced by something else. The foundation of this order is a certain axiology. In the third part I show how the sketched concept of memory is used to describe the mechanism of the evolution of philosophical thought. The “on the way” philosophy would consist of two constantly repeated activities: on reconstructing what is to be denied, and thus on the recognition of the previous philosophical achievements in its totality, and on its negation. This denial would concern the whole of this achievement as an axiologically reconstructed unity. The new system is only realized as a series of consequences of the negation of the current state. The vast majority of philosophical reflection focuses on the constitution of this current state, its supposed unity. In the short part of the fourth, I draw up prospects for further deliberations.

scholarly journals The Emerging Role of Electrophiles as a Key Regulator for Endoplasmic Reticulum (ER) Stress

2019 ◽  
Vol 20 (7) ◽  
pp. 1783 ◽  
Author(s):  
Takasugi ◽  
Hiraoka ◽  
Nakahara ◽  
Akiyama ◽  
Fujikawa ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Unfolded Proteins ◽  
Unfolded Protein ◽  
Stress Sensors ◽  
The Unfolded Protein Response ◽  
Protein Response ◽  
Protein Disulfide ◽  
The Relationship

The unfolded protein response (UPR) is activated by the accumulation of misfolded proteins in the endoplasmic reticulum (ER), which is called ER stress. ER stress sensors PERK, IRE1, and ATF6 play a central role in the initiation and regulation of the UPR; they inhibit novel protein synthesis and upregulate ER chaperones, such as protein disulfide isomerase, to remove unfolded proteins. However, when recovery from ER stress is difficult, the UPR pathway is activated to eliminate unhealthy cells. This signaling transition is the key event of many human diseases. However, the precise mechanisms are largely unknown. Intriguingly, reactive electrophilic species (RES), which exist in the environment or are produced through cellular metabolism, have been identified as a key player of this transition. In this review, we focused on the function of representative RES: nitric oxide (NO) as a gaseous RES, 4-hydroxynonenal (HNE) as a lipid RES, and methylmercury (MeHg) as an environmental organic compound RES, to outline the relationship between ER stress and RES. Modulation by RES might be a target for the development of next-generation therapy for ER stress-associated diseases.

scholarly journals The Transient Receptor Potential Channel Yvc1 Deletion Recovers the Growth Defect of Calcineurin Mutant Under Endoplasmic Reticulum Stress in Candida albicans

2021 ◽  
Vol 12 ◽  
Author(s):  
Liping Peng ◽  
Jiawen Du ◽  
Runfan Zhang ◽  
Nali Zhu ◽  
He Zhao ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Stress Response ◽  
Er Stress ◽  
Calcium Concentration ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Cellular Calcium ◽  
Er Stress Response ◽  
Transient Receptor ◽  
The Relationship

Transient receptor potential (TRP) channel Yvc1 was related with hyphal growth, oxidative stress response, and pathogenicity. Calcineurin subunit Cnb1 was activated immediately in yeasts when exposed to severe stimulation. However, the relationship between Yvc1 and Cnb1-governed calcium ions and endoplasmic reticulum (ER) stress response remains unrevealed. In this study, we found that the mutant cnb1Δ/Δ was sensitive to TN, which was related with the overexpression of membrane calcium ion channels that could increase the cytosol calcium concentration. However, the growth of the cnb1Δ/Δyvc1Δ/Δ mutant was recovered and its cell vitality was better than the cnb1Δ/Δ strain. Meanwhile, the cellular calcium concentration was decreased and its fluctuation was weakened under ER stress in the cnb1Δ/Δyvc1Δ/Δ strain. To verify the regulation role of Yvc1 in the calcium concentration, we found that the addition of CaCl2 led to the worse viability, while the growth state was relieved under the treatment of EGTA in the cnb1Δ/Δ strain. In conclusion, the deletion of YVC1 could reduce the cellular calcium and relieve the ER stress sensitivity of the cnb1Δ/Δ strain. Thereby, our findings shed a novel light on the relationship between the Yvc1-governed cellular calcium concentration and ER stress response in C. albicans.

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