Assessing ClO- level during ER stress and cellular senescence through a ratio fluorescent probe with dual organelle targeting ability

2022 ◽  
pp. 131383
Author(s):  
Yi-Min Shan ◽  
Kang-Kang Yu ◽  
Nan Wang ◽  
Fan-Yuan Yu ◽  
Kun Li ◽  
...  
Keyword(s):  
Er Stress ◽  
Fluorescent Probe ◽  
Cellular Senescence ◽  
Targeting Ability ◽  
Organelle Targeting

The p38‐activated ER stress‐ATF6α axis mediates cellular senescence

2018 ◽  
Vol 33 (2) ◽  
pp. 2422-2434 ◽  
Author(s):  
Hee Suk Kim ◽  
Yongjin Kim ◽  
Min Jae Lim ◽  
Yun-Gyu Park ◽  
Serk In Park ◽  
...  
Keyword(s):  
Er Stress ◽  
Cellular Senescence

Bile Acids and Deregulated Cholangiocyte Autophagy in Primary Biliary Cholangitis

2017 ◽  
Vol 35 (3) ◽  
pp. 210-216 ◽  
Author(s):  
Motoko Sasaki ◽  
Yasuni Nakanuma
Keyword(s):  
Bile Duct ◽  
Er Stress ◽  
Bile Acids ◽  
Cellular Senescence ◽  
Primary Biliary Cholangitis ◽  
Biliary Cirrhosis ◽  
Chemical Chaperone ◽  
Abnormal Expression ◽  
Bile Duct Lesions ◽  
Mitochondrial Antigens

Background: Primary biliary cholangitis (PBC) is characterized by a high prevalence of serum anti-mitochondrial antibodies against the E2 subunit of the pyruvate dehydrogenase complex and bile duct lesions called chronic non-suppurative destructive cholangitis (CNSDC) in small bile ducts, eventually followed by extensive bile duct loss and biliary cirrhosis. Macroautophagy (a major type of autophagy) is a process of cellular self-digestion that plays a critical role in energy homeostasis and in the cytoprotection to various stresses. Deregulated autophagy is thought to be associated with various human diseases. Key Messages: Accumulating evidences suggest that deregulated autophagy may be a central player in the pathogenesis of PBC. Damaged cholangiocytes involved in CNSDC show vesicular expression of autophagy marker LC3 and accumulation of p62/sequestosome-1, suggesting deregulated autophagy. Deregulated autophagy may be involved in the autoimmune process via the abnormal expression of mitochondrial antigens and also in cholangiocyte senescence in bile duct lesions in PBC. In vitro study showed that hydrophobic bile acids, such as glycochenodeoxycholic acid (GCDC), as well as serum deprivation and oxidative stress, cause autophagy, deregulated autophagy and abnormal expression of mitochondrial antigens followed by cellular senescence in cholangiocytes. Although exact mechanisms of deregulated autophagy remain to be clarified, endoplasmic reticulum (ER) stress may be a plausible cause of deregulated autophagy induced by GCDC in cholangiocytes. Impaired ‘biliary bicarbonate umbrella' may further exacerbate the toxicity of GCDC to cholangiocytes. Interestingly, pretreatment with ursodeoxycholic acid (UDCA) and tauro-UDCA, which is a chemical chaperone enhancing the adaptive capacity of the ER, significantly suppressed ER stress, deregulated autophagy and cellular senescence induced by GCDC and other stresses in cholangiocytes. Conclusions: GCDC may play a role in the occurrence of deregulated autophagy and cellular senescence at least partly through the induction of ER stress in PBC. Deregulated autophagy and cellular senescence can be a promising therapeutic target in PBC.

scholarly journals The unfolded protein response and cellular senescence. A Review in the Theme: Cellular Mechanisms of Endoplasmic Reticulum Stress Signaling in Health and Disease

2015 ◽  
Vol 308 (6) ◽  
pp. C415-C425 ◽  
Author(s):  
Olivier Pluquet ◽  
Albin Pourtier ◽  
Corinne Abbadie
Keyword(s):  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Unfolded Protein Response ◽  
Cellular Senescence ◽  
Cell Phenotype ◽  
Cellular Mechanisms ◽  
Telomere Attrition ◽  
Unfolded Protein ◽  
The Unfolded Protein Response ◽  
Protein Response

The endoplasmic reticulum (ER) is a multifunctional organelle critical for the proper folding and assembly of secreted and transmembrane proteins. Perturbations of ER functions cause ER stress, which activates a coordinated system of transcriptional and translational controls called the unfolded protein response (UPR), to cope with accumulation of misfolded proteins and proteotoxicity. It results in ER homeostasis restoration or in cell death. Senescence is a complex cell phenotype induced by several stresses such as telomere attrition, DNA damage, oxidative stress, and activation of some oncogenes. It is mainly characterized by a cell enlargement, a permanent cell-cycle arrest, and the production of a secretome enriched in proinflammatory cytokines and components of the extracellular matrix. Senescent cells accumulate with age in tissues and are suspected to play a role in age-associated diseases. Since senescence is a stress response, the question arises of whether an ER stress could occur concomitantly with senescence and participate in the onset or maintenance of the senescent features. Here, we described the interconnections between the UPR signaling and the different aspects of the cellular senescence programs and discuss the implication of UPR modulations in this context.

scholarly journals OC-STAMP Overexpression Drives Lung Alveolar Epithelial Cell Type II Senescence in Silicosis

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Tian Li ◽  
Xin-yu Yang ◽  
Ding-jie Xu ◽  
Zi-yi Gao ◽  
Yi-bing Gao ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Er Stress ◽  
Cellular Senescence ◽  
Alveolar Epithelial Cell ◽  
Type Ii ◽  
Cell Type ◽  
Mesenchymal Transition ◽  
Epithelial Cell Type ◽  
Alveolar Epithelial ◽  
Chronic Lung Diseases

Cellular senescence has been considered an important driver of many chronic lung diseases. However, the specific mechanism of cellular senescence in silicosis is still unknown. In the present study, silicotic rats and osteoclast stimulatory transmembrane protein (Ocstamp) overexpression of MLE-12 cells were used to explore the mechanism of OC-STAMP in cellular senescence in alveolar epithelial cell type II (AEC2). We found an increasing level of OC-STAMP in AEC2 of silicotic rats. Overexpression of Ocstamp in MLE-12 cells promoted epithelial-mesenchymal transition (EMT), endoplasmic reticulum (ER) stress, and cellular senescence. Myosin heavy chain 9 (MYH9) was a potential interacting protein of OC-STAMP. Knockdown of Ocstamp or Myh9 inhibited cellular senescence in MLE-12 cells transfected with pcmv6-Ocstamp. Treatment with 4-phenylbutyrate (4-PBA) to inhibit ER stress also attenuated cellular senescence in vitro or in vivo. In conclusion, OC-STAMP promotes cellular senescence in AEC2 in silicosis.

A facile two-photon fluorescent probe: an endoplasmic reticulum tracker monitoring ER stress and vesicular transport to lysosomes

2019 ◽  
Vol 55 (3) ◽  
pp. 294-297 ◽  
Author(s):  
Pratibha Kumari ◽  
Sanjay K. Verma ◽  
Shaikh M. Mobin
Keyword(s):  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Fluorescent Probe ◽  
Vesicular Transport ◽  
Living Cells ◽  
Vesicle Transport ◽  
Live Cells ◽  
Tumor Spheroids ◽  
Dynamic Changes ◽  
Two Photon

The two-photon fluorescent organic probe ERLp selectively labels the endoplasmic reticulum in live cells and tumor spheroids. ERLp can also monitor ER dynamic changes during ER stress and vesicle transport from the ER to the lysosome in living cells.

An endoplasmic reticulum-targeting fluorescent probe for imaging ˙OH in living cells

2020 ◽  
Vol 56 (47) ◽  
pp. 6344-6347 ◽  
Author(s):  
Yanyan Zhao ◽  
Hongyu Li ◽  
Ziyin Chai ◽  
Wen Shi ◽  
Xiaohua Li ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Fluorescent Probe ◽  
Lipid Droplet ◽  
Droplet Formation ◽  
Living Cells ◽  
Lipid Droplet Formation ◽  
Er Targeting ◽  
Endoplasmic Reticulum Targeting

A new ER-targeting fluorescent probe for ˙OH is developed and applied to imaging ˙OH generation as well as lipid droplet formation in ER stress.

scholarly journals Organelle targeting using a fluorescent probe that selectively penetrates the zona pellucida

2021 ◽  
pp. 121282
Author(s):  
Sujin Lee ◽  
Hye Jin Kim ◽  
Ji-In Park ◽  
Hui Bang Cho ◽  
Ji Sun Park ◽  
...  
Keyword(s):  
Fluorescent Probe ◽  
Zona Pellucida ◽  
Organelle Targeting

Lamin B receptor: role on chromatin structure, cellular senescence and possibly aging

2020 ◽  
Vol 477 (14) ◽  
pp. 2715-2720
Author(s):  
Susana Castro-Obregón
Keyword(s):  
Cellular Senescence ◽  
Nuclear Membrane ◽  
Chromatin Structure ◽  
Cholesterol Synthesis ◽  
Reductase Activity ◽  
Chimeric Protein ◽  
Nuclear Lamina ◽  
Lamin B ◽  
Inner Nuclear Membrane ◽  
Lamin B Receptor

The nuclear envelope is composed by an outer nuclear membrane and an inner nuclear membrane, which is underlain by the nuclear lamina that provides the nucleus with mechanical strength for maintaining structure and regulates chromatin organization for modulating gene expression and silencing. A layer of heterochromatin is beneath the nuclear lamina, attached by inner nuclear membrane integral proteins such as Lamin B receptor (LBR). LBR is a chimeric protein, having also a sterol reductase activity with which it contributes to cholesterol synthesis. Lukasova et al. showed that when DNA is damaged by ɣ-radiation in cancer cells, LBR is lost causing chromatin structure changes and promoting cellular senescence. Cellular senescence is characterized by terminal cell cycle arrest and the expression and secretion of various growth factors, cytokines, metalloproteinases, etc., collectively known as senescence-associated secretory phenotype (SASP) that cause chronic inflammation and tumor progression when they persist in the tissue. Therefore, it is fundamental to understand the molecular basis for senescence establishment, maintenance and the regulation of SASP. The work of Lukasova et al. contributed to our understanding of cellular senescence establishment and provided the basis that lead to the further discovery that chromatin changes caused by LBR reduction induce an up-regulated expression of SASP factors. LBR dysfunction has relevance in several diseases and possibly in physiological aging. The potential bifunctional role of LBR on cellular senescence establishment, namely its role in chromatin structure together with its enzymatic activity contributing to cholesterol synthesis, provide a new target to develop potential anti-aging therapies.

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