Calreticulin Protects Rat Microvascular Endothelial Cells against Microwave Radiation‐induced Injury by Attenuating Endoplasmic Reticulum Stress

Li, Weihong; Li, Yuzhen; Song, Dandan; Wang, Xiao-Reng; Liu, Mi; Wang, Xudong; Li, Xiuhua

doi:10.1111/micc.12126

Cited by 10 publications

(2 citation statements)

References 30 publications

(45 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Calreticulin, a major Ca 2+ binding ER chaperone plays an important role in the adequate folding of newly synthesized proteins [73]. Therefore, fluctuations or alterations in Ca 2+ level in the ER might impact folding capacity and initiate the components of cell death.…”

Section: Introductionmentioning

confidence: 99%

Endoplasmic Reticulum Stress in Sepsis

Khan

Yang

Wang

2015

Shock

115

View full text Add to dashboard Cite

Sepsis is an enormous public health issue and the leading cause of death in critically ill patients in intensive care units (ICU). Overwhelming inflammation, characterized by cytokine storm, oxidative threats, and neutrophil sequestration is an underlying component of sepsis-associated organ failure. Despite recent advances in sepsis research, there is still no effective treatment available beyond the standard of care and supportive therapy. To reduce sepsis-related mortality, a better understanding of the biological mechanism associated with the sepsis is essential. Endoplasmic reticulum (ER), a subcellular organelle is responsible for the facilitation of protein folding and assembly and involved in several other physiological activities. Under the stress and inflammation condition, ER loses the homeostasis in its function, which is termed as ER stress. During ER stress, unfolded protein response (UPR) is activated to restore ER function to its normal balance. However, once the stress is beyond the compensatory capacity of UPR or protracted, the apoptosis would be initiated by triggering cell injuries, even to cell death. As such, ER stress and UPR are reported to be implicated in several pathological and inflammatory conditions. Although the detrimental role of ER stress during infections has been demonstrated, there is growing evidences that ER stress participate in the pathogenesis of sepsis. In this review, we summarize the current research in the context of ER stress and UPR signaling associated with sepsis and its related clinical conditions, such as trauma- hemorrhage, and ischemia/reperfusion (I/R) injury. We also discuss the potential implication of ER stress as a novel therapeutic target and prognostic marker in patients with sepsis.

show abstract

Section: Introductionmentioning

confidence: 99%

Endoplasmic Reticulum Stress in Sepsis

Khan

Yang

Wang

2015

Shock

115

View full text Add to dashboard Cite

show abstract

“…Their data showed that exposure to the highest power level (12 W) resulted in a decrease in HSP90 levels in the thymus, while the expression of HSP70 remained relatively unchanged in both groups, consistent with the results of this experiment. Currently, research on microwave irradiation and CRT protein is mainly focused on investigating the protective role of CRT against microvascular endothelial cell damage after irradiation by reducing endoplasmic reticulum stress [24]. In our study, we primarily investigated the expression of CRT protein in rat spleens after microwave irradiation and explored its potential as an indicator of the immune status of the rat spleen after irradiation.…”

Section: Discussionmentioning

confidence: 99%

Microwaves activate immune response and promote lymphocytes proliferation of Wistar rats

Ma,

Cao,

Zou

et al. 2024

Preprint

View full text Add to dashboard Cite

Objective The potential effects of microwave radiation on human health have been increasingly emphasized with its widespread application in human production and daily life. This study aimed to investigate microwave radiation effects on rat spleen tissue structure and immune function. Methods Male Wistar rats weighed approximately 320 to 350 g were subjected to S band (2.856 GHz) microwave radiation for 20 minutes at an average power density of 50 mW/cm2. At 0 and 7 days after exposure, the concentration of IL-1, IL-1β, IL-2, IL-4, IL-8, IL-10, TNF-α and IFN-γ in rat serum were detected by ELISA. HE staining was used to observe the structure of rat spleen. Western blotting was used to assess the expression of HSP70 and CRT in rat spleen. Additionally, mixed lymphocytes from rat spleens were isolated, and the morphology and proliferation of rat spleen mixed lymphocytes was observed after 24 hours of culture, and their proliferation was evaluated using the CCK-8 assay. Results After exposure to 50 mW/cm2 for 20 minutes, rats showed an increased secretion of inflammatory factors in their serum. This was observed both in the immediately irradiated group (R-0d) and in the irradiated group observed after 7 days (R-7d). The R-0d group exhibited lower levels of IL-1 and IL-8 than the control group (C-0d), while IL-2 and IL-10 secretion was elevated. Conversely, in the R-7d group, levels of IL-1, IL-2, and IL-10 were lower than those in the C-0d group, and IL-8 levels were lower compared to the control group. TNF-α and IFN-γ levels were elevated. Structural examination of rat spleen tissue revealed no significant damage. However, compared to the control group, the irradiated groups (R-0d and R-7d) showed a significant increase and thickening of the white pulp. Additionally, the boundary between the red and white medulla in the R-7d group appeared blurred. Western blotting showed no significant difference in the expression of HSP70 and CRT between the exposed and control groups. In addition, the splenic mixed lymphocytes in the irradiated group showed a significant proliferation of cell colonies. The results of the CCK-8 assay showed that the cell viability and proliferation capacity of the irradiated group were significantly increased compared to the control group. Conclusion The immune system of rats was activated, the pattern of cytokine secretion in rat serum was altered, splenocytes proliferation was promoted, potentially triggering an inflammatory immune response after exposure to 50 mW/cm² of microwave for 20 minutes.

show abstract

The Role of Endoplasmic Reticulum Stress in Diabetic Nephropathy

et al. 2017

View full text Add to dashboard Cite

As maladaptive ER stress response caused by excessively prolonged UPR will eventually cause cell death and increase kidney injury, several ER stress inhibitors have been shown to improve DN in animal models, albeit blocking both adaptive and maladaptive UPR. More recently, reticulon-1A (RTN1A), an ER-associated protein, was shown to be increased in both human and mouse diabetic kidneys. Its expression correlates with the progression of DN, and its polymorphisms are associated with kidney disease in people with diabetes. Increased RTN1A expression heightened the ER stress response and renal cell apoptosis, and conversely reduced RTN1A in renal cells decreased apoptosis and ameliorated kidney injury and DN progression, suggesting that RTN1A may be a novel target to specifically restrain the maladaptive UPR. These findings suggest that ER stress response in renal cells is a key driver of progression of DN and that the inhibition of the unchecked ER stress response in DN, such as by inhibition of RTN1A function, may be a promising therapeutic approach against DN.

show abstract

Calreticulin Protects Rat Microvascular Endothelial Cells against Microwave Radiation‐induced Injury by Attenuating Endoplasmic Reticulum Stress

Abstract: Exogenous CRT attenuates MR-induced ER stress-related apoptosis by suppressing CHOP-mediated apoptotic signaling pathways in MMECs.

Cited by 10 publications

References 30 publications

Endoplasmic Reticulum Stress in Sepsis

Endoplasmic Reticulum Stress in Sepsis

Microwaves activate immune response and promote lymphocytes proliferation of Wistar rats

The Role of Endoplasmic Reticulum Stress in Diabetic Nephropathy

Contact Info

Product

Resources

About