Restraint stress aggravates rat kidney injury caused by a crush injury through endoplasmic reticulum stress

Geng, Jing; Zhang, Xiao Jing; Ling, Chun; Li, Ying Min; Zhang, Guo Zhong; Ren, Feng; Zhang, Yue; Cong, Bin

doi:10.1097/ta.0b013e3182a685ff

Cited by 6 publications

(4 citation statements)

References 35 publications

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“…Firstly, apoptosis has been reported to be involved in kidney damage at the cellular level after experimental CS [25, 30]. In fact, necrosis is also involved in kidney damage [25].…”

Section: Discussionmentioning

confidence: 99%

Anti-high mobility group box-1 (HMGB1) antibody attenuates kidney damage following experimental crush injury and the possible role of the tumor necrosis factor-α and c-Jun N-terminal kinase pathway

et al. 2017

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BackgroundInflammation plays a crucial role in kidney damage after crush syndrome (CS). Several researchers report that high mobility group box-1 protein (HMGB1) may be the vital trigger in kidney damage, and tumor necrosis factor-α (TNF-α) and c-Jun N-terminal kinase (JNK) are involve in this pathophysiological process, but their biological roles are unclear. This study aimed to explore the relationship between HMGB1, JNK, and TNF-α in kidney damage.MethodsThe crush injury model was established using weight compression. The reliability of the crush injury model was determined by hematoxylin-eosin (HE) staining. Western blot was used to detect the expression of HMGB1, JNK, and TNF-α, and TUNEL was used to mark apoptotic cells in the renal cortex.ResultsThe results showed that the highest expression of HMGB1 in muscle was 12 h after CS. JNK and TNF-α increased and peaked at 1 day after CS in kidneys. Western blot analysis revealed that anti-HMGB1 antibody could downregulate the expression of JNK and TNF-α. Anti-TNF-α could downregulate activation of JNK, and SP600125 could downregulate expression of TNF-α in the kidneys. In addition, anti-HMGB1 antibody, anti-TNF-α antibody, and SP600125 could reduce cellular apoptosis in the renal cortex.ConclusionsIt is possible that JNK and TNF-α commonly contribute to kidney damage by assembling a positive feedback cycle after CS, leading to increased apoptosis in the renal cortex. HMGB1 from the muscle may be the trigger.

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“…Firstly, apoptosis has been reported to be involved in kidney damage at the cellular level after experimental CS [25, 30]. In fact, necrosis is also involved in kidney damage [25].…”

Section: Discussionmentioning

confidence: 99%

Anti-high mobility group box-1 (HMGB1) antibody attenuates kidney damage following experimental crush injury and the possible role of the tumor necrosis factor-α and c-Jun N-terminal kinase pathway

et al. 2017

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“…ER stress was also involved in METH-induced umbilical vein endothelial cell injury ( Cai et al, 2016 ). Our previous studies have found that ER stress is related to restraint stress-induced rat kidney injury and hippocampal damage ( Geng et al, 2013 ; Zhang et al, 2014 ). Whether ER stress is involved in METH-induced BBB damage has not been determined yet.…”

Section: Introductionmentioning

confidence: 99%

Endoplasmic Reticulum Stress Mediates Methamphetamine-Induced Blood–Brain Barrier Damage

et al. 2017

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Methamphetamine (METH) abuse causes serious health problems worldwide, and long-term use of METH disrupts the blood–brain barrier (BBB). Herein, we explored the potential mechanism of endoplasmic reticulum (ER) stress in METH-induced BBB endothelial cell damage in vitro and the therapeutic potential of endoplasmic reticulum stress inhibitors for METH-induced BBB disruption in C57BL/6J mice. Exposure of immortalized BMVEC (bEnd.3) cells to METH significantly decreased cell viability, induced apoptosis, and diminished the tightness of cell monolayers. METH activated ER stress sensor proteins, including PERK, ATF6, and IRE1, and upregulated the pro-apoptotic protein CHOP. The ER stress inhibitors significantly blocked the upregulation of CHOP. Knockdown of CHOP protected bEnd.3 cells from METH-induced cytotoxicity. Furthermore, METH elevated the production of reactive oxygen species (ROS) and induced the dysfunction of mitochondrial characterized by a Bcl2/Bax ratio decrease, mitochondrial membrane potential collapse, and cytochrome c. ER stress release was partially reversed by ROS inhibition, and cytochrome c release was partially blocked by knockdown of CHOP. Finally, PBA significantly attenuated METH-induced sodium fluorescein (NaFluo) and Evans Blue leakage, as well as tight junction protein loss, in C57BL/6J mice. These data suggest that BBB endothelial cell damage was caused by METH-induced endoplasmic reticulum stress, which further induced mitochondrial dysfunction, and that PBA was an effective treatment for METH-induced BBB disruption.

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“…The liver and kidney, as the main organs of animal, have some functions that cannot be compensated by other organs. Many types of stresses such as endoplasmic reticulum stress and oxidative stress can cause some damages to the liver and kidney (Gallazzini & Pallet, 2018;Geng et al, 2013;Yang et al, 2016;Yao et al, 2015). A previous study has demonstrated that HSP70 protein was increased in the kidney of pig after transport stress (Yu et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Detection of heat shock protein 27, 70, 90 expressions in primary parenchymatous organs of goats after transport stress by real‐time PCR and ELISA

Fang

Yang

et al. 2020

Veterinary Medicine & Sci

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Transport stress causes a series of problems to goat production, such as tissue injury and immunity damage. As a pro‐survival pathway, the heat shock response protects healthy cells of goat from stressors. To evaluate the effects of transport stress on heat shock protein (HSPs) expression on goat primary parenchymatous organs, a total of three batches of goats were treated in this study. For each batch, 12 healthy adult male goats were randomly and averagely divided into three groups: Control group (non‐transported group), 2 hr transported group and 6 hr transported group. Real‐time PCR results indicated that the mRNA expression level of heat shock protein 27 (HSP27) in all examined organs of 2 hr transport‐treated goats were upregulated (p < .05) except lung, and heat shock protein 70 (HSP70; except spleen) and heat shock protein 90 (HSP90; except liver and lung) were also increased (p < .05). In 6 hr transported group, the transcription levels of HSP27 (except heart and kidney), HSP70 (except heart, liver and lymph nodes) and HSP90 (except heart and spleen) were all backed to the original levels or even reduced (p < .05). Enzyme‐linked immunosorbent assay (ELISA) results showed that the protein levels of HSP27 (except lymph nodes), HSP70 (except spleen) and HSP90 (except liver and lung) were all increased after 2 hr transport (p < .05). After 6 hr transport, HSP27 only in kidney and HSP70 only in heart and liver were upregulated (p < .05), while HSP90 in all the examined organs except liver and lung were also maintained in relatively high levels (p < .05). Taken together, these results suggested that the expression of HSPs in goat primary parenchymatous organs may be regulated by transport stress time. Moreover, this study also provides some new data to advocate reducing transport stress of goats and improving animal welfare.

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Restraint stress aggravates rat kidney injury caused by a crush injury through endoplasmic reticulum stress

Abstract: Apoptosis and inflammation induced by ERS are important mechanisms by which restraint stress aggravates kidney injury caused by a crush injury.

Cited by 6 publications

References 35 publications

Anti-high mobility group box-1 (HMGB1) antibody attenuates kidney damage following experimental crush injury and the possible role of the tumor necrosis factor-α and c-Jun N-terminal kinase pathway

Anti-high mobility group box-1 (HMGB1) antibody attenuates kidney damage following experimental crush injury and the possible role of the tumor necrosis factor-α and c-Jun N-terminal kinase pathway

Endoplasmic Reticulum Stress Mediates Methamphetamine-Induced Blood–Brain Barrier Damage

Detection of heat shock protein 27, 70, 90 expressions in primary parenchymatous organs of goats after transport stress by real‐time PCR and ELISA

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