Protective effect of FBXL10 in myocardial ischemia reperfusion injury via inhibiting endoplasmic reticulum stress

Gao, Jie; Guo, Yulin; Liu, Yan; Yan, Jun; Zhou, Jian; An, Xiangguang; Su, Pixiong

doi:10.1016/j.rmed.2019.105852

Cited by 16 publications

(14 citation statements)

References 21 publications

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“…Fbxl10 expression reduced myocardial infarction, remodeling, and inflammatory response in myocardial ischemia-reperfusion rats by suppressing the expression of endoplasmic reticulum stress proteins including DNA damage-inducible transcript 3 (Ddit3, also known as Chop), heat shock protein family A member 5 (Hspa5, also known as Grp78), activating transcription factor 4 (Atf4, also known as Creb2), and phospho-Erk (mitogen-activated protein kinase) [ 122 ].…”

Section: The Role Of Cullin-1 Based Crls In Cross-striated Musclesmentioning

confidence: 99%

The Role of Cullin-RING Ligases in Striated Muscle Development, Function, and Disease

Blondelle

Biju

Lange

2020

IJMS

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The well-orchestrated turnover of proteins in cross-striated muscles is one of the fundamental processes required for muscle cell function and survival. Dysfunction of the intricate protein degradation machinery is often associated with development of cardiac and skeletal muscle myopathies. Most muscle proteins are degraded by the ubiquitin–proteasome system (UPS). The UPS involves a number of enzymes, including E3-ligases, which tightly control which protein substrates are marked for degradation by the proteasome. Recent data reveal that E3-ligases of the cullin family play more diverse and crucial roles in cross striated muscles than previously anticipated. This review highlights some of the findings on the multifaceted functions of cullin-RING E3-ligases, their substrate adapters, muscle protein substrates, and regulatory proteins, such as the Cop9 signalosome, for the development of cross striated muscles, and their roles in the etiology of myopathies.

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Section: The Role Of Cullin-1 Based Crls In Cross-striated Musclesmentioning

confidence: 99%

The Role of Cullin-RING Ligases in Striated Muscle Development, Function, and Disease

Blondelle

Biju

Lange

2020

IJMS

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“…underlying mechanism involves excessive oxidative damage, ATP depletion and energy imbalance, calcium homeostasis and other factors. A number of studies have elucidated the effects of ameliorating ERS on the prognosis of MIRI in animal models and in vitro cell models (11)(12)(13). Furthermore, numerous signaling pathways, such as the miR-34a/sirtuin 1/nuclear factor erythroid 2-related factor 2 (Nrf2) (14), AMP-activated protein kinase/Nrf2 (15), PI3K/AKT (16) and Toll-like receptor 4/myeloid differentiation factor 88/NF-κB pathways (17), have been demonstrated to mediate ERS.…”

Section: Dexmedetomidine At a Dose Of 1 µM Attenuates H9c2 Cardiomyocmentioning

confidence: 99%

Dexmedetomidine at a dose of 1 µM attenuates H9c2 cardiomyocyte injury under 3 h of hypoxia exposure and 3 h of reoxygenation through the inhibition of endoplasmic reticulum stress

et al. 2020

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Myocardial ischemia-reperfusion injury (MIRI) has been confirmed to induce endoplasmic reticulum stress (ERS) during downstream cascade reactions after the sufficient deterioration of cardiomyocyte function. However, clinically outcomes have been inconsistent with experimental findings because the mechanism has not been entirely elucidated. Dexmedetomidine (DEX), an α 2 adrenergic receptor agonist with anti-inflammatory and organ-protective activity, has been shown to attenuate IRI in the heart. The present study aimed to determine whether DEX is able to protect injured cardiomyocytes under in vitro hypoxia/reoxygenation (H/R) conditions and evaluate the conditions under which ERS is efficiently ameliorated. The cytotoxicity of DEX in H9c2 cells was evaluated 24 h after treatment with several different concentrations of DEX. The most appropriate H/R model parameters were determined by the assessment of cell viability and injury with Cell Counting Kit-8 and lactate dehydrogenase (LDH) release assays after incubation under hypoxic conditions for 3 h and reoxygenation conditions for 3, 6, 12 and 24 h. Additionally, the aforementioned methods were used to assess cardiomyocytes cultured with various concentrations of DEX under H/R conditions. Furthermore, the degree of apoptosis and the mRNA and protein expression levels of glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP) and caspase-12 were evaluated in all groups. The addition of 1, 5 and 10 µM DEX to the cell culture significantly increased the proliferation of H9c2 cells by >80% under normal culture conditions. In the H/R model assessment, following 3 h of anoxia exposure, H9c2 cell viability decreased to 62.67% with 3 h of reoxygenation and to 36% with 6 h of reoxygenation compared with the control. The viability of H9c2 cells subjected to hypoxia for 3 h and reoxygenation for 3 h increased by 61.3% when pretreated with 1 µM DEX, and the LDH concentration in the supernatant was effectively decreased by 13.7%. H/R significantly increased the percentage of apoptotic cells, as detected by flow cytometry, and increased the expression levels of GRP78, CHOP and caspase-12, while treatment with either DEX or 4-phenylbutyric acid (4-PBA) significantly attenuated these effects. Additionally, despite the protective effect of DEX against H/R injury, 4-PBA attenuated the changes induced by DEX and H/R. In conclusion, treatment with 1 µM DEX alleviated cell injury, apoptosis and the increases in GRP78, CHOP and caspase-12 expression levels in H9c2 cells induced by 3 h of hypoxia and 3 h of reoxygenation.

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“…However, re-establishing blood to ischemic areas yields additional myocardial damage including inflammation, apoptosis and autophagy, which is known as myocardial ischemia/reperfusion (I/R) injury (MIRI) (1)(2)(3). The pathophysiological mechanism of MIRI is complex and numerous studies have confirmed that endoplasmic reticulum (ER) stress (ERS)-induced apoptosis serves important roles in the progression of MIRI (4,5). Conventionally, the ER is indispensable for the biosynthesis, folding, processing, excretion and transportation of proteins (4,5).…”

Section: Introductionmentioning

confidence: 99%

“…The pathophysiological mechanism of MIRI is complex and numerous studies have confirmed that endoplasmic reticulum (ER) stress (ERS)-induced apoptosis serves important roles in the progression of MIRI (4,5). Conventionally, the ER is indispensable for the biosynthesis, folding, processing, excretion and transportation of proteins (4,5). However, the disruption of ER homeostasis caused by MIRI, which is referred to as ERS, leads to inaccurate synthesis and assembly of proteins (4,5).…”

Section: Introductionmentioning

confidence: 99%

PHLDA3 inhibition attenuates endoplasmic reticulum stress‑induced apoptosis in myocardial hypoxia/reoxygenation injury by activating the PI3K/AKT signaling pathway

Chen

et al. 2021

Exp Ther Med

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Protective effect of FBXL10 in myocardial ischemia reperfusion injury via inhibiting endoplasmic reticulum stress

Cited by 16 publications

References 21 publications

The Role of Cullin-RING Ligases in Striated Muscle Development, Function, and Disease

The Role of Cullin-RING Ligases in Striated Muscle Development, Function, and Disease

Dexmedetomidine at a dose of 1 µM attenuates H9c2 cardiomyocyte injury under 3 h of hypoxia exposure and 3 h of reoxygenation through the inhibition of endoplasmic reticulum stress

PHLDA3 inhibition attenuates endoplasmic reticulum stress‑induced apoptosis in myocardial hypoxia/reoxygenation injury by activating the PI3K/AKT signaling pathway

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