FPR1 gene silencing suppresses cardiomyocyte apoptosis and ventricular remodeling in rats with ischemia/reperfusion injury through the inhibition of MAPK signaling pathway

Zhou, Qingling; Teng, Fei; Zhang, Yongshan; Sun, Qiang; Cao, Yong; Meng, Guowei

doi:10.1016/j.yexcr.2018.07.016

Cited by 42 publications

(25 citation statements)

References 47 publications

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“…The role of ERK signaling following IR injury is not yet completely elucidated, but most studies to date show decreased ERK signaling and/or decreased ERK1/2 phosphorylation in the injured tissue to be beneficial for tissue survival and regeneration [38][39][40][41][42][43] and ERK signaling has also been implicated in fibrotic diseases. 36,37,[65][66][67] In order to investigate the role of ERK signaling in IR injury, we analyzed the IR + ctx single-cell data set to characterize Erk1 and Erk2 gene expression in uninjured and injured skeletal muscle without treatment interventions.…”

Section: Treatment With Hcq Inhibited Erk1/2 Phosphorylation After mentioning

confidence: 99%

“…37 Furthermore, inhibition of Mapk genes and decreased phosphorylation of ERK1/2 have protective effects in multiple organ systems by decreasing apoptosis and increasing cellular turnover. [38][39][40][41][42][43] In contrast, contradicting reports have shown increased activation of the same ERK pathways provide protection. [44][45][46] These differences suggest ERK signaling may vary depending on pathologic state/condition, thus the precise role in IR injury remains to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

“…Studies have shown inhibition of ERK1/2 signaling has been shown to attenuate fibrosis by minimizing extracellular matrix deposition in several mouse models, including hepatic IR injury 36 and kidney fibrosis 37 . Furthermore, inhibition of Mapk genes and decreased phosphorylation of ERK1/2 have protective effects in multiple organ systems by decreasing apoptosis and increasing cellular turnover 38‐43 . In contrast, contradicting reports have shown increased activation of the same ERK pathways provide protection 44‐46 .…”

Section: Introductionmentioning

confidence: 99%

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The role of neutrophil extracellular traps and TLR signaling in skeletal muscle ischemia reperfusion injury

et al. 2020

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Ischemia reperfusion (IR) injury results in devastating skeletal muscle fibrosis. Here, we recapitulate this injury with a mouse model of hindlimb IR injury which leads to skeletal muscle fibrosis. Injury resulted in extensive immune infiltration with robust neutrophil extracellular trap (NET) formation in the skeletal muscle, however, direct targeting of NETs via the peptidylarginine deiminase 4 (PAD4) mechanism was insufficient to reduce muscle fibrosis. Circulating levels of IL-10 and TNFα were significantly elevated post injury, indicating toll-like receptor (TLR) signaling may be involved in muscle injury. Administration of hydroxychloroquine (HCQ), a small molecule inhibitor of TLR7/8/9, following injury reduced NET formation, IL-10, and TNFα levels and ultimately mitigated muscle fibrosis and improved myofiber regeneration following IR injury. HCQ treatment decreased fibroadipogenic progenitor cell proliferation and partially inhibited ERK1/2 phosphorylation in the injured tissue, suggesting it may act through a combination of TLR7/8/9 and ERK signaling mechanisms. We demonstrate that treatment with FDA-approved HCQ leads to decreased muscle fibrosis and increased myofiber regeneration following IR injury, suggesting short-term HCQ treatment may be a viable treatment to prevent muscle fibrosis in ischemia reperfusion and traumatic extremity injury.

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Section: Treatment With Hcq Inhibited Erk1/2 Phosphorylation After mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The role of neutrophil extracellular traps and TLR signaling in skeletal muscle ischemia reperfusion injury

et al. 2020

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“…9 Moreover, Fpr1 −/mice subjected to ischemia-reperfusion damage to the heart present reduced inflammation, cardiomyocyte apoptosis and ventricular remodeling, accompanied by the inhibition of the mitogen-activated protein kinases (MAPK) pathway. 10 Similarly, FPR1 plays a negative role in celiac disease, a highly prevalent autoimmune disorder that can be attenuated but not cured by a gluten-free diet. Indeed, FPR1 promotes the proinflammatory migration of neutrophils into the gut following exposure to gliadin (the pathogenic component of gluten).…”

Section: Editorialmentioning

confidence: 99%

The ambiguous role of FPR1 in immunity and inflammation

2020

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“…Myocardial ischemia/reperfusion (I/R) injury is a common cardiovascular disease accompanied with high morbidity and mortality globally, which derives from acute myocardial infarction and coronary artery disease [1,2]. Myocardial I/R injury arises from temporary interruption of blood supply followed by the recovery of perfusion and concomitant reoxygenation, which exacerbates the dysfunction and leads to structural damage [3]. Mounting evidence supported that myocardial I/R is a long-term myocardial injury secondary to the excessive release of inflammatory mediators and formation of reactive oxygen species (ROS), which together contribute to the occurrence and development of myocardial I/R injury [4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Sufentanil attenuates inflammation and oxidative stress in myocardial ischemia reperfusion injury via upregulating Sestrin 2 expression and activating AMPK signalling pathway

Jiang

Zou

et al. 2020

Biotechnology & Biotechnological Equipment

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This study explored whether sufentanil, a lipophilic opioid, can protect against myocardial ischemia-reperfusion (I/R) injury via regulating Sestrin 2 (Sesn2) expression. The expression of Sesn2 was measured in the blood of patients with myocardial I/R after sufentanil administration. H9c2 cells were applied to establish I/R injury by oxygen-glucose deprivation and reoxygenation (OGD/R). After treatment with 5, 10 and 20 lmol/L sufentanil, the expression of Sesn2 was examined. Then, shRNA-Sesn2 was transfected into H9c2 cells. The concentrations of creatine kinase (CK), CK isoenzymes (CK-MB), cardiac troponin I (cTnI), inflammation-related factors and oxidative-related factors were sequentially determined by kits. Western blotting was exploited to determine the expression of AMP-activated protein kinase (AMPK) pathway proteins. The results revealed that the expression of Sesn2 was increased in patients after administration with sufentanil. OGD/R intervention upregulated the expression of Sesn2, which continued to increase in a dose-dependent manner following treatment with sufentanil. Moreover, sufentanil attenuated the concentrations of CK, CK-MB and cTnl induced by OGD/R in H9c2 cells. This effect was reversed after Sesn2 silencing. Meanwhile, the levels of inflammatory factors and oxidative stress were notably decreased when cells were treated with sufentanil, and these inhibitory effects were alleviated after transfection with shRNA-Sesn2. Furthermore, sufentanil enhanced the phosphorylation of AMPK and its downstream acetyl CoA carboxylase (ACC), whereas Sesn2 silencing inhibited the expression of the above proteins. These findings demonstrated that sufentanil could attenuate inflammation and oxidative stress in myocardial I/R injury via upregulating Sesn2 expression and activating the AMPK pathway.

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FPR1 gene silencing suppresses cardiomyocyte apoptosis and ventricular remodeling in rats with ischemia/reperfusion injury through the inhibition of MAPK signaling pathway

Cited by 42 publications

References 47 publications

The role of neutrophil extracellular traps and TLR signaling in skeletal muscle ischemia reperfusion injury

The role of neutrophil extracellular traps and TLR signaling in skeletal muscle ischemia reperfusion injury

The ambiguous role of FPR1 in immunity and inflammation

Sufentanil attenuates inflammation and oxidative stress in myocardial ischemia reperfusion injury via upregulating Sestrin 2 expression and activating AMPK signalling pathway

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