Effects of interleukin-6 and IL-6/AMPK signaling pathway on mitochondrial biogenesis and astrocytes viability under experimental septic condition

Chen, Xiaolan; Wang, Yan; Peng, Wanwan; Zheng, Yijun; Zhang, Tiannan; Wang, Ping-Jun; Huang, Jinda; Zeng, Qing

doi:10.1016/j.intimp.2018.04.020

Cited by 31 publications

(17 citation statements)

References 39 publications

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“…Notably, we predicted that the target mRNAs of these confirmed circRNAs may regulate various biological processes, cellular components and molecular functions, suggesting the functional roles of these circRNAs in pathophysiologic processes. Lastly, target mRNAs were revealed to participate in multiple cell signaling pathways of metabolism, including the AMPK signaling pathway and peroxisome activity, which play a pivotal role in the regulation of cell energy homeostasis, significantly affecting cell survival, death, differentiation, proliferation, and inflammation (Chen et al, 2018b; Di Cara et al, 2018). Taken together, the observations from this study suggest that these altered circRNAs are extensively involved in pathophysiologic processes after traumatic SCI.…”

Section: Discussionmentioning

confidence: 99%

Circular RNA Expression Alteration and Bioinformatics Analysis in Rats After Traumatic Spinal Cord Injury

Qin

Liu

Yang

et al. 2019

Front. Mol. Neurosci.

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Spinal cord injury (SCI) is mostly caused by trauma. As primary mechanical injury is unavoidable in SCI, a focus on the pathophysiology and underlying molecular mechanisms of SCI-induced secondary injury is necessary to develop promising treatments for SCI patients. Circular RNAs (circRNAs) are associated with various diseases. Nevertheless, studies to date have not yet determined the functional roles of circRNAs in traumatic SCI. We examined circRNA expression profiles in the contused spinal cords of rats using microarray and quantitative reverse transcription-PCR (qRT-PCR) then predict their potential roles in post-SCI pathophysiology with bioinformatics. We found a total of 1676 differentially expressed circRNAs (fold change ≥ 2.0; P < 0.05) in spinal cord 3 days after contusion using circRNA microarray; 1261 circRNAs were significantly downregulated, whereas the remaining 415 were significantly upregulated. Then, five selected circRNAs, namely, rno_circRNA_005342, rno_circRNA_015513, rno_circRNA_002948, rno_circRNA_006096, and rno_circRNA_013017 were all significantly downregulated in the SCI group after verification by qRT-PCR, demonstrating a similar expression pattern in both microarray and PCR data. The next section of the study was concerned with the prediction of circRNA/miRNA/mRNA interactions using bioinformatics analysis. In the final part of the study, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes analyses indicated carbohydrate metabolic process was one of the most significant enrichments and meaningful terms after GO analysis, and the top two signaling pathways affected by the circRNAs-miRNAs axes were the AMP-activated protein kinase signaling pathway and the peroxisome related pathway. In summary, this study showed an altered circRNA expression pattern that may be involved in physiological and pathological processes in rats after traumatic SCI, providing deep insights into numerous possibilities for SCI treatment targets by regulating circRNAs.

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Section: Discussionmentioning

confidence: 99%

Circular RNA Expression Alteration and Bioinformatics Analysis in Rats After Traumatic Spinal Cord Injury

Qin

Liu

Yang

et al. 2019

Front. Mol. Neurosci.

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“…Our group has reported the mechanisms of sepsis-induced mitochondrial dysfunction in various organs; these mechanisms are gradually assuming an important role in sepsis research and its potential treatment (6,19–21). To establish the mechanisms underlying the sepsis-induced brain inflammatory process, we have observed numerous cellular and molecular changes that, with time and increased understanding, broaden the list of new molecules that may contribute to the pathological state of the disease.…”

Section: Discussionmentioning

confidence: 99%

“…Neonatal rat cerebral cortical astrocytes were prepared using enzymatic dissociation and culture from 1-day-old newborn Sprague-Dawley rat brains from animals obtained from the Laboratory Animal Center of Southern Medical University (Guangzhou, China) according to a protocol described previously (6). This study was approval by the Nanfang Hospital Ethics Committee (NFYY-2017-39).…”

Section: Methodsmentioning

confidence: 99%

“…Many studies of both septic patients and animal models have concluded that mitochondrial disruption appears to be related to the progression and outcome of sepsis (4,5). A previous study (6) demonstrated that elements of mitochondrial disorder are conducive to SAE, including increases in reactive oxygen species (ROS), and mitochondrial biogenesis, generation of cellular ATP and reduction in the mitochondrial membrane potential (MMP or ΔΨm). Astrocytes account for 90% of the total brain cells and play an important role in the pathophysiology of the central nervous system (CNS) (7).…”

Section: Introductionmentioning

confidence: 99%

“…Inflammatory signaling activation is an important mechanism leading to increased ROS production and mitochondrial dysfunction (14). In experimental sepsis, after co-stimulation with LPS and interferon (IFN)-γ, a potent inflammatory state and significant mitochondrial damage can be observed (6,15). UCP2 is considered an important neuroprotective element in many inflammatory and degenerative states of the CNS (16).…”

Section: Introductionmentioning

confidence: 99%

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UCP2 silencing aggravates mitochondrial dysfunction in astrocytes under septic conditions

et al. 2019

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Uncoupling protein 2 (UCP2) plays a positive role in sepsis. However, the role of UCP2 in experimental sepsis in astrocytes remains unknown. The present study was designed to determine whether UCP2 has a protective effect in an experimental sepsis model in astrocytes asnd to clarify the mechanisms responsible for its neuroprotective effects after sepsis. An experimental astrocyte model mimicking sepsis-induced brain injury was established using lipopolysaccharide (LPS) and interferon (IFN)-γ. Additionally, UCP2 knockdown in astrocytes was achieved by adenovirus transfection. Tumor necrosis factor (TNF)-α and interleukin (IL)-1β activity, mitochondrial membrane potential (MMP) and reactive oxygen species (ROS), and adenosine triphosphate (ATP) levels were assessed. The mitochondrial ultrastructure was evaluated, and the expression of UCP2 was determined by western blotting. LPS with IFN-γ co-stimulation increased the mRNA and protein expression levels of UCP2 in astrocytes, damaged the mitochondrial structure, and accelerated the release of TNF-α and IL-1β, resulting in a decrease in the MMP, and the excessive generation of ROS. Moreover, sepsis also caused a reduction in ATP production. The knockdown of UCP2 exacerbated astrocyte injury and mitochondrial impairment. In conclusion, both the function and morphology of mitochondria were damaged in an experimental model of sepsis in astrocytes, and knockdown of UCP2 using shRNA exacerbated this impairment, suggesting that UCP2 has a positive effect on astrocytes as determined in an experimental sepsis model.

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Myokines: A central point in managing redox homeostasis and quality of life

Rathor,

Suryakumar

2024

BioFactors

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Redox homeostasis is a crucial phenomenon that is obligatory for maintaining the healthy status of cells. However, the loss of redox homeostasis may lead to numerous diseases that ultimately result in a compromised quality of life. Skeletal muscle is an endocrine organ that secretes hundreds of myokines. Myokines are peptides and cytokines produced and released by muscle fibers. Skeletal muscle secreted myokines act as a robust modulator for regulating cellular metabolism and redox homeostasis which play a prime role in managing and improving metabolic function in multiple organs. Further, the secretory myokines maintain redox homeostasis not only in muscles but also in other organs of the body via stabilizing oxidants and antioxidant levels. Myokines are also engaged in maintaining mitochondrial dynamics as mitochondria is a central point for the generation of reactive oxygen species (ROS). Ergo, myokines also act as a central player in communicating signals to other organs, including the pancreas, gut, liver, bone, adipose tissue, brain, and skin via their autocrine, paracrine, or endocrine effects. The present review provides a comprehensive overview of skeletal muscle‐secreted myokines in managing redox homeostasis and quality of life. Additionally, probable strategies will be discussed that provide a solution for a better quality of life.

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Effects of interleukin-6 and IL-6/AMPK signaling pathway on mitochondrial biogenesis and astrocytes viability under experimental septic condition

Cited by 31 publications

References 39 publications

Circular RNA Expression Alteration and Bioinformatics Analysis in Rats After Traumatic Spinal Cord Injury

Circular RNA Expression Alteration and Bioinformatics Analysis in Rats After Traumatic Spinal Cord Injury

UCP2 silencing aggravates mitochondrial dysfunction in astrocytes under septic conditions

Myokines: A central point in managing redox homeostasis and quality of life

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