RETRACTED ARTICLE: Yin Yang 1 (YY1)-induced long intergenic non-protein coding RNA 472 (LINC00472) aggravates sepsis-associated cardiac dysfunction via the micro-RNA-335-3p (miR-335-3p)/Monoamine oxidase A (MAOA) cascade

Mo, Guixi; Mo, Jian; Tan, Xiujuan; Wang, Jingjing; Yan, Zhenyi; Liu, Yijun

doi:10.1080/21655979.2021.2017589

Cited by 8 publications

(7 citation statements)

References 49 publications

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“…MAOA is a mitochondrial enzyme that catalyzes the oxidative deamination of dietary amines and monoamine neurotransmitters, such as serotonin, norepinephrine, and dopamine [ 28 , 29 ]. Recent studies have shown that MAOA is correlated with sepsis-induced cardiac dysfunction [ 30 ]. Neutrophil myeloperoxidase (MPO) is a peroxidase enzyme abundant in neutrophil granulocytes.…”

Section: Discussionmentioning

confidence: 99%

Predicting the prognosis in patients with sepsis by an endoplasmic reticulum stress gene signature

Liu,

Wang,

Xiao

et al. 2023

Aging

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Background: Prognostic stratification of patients with sepsis is important for the development of individualized treatment strategies. Endoplasmic reticulum stress (ERS) plays a key role in sepsis. This study aimed to identify a set of genes related to ER stress to construct a predictive model for the prognosis of sepsis. Methods: The transcriptomic and clinical data of 479 sepsis patients were obtained from GSE65682 and divided into a training set (n=288) and a validation set (n=191) at a ratio of 3:2. The external test set was GSE95233 (n=51). LASSO and Cox regression analyses were performed to establish a signature to predict the prognosis of patients with sepsis. Moreover, we developed a nomogram that included the risk signature and clinical features to predict survival probability. Results: A prognostic signature was constructed with ten endoplasmic reticulum related genes (ADRB2, DHCR7, GABARAPL2, MAOA, MPO, PDZD8, QDPR, SCAP, TFRC, and TLR4) in the training set, which significantly divided patients with sepsis into high- and low-risk groups in terms of survival. This signature was validated using validation and external test sets. A nomogram based on the risk signature was constructed to quantitatively predict the prognosis of patients with sepsis. Conclusions: We constructed an ERS signature as a novel prognostic marker for predicting survival in sepsis patients, which could be used to develop novel biomarkers for the diagnosis, treatment, and prognosis of sepsis and to provide new ideas and prospects for future clinical research.

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Section: Discussionmentioning

confidence: 99%

Predicting the prognosis in patients with sepsis by an endoplasmic reticulum stress gene signature

Liu,

Wang,

Xiao

et al. 2023

Aging

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“…RIP assay was performed by using the Magna RIP RNA binding protein immunoprecipitation kit (Merck Millipore) . RGCs transfected with miR-203-3p or miR-NC were lysed at 4 °C with RIP buffer containing magnetic beads, and lysates were coupled to the anti-Ago2 antibody or IgG antibody as NCs.…”

Section: Methodsmentioning

confidence: 99%

“…RIP assay was performed by using the Magna RIP RNA binding protein immunoprecipitation kit (Merck Millipore). 23 RGCs transfected with miR-203-3p or miR-NC were lysed at 4 °C with RIP buffer containing magnetic beads, and lysates were coupled to the anti-Ago2 antibody or IgG antibody as NCs. Next, the immunoprecipitated RNA was isolated by TRIzol washing, and the expression levels of MIAT and miR-203-3p were tested by RT-qPCR.…”

Section: Genesmentioning

confidence: 99%

Long Noncoding RNA MIAT Modulates Chronic Retinal Ischemia-Reperfusion Injury in Mice via the microRNA-203-3p/SNAI2 Axis

Fu,

Gu,

2023

Chem. Res. Toxicol.

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Retinal ischemia-reperfusion injury (RIRI) is a vital pathological process of multiple ocular diseases. This study aimed at investigating the effects of the MIAT/miR-203-3p/SNAI2 axis on RIRI. RIRI was produced by inducing an exceedingly high intraocular pressure (IOP) in mice. Mouse retinal ganglion cells (RGCs) were subjected to oxygenglucose deprivation/reoxygenation (OGD/R) to mimic in vitro models. Relevant oligonucleotides or plasmids were transfected into OGD/R-induced RGCs in vitro or injected into RIRI mice models in vivo via a vitreous cavity. The findings of our paper indicated that MIAT and SNAI2 were highly expressed and miR-203-3p was lowly expressed in mouse RIRI tissues and OGD/R-induced RGCs. Interfering MIAT promoted the viability of OGD/R-induced RGCs, decreased apoptosis, and reduced oxidative stress in vitro. Silencing MIAT increased retinal neuronal cell numbers and decreased retinal neuronal cell apoptosis in mouse RIRI tissues in vivo. MIAT sponged miR-203-3p, and miR-203-3p targeted and inhibited SNAI2 expression. SNAI2 up-regulation or miR-203-3p down-regulation reversed the protective effects of MIAT down-regulation on RIRI in mice and OGD/R-induced RGCs. MIAT sponges miR-203-3p upregulated the expression of SNAI2, thereby promoting RIRI in mice. In summary, MIAT may be a therapeutic target for the treatment of chronic RIRI.

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“…In AC16 cardiomyocytes, MAO-A mRNA and protein expressions are affected by non-coding RNAs since knockdown of the non-protein coding RNA 472 (LINC00472) reduced MAO-A expression, the results being partly abolished by miR-335-3p inhibition. Thus, LINC00472 positively regulates MAOA expression via interaction with miR-335-3p [ 158 ].…”

Section: Monoamine Oxidases (Mao)mentioning

confidence: 99%

Importance of Mitochondria in Cardiac Pathologies: Focus on Uncoupling Proteins and Monoamine Oxidases

Schulz

Schlüter

2023

IJMS

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On the one hand, reactive oxygen species (ROS) are involved in the onset and progression of a wide array of diseases. On the other hand, these are a part of signaling pathways related to cell metabolism, growth and survival. While ROS are produced at various cellular sites, in cardiomyocytes the largest amount of ROS is generated by mitochondria. Apart from the electron transport chain and various other proteins, uncoupling protein (UCP) and monoamine oxidases (MAO) have been proposed to modify mitochondrial ROS formation. Here, we review the recent information on UCP and MAO in cardiac injuries induced by ischemia-reperfusion (I/R) as well as protection from I/R and heart failure secondary to I/R injury or pressure overload. The current data in the literature suggest that I/R will preferentially upregulate UCP2 in cardiac tissue but not UCP3. Studies addressing the consequences of such induction are currently inconclusive because the precise function of UCP2 in cardiac tissue is not well understood, and tissue- and species-specific aspects complicate the situation. In general, UCP2 may reduce oxidative stress by mild uncoupling and both UCP2 and UCP3 affect substrate utilization in cardiac tissue, thereby modifying post-ischemic remodeling. MAOs are important for the physiological regulation of substrate concentrations. Upon increased expression and or activity of MAOs, however, the increased production of ROS and reactive aldehydes contribute to cardiac alterations such as hypertrophy, inflammation, irreversible cardiomyocyte injury, and failure.

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RETRACTED ARTICLE: Yin Yang 1 (YY1)-induced long intergenic non-protein coding RNA 472 (LINC00472) aggravates sepsis-associated cardiac dysfunction via the micro-RNA-335-3p (miR-335-3p)/Monoamine oxidase A (MAOA) cascade

Cited by 8 publications

References 49 publications

Predicting the prognosis in patients with sepsis by an endoplasmic reticulum stress gene signature

Predicting the prognosis in patients with sepsis by an endoplasmic reticulum stress gene signature

Long Noncoding RNA MIAT Modulates Chronic Retinal Ischemia-Reperfusion Injury in Mice via the microRNA-203-3p/SNAI2 Axis

Importance of Mitochondria in Cardiac Pathologies: Focus on Uncoupling Proteins and Monoamine Oxidases

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