Author Correction: Therapeutic potential of KLF2-induced exosomal microRNAs in pulmonary hypertension

Sindi, Hebah A.; Russomanno, Giusy; Satta, Sandro; Abdul-Salam, Vahitha B.; Jo, Kyeong Beom; Qazi-Chaudhry, Basma; Ainscough, Alexander J.; Szulcek, Robert; Bogaard, Harm Jan; Morgan, Claire C.; Pullamsetti, Soni Savai; Alzaydi, Mai M.; Rhodes, Christopher J.; Piva, Roberto; Eichstaedt, Christina A.; Grünig, Ekkehard; Wilkins, Martin R.; Wójciak-Stothard, Beata

doi:10.1038/s41467-020-17273-7

Cited by 4 publications

(4 citation statements)

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“…Cardiovascular health and protection. Some studies have suggested that exosomes have cardioprotective effects (Liao et al, 2021;Ren et al, 2020;Sindi et al, 2020;Weber et al, 2021;Zamani et al, 2019; Table 1). Recent findings suggested that exosomes derived from induced pluripotent stem cells (iPSCs) can transfer cardioprotective miRNAs to cardiomyocytes.…”

Section: J Physiol 60122mentioning

confidence: 99%

“…Promising data regarding the therapeutic use of native exosomes come from MSCs, which have been shown to be protective in cardiovascular diseases, including pulmonary arterial hypertension (Zhang et al., 2020), aneurysm (Yang et al., 2021), chronic heart failure (Wang et al., 2021) and kidney disease (Eirin & Lerman, 2021). Mechanisms are mainly mediated by transferring protective miRNAs, including miR‐144‐5p (Yang et al., 2021), miR‐1246 (Wang et al., 2021), miR‐181‐5p and miR‐324‐5p (Sindi et al., 2020). However, identification of the intracellular targets of these protective miRNAs remains unclear.…”

Section: Introductionmentioning

confidence: 99%

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Exosomes and the cardiovascular system: role in cardiovascular health and disease

Neves

Sevilla-Montero

Montezano

et al. 2022

The Journal of Physiology

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Section: J Physiol 60122mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Exosomes and the cardiovascular system: role in cardiovascular health and disease

Neves

Sevilla-Montero

Montezano

et al. 2022

The Journal of Physiology

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“…So far, no study reported the relation of Glis3 and the BMPR2 gene or any PAH pathway related gene. However, the new PAH gene Krüppel-like transcription factor 2 ( KLF2 ) could indicate a possible relation to this Zinc finger family member and PAH pathogenesis [ 23 , 24 ]. The promoter variant c.-910C>T did not cosegregate with PAH in the family but with a hypertensive PASP during exercise.…”

Section: Discussionmentioning

confidence: 99%

BMPR2 Promoter Variants Effect Gene Expression in Pulmonary Arterial Hypertension Patients

Song

Hinderhofer

Kaufmann

et al. 2020

Genes

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Pathogenic variants have been identified in 85% of heritable pulmonary arterial hypertension (PAH) patients. These variants were mainly located in the bone morphogenetic protein receptor 2 (BMPR2) gene. However, the penetrance of BMPR2 variants was reduced leading to a disease manifestation in only 30% of carriers. In these PAH patients, further modifiers such as additional pathogenic BMPR2 promoter variants could contribute to disease manifestation. Therefore, the aim of this study was to identify BMPR2 promoter variants in PAH patients and to analyze their transcriptional effect on gene expression and disease manifestation. BMPR2 promoter variants were identified in PAH patients and cloned into plasmids. These were transfected into human pulmonary artery smooth muscle cells to determine their respective transcriptional activity. Nine different BMPR2 promoter variants were identified in seven PAH families and three idiopathic PAH patients. Seven of the variants (c.-575A>T, c.-586dupT, c.-910C>T, c.-930_-928dupGGC, c.-933_-928dupGGCGGC, c.-930_-928delGGC and c.-1141C>T) led to a significantly decreased transcriptional activity. This study identified novel BMPR2 promoter variants which may affect BMPR2 gene expression in PAH patients. They could contribute to disease manifestations at least in some families. Further studies are needed to investigate the frequency of BMPR2 promoter variants and their impact on penetrance and disease manifestation.

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“…KLF2 could negatively regulate the expression of inflammatory cytokines and the production of adhesion molecules [ 21 ]. It has recently been discovered to participate in the occurrence and development of various lung diseases, including acute lung injury, asthma, and chronic obstructive pulmonary disease [ 18 , 22 – 25 ]. Lung inflammation induced by lipopolysaccharide (LPS) or influenza A H1N1 virus could lead to reduced KLF2 [ 22 ].…”

Section: Introductionmentioning

confidence: 99%

Simvastatin Inhibits NLRP3 Inflammasome Activation and Ameliorates Lung Injury in Hyperoxia-Induced Bronchopulmonary Dysplasia via the KLF2-Mediated Mechanism

Wang

Huo

Liang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Bronchopulmonary dysplasia (BPD) is a chronic lung disease commonly found in premature infants. Excessive inflammation and oxidative stress contribute to BPD occurrence and development. Simvastatin, as an inhibitor of HMG-CoA reductase, has been reported to have antioxidative and anti-inflammatory effects. However, its effect and possible mechanisms in hyperoxia-induced lung injury are rarely reported. In this study, in vivo and in vitro experiments were conducted to investigate whether simvastatin could ameliorate hyperoxia-induced lung injury and explore its potential mechanism. For the in vivo study, simvastatin could improve alveolar development after hyperoxic lung injury and reduce hyperoxic stress and inflammation. The in vitro study revealed that simvastatin can reduce inflammation in A549 cells after high-oxygen exposure. Simvastatin suppressed NLRP3 inflammasome activation and played anti-inflammatory and antioxidant roles by increasing KLF2 (Krüppel-like factor 2) expression. In vitro experiments also revealed that these effects of simvastatin were partially reversed by KLF2 shRNA, indicating that KLF2 was involved in simvastatin effects. In summary, our findings indicate that simvastatin could downregulate NLRP3 inflammasome activation and attenuate lung injury in hyperoxia-induced bronchopulmonary dysplasia via KLF2-mediated mechanism.

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Author Correction: Therapeutic potential of KLF2-induced exosomal microRNAs in pulmonary hypertension

Abstract: An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Cited by 4 publications

References 0 publications

Exosomes and the cardiovascular system: role in cardiovascular health and disease

Exosomes and the cardiovascular system: role in cardiovascular health and disease

BMPR2 Promoter Variants Effect Gene Expression in Pulmonary Arterial Hypertension Patients

Simvastatin Inhibits NLRP3 Inflammasome Activation and Ameliorates Lung Injury in Hyperoxia-Induced Bronchopulmonary Dysplasia via the KLF2-Mediated Mechanism

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