Roles of different mitochondrial electron transport chain complexes in hypoxia‐induced pulmonary vasoconstriction

Yang, Zhao; Zhuan, Bing; Yan, Yan; Jiang, Simin; Wang, Tao

doi:10.1002/cbin.10550

Cited by 6 publications

(3 citation statements)

References 21 publications

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“…Superoxide from complex I is generated within the mitochondrial matrix, where it is converted to peroxide by manganese superoxide dismutase that is expressed in the mitochondria (MnSOD). Recent pharmacological studies in pulmonary arterial myocytes isolated from lung resections of human patients provide important insights into its function (1118). The studies show that complex I as well as II and the Q(0) site of complex III are important to hypoxic pulmonary vasoconstriction.…”

Section: Ros and Association With Hypoxia-induced Diseasementioning

confidence: 99%

Gestational Hypoxia and Developmental Plasticity

Ducsay

Goyal

Pearce

et al. 2018

Physiological Reviews

142

145

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Hypoxia is one of the most common and severe challenges to the maintenance of homeostasis. Oxygen sensing is a property of all tissues, and the response to hypoxia is multidimensional involving complicated intracellular networks concerned with the transduction of hypoxia-induced responses. Of all the stresses to which the fetus and newborn infant are subjected, perhaps the most important and clinically relevant is that of hypoxia. Hypoxia during gestation impacts both the mother and fetal development through interactions with an individual's genetic traits acquired over multiple generations by natural selection and changes in gene expression patterns by altering the epigenetic code. Changes in the epigenome determine "genomic plasticity," i.e., the ability of genes to be differentially expressed according to environmental cues. The genomic plasticity defined by epigenomic mechanisms including DNA methylation, histone modifications, and noncoding RNAs during development is the mechanistic substrate for phenotypic programming that determines physiological response and risk for healthy or deleterious outcomes. This review explores the impact of gestational hypoxia on maternal health and fetal development, and epigenetic mechanisms of developmental plasticity with emphasis on the uteroplacental circulation, heart development, cerebral circulation, pulmonary development, and the hypothalamic-pituitary-adrenal axis and adipose tissue. The complex molecular and epigenetic interactions that may impact an individual's physiology and developmental programming of health and disease later in life are discussed.

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Section: Ros and Association With Hypoxia-induced Diseasementioning

confidence: 99%

Gestational Hypoxia and Developmental Plasticity

Ducsay

Goyal

Pearce

et al. 2018

Physiological Reviews

142

145

View full text Add to dashboard Cite

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“…Pathogenesis of AR and asthma has not yet been completely elucidated owing to the complex influence of environmental and genetic factors, such as immune-inflammatory response, neural, and airway hyperresponsiveness mechanisms [ 8 , 9 ]. Inflammation associated with asthma and AR is thought to be mediated by the involvement of multiple cells and cytokines.…”

Section: Introductionmentioning

confidence: 99%

Bioinformatic Analysis and Cellular Assays Identify Substance P Influencing Th17/Treg Differentiation via the MyD88 Pathway as a Potential Contributor to the Progression of Asthma and Allergic Rhinitis

Liu

et al. 2022

Disease Markers

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Objective. This study is aimed at investigating the role of substance P (SP) in the development of asthma. Methods. The Gene Expression Omnibus (GEO) database was used to characterize SP expression in allergic rhinitis (AR) and asthma. Peripheral blood was collected from patients with asthma or AR. The expression of relevant cytokines and neuropeptides was measured. Enzyme-linked immunosorbent assay (ELISA) was also performed. The mast cell line LAD2 and the lung bronchial epithelial cell line BEAS-2B were treated with different concentrations of SP concentration. Then, the qRT-PCR method was used to determine the mRNA expression. Furthermore, p38 and p65 and their associated phosphorylated proteins (p-p38 and p-p65) were further validated by western blotting. Result. Clinical and GSE75011 data analysis suggested that MyD88 expression was upregulated in AR and asthma. Through the gene set variation analysis (GSVA), MyD88-related pathways were noticed and further investigated. ELISA results suggested that the SP expression was significantly increased in AR and asthma and IL-10 expression was decreased, whereas the expression of IL-6, IL-17A, IL-23, and TGF-β expressions increased. The mast cell line LAD2 was treated with different SP concentrations, and ELISA results showed that the expression of IL-6, IL-17A, IL-23, and TGF-β in the cell supernatant gradually increased with increasing SP concentrations, whereas that of IL-10 decreased. The lung bronchial epithelial cell line BEAS-2B was treated with different SP concentrations, and the expression of myeloid differentiation factor 88 (MyD88) and its related proteins was elevated. The expression of p38 and p-p38 proteins was elevated after SP treatment, and their expression levels elevated as SP concentrations increased. Finally, MyD88 expression at the single-cell level was also demonstrated. Conclusion. SP may affect the cytokine expression through the MyD88 pathway, thereby influencing Th17/Treg differentiation and eventually participating in the pathological process of asthma and AR. There are many pathological similarities between allergic rhinitis (AR) and bronchial asthma. In the present study, SP was found to possibly activate downstream inflammatory signaling pathways via MyD88, thereby affecting Th17/Treg differentiation and ultimately participating in the pathological process of asthma and AR.

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“…TCMK-1 cells were cultured in Forma Series II Water Jacketed CO 2 incubator (ThermoFisher) with 94 % N 2 and 5 % CO 2 to keep 1 % oxygen concentration for hypoxia treatment. After that, cells were transferred to normoxic chamber (21 % O 2, 74 % N 2 , and 5 % CO 2 ) during reoxygenation incubation [ 20 ].…”

Section: Methodsmentioning

confidence: 99%

Long non-coding RNA TUG1 knockdown promotes autophagy and improves acute renal injury in ischemia-reperfusion-treated rats by binding to microRNA-29 to silence PTEN

Xu¹,

Huang²,

Lin³

et al. 2021

BMC Nephrol

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Objective Long noncoding RNA (lncRNA) taurine upregulated gene 1 (TUG1) is increased under the condition of ischemia. This study intended to identify the mechanism of TUG1 in renal ischemia-reperfusion (I/R). Methods First, a rat model of acute renal injury induced by I/R was established, followed by the measurement of blood urea nitrogen (BUN), serum creatine (SCr), methylenedioxyphetamine (MDA) and superoxide dismutase (SOD) in the serum of rats. TUG1 was knocked down in I/R rats (ko-TUG1 group). Next, histological staining was used to evaluate the pathological damage and apoptosis of rat kidney. Western blot analysis was used to detect the levels of apoptosis- and autophagy-related proteins and transmission electron microscope was used to observe autophagosomes. Autophagy and apoptosis were evaluated after inhibition of the autophagy pathway using the inhibitor 3-MA. The targeting relation among TUG1, microRNA (miR)-29 and phosphatase and tensin homolog (PTEN) were validated. Lastly, the effects of TUG1 on biological behaviors of renal tubular cells were evaluated in vitro. Results In vivo, the levels of BUN, SCr and MDA in the serum of I/R-treated rats were increased while SOD level and autophagosomes were reduced, tubule epithelial cells were necrotic, and TUG1 was upregulated in renal tissues of I/R-treated rats, which were all reversed in rats in the ko-TUG1 group. Autophagy inhibition (ko-TUG1 + 3-MA group) averted the protective effect of TUG1 knockdown on I/R-treated rats. TUG1 could competitively bind to miR-29 to promote PTEN expression. In vitro, silencing TUG1 (sh-TUG1 group) promoted viability and autophagy of renal tubular cells and inhibited apoptosis. Conclusions LncRNA TUG can promote PTEN expression by competitively binding to miR-29 to promote autophagy and inhibited apoptosis, thus aggravating acute renal injury in I/R-treated rats.

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Roles of different mitochondrial electron transport chain complexes in hypoxia‐induced pulmonary vasoconstriction

Cited by 6 publications

References 21 publications

Gestational Hypoxia and Developmental Plasticity

Gestational Hypoxia and Developmental Plasticity

Bioinformatic Analysis and Cellular Assays Identify Substance P Influencing Th17/Treg Differentiation via the MyD88 Pathway as a Potential Contributor to the Progression of Asthma and Allergic Rhinitis

Long non-coding RNA TUG1 knockdown promotes autophagy and improves acute renal injury in ischemia-reperfusion-treated rats by binding to microRNA-29 to silence PTEN

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