Bone morphogenetic protein‐7 inhibits endothelial‐mesenchymal transition in pulmonary artery endothelial cell under hypoxia

Zhang, Hongyue; Liu, Ying; Yan, Lei; Du, Wei; Zhang, Xiaodan; Zhang, Min; Chen, He; Zhang, Yafeng; Zhou, Jianqiu; Sun, Hanliang; Zhu, Daling

doi:10.1002/jcp.26195

Cited by 41 publications

(30 citation statements)

References 42 publications

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“…PASMCs and PAECs were cultured in Dulbecco's modified Eagle's medium supplemented with 10% fetal bovine serum (FBS) and 20% FBS for 48h, respectively [32,53]. The cells were incubated in a 37°C, 21% O 2 or 1% O 2 -5% CO 2 humidified incubator.…”

Section: Isolation and Hypoxia-treatment Of Pasmcs And Paecsmentioning

confidence: 99%

Transcriptome-wide map of m6A circRNAs identified in a rat model of hypoxia mediated pulmonary hypertension

Wang

et al. 2020

Preprint

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Background: Hypoxia mediated pulmonary hypertension (HPH) is a lethal disease and lacks effective therapy. CircRNAs play significant roles in physiological process. Recently, circRNAs are found to be m 6 A-modified. The abundance of circRNAs was influenced by m 6 A. Furthermore, the significance of m 6 A circRNAs has not been elucidated in HPH yet. Here we aim to investigate the transcriptome-wide map of m 6 A circRNAs in HPH. Results: Differentially expressed m 6 A abundance was detected in lungs of HPH rats. M 6 A abundance in circRNAs was significantly reduced in hypoxia in vitro . M 6 A circRNAs were mainly from protein-coding genes spanned single exons in control and HPH groups. Moreover, m 6 A influenced the circRNA–miRNA–mRNA co-expression network in hypoxia. M 6 A circXpo6 and m 6 A circTmtc3 were firstly identified to be downregulated in HPH. Conclusion: Our study firstly identified the transcriptome-wide map of m 6 A circRNAs in HPH. M 6 A can influence circRNA–miRNA–mRNA network. Furthermore, we firstly identified two HPH-associated m 6 A circRNAs: circXpo6 and circTmtc3. However, the clinical significance of m 6 A circRNAs for HPH should be further validated. Key words: m 6 A circRNAs; hypoxia mediated pulmonary hypertension; m 6 A circXpo6; m 6 A circTmtc3

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Section: Isolation and Hypoxia-treatment Of Pasmcs And Paecsmentioning

confidence: 99%

Transcriptome-wide map of m6A circRNAs identified in a rat model of hypoxia mediated pulmonary hypertension

Wang

et al. 2020

Preprint

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“…TGF-β1, TGF-β2, and bone morphogenetic proteins are also well-known to cause EndMT 5,6 . Several groups have reported on signaling systems and molecules that induce EndMT, including Wnt/β-catenin 7 and Notch signaling 8 , as well as hypoxia 9 and oxidative stress 10 . These signaling pathways are related to transcription factors involved in mesenchymal transition, such as Snail, Slug, ZEB1, and ZEB2 11,12 .…”

Section: Introductionmentioning

confidence: 99%

Endothelial-to-mesenchymal transition in anticancer therapy and normal tissue damage

et al. 2020

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Endothelial-to-mesenchymal transition (EndMT) involves the phenotypic conversion of endothelial-to-mesenchymal cells, and was first discovered in association with embryonic heart development. EndMT can regulate various processes, such as tissue fibrosis and cancer. Recent findings have shown that EndMT is related to resistance to cancer therapy, such as chemotherapy, antiangiogenic therapy, and radiation therapy. Based on the known effects of EndMT on the cardiac toxicity of anticancer therapy and tissue damage of radiation therapy, we propose that EndMT can be targeted as a strategy for overcoming tumor resistance while reducing complications, such as tissue damage. In this review, we discuss EndMT and its roles in damaging cardiac and lung tissues, as well as EndMT-related effects on tumor vasculature and resistance in anticancer therapy. Modulating EndMT in radioresistant tumors and radiationinduced tissue fibrosis can especially increase the efficacy of radiation therapy. In addition, we review the role of hypoxia and reactive oxygen species as the main stimulating factors of tissue damage due to vascular damage and EndMT. We consider drugs that may be clinically useful for regulating EndMT in various diseases. Finally, we argue the importance of EndMT as a therapeutic target in anticancer therapy for reducing tissue damage.

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“…The lysates were sonicated, centrifuged at 13, 500 g at 4ºC for 15 min, the insoluble fraction was discarded and the supernatants were collected and used in the western blot assays. The protein concentration was determined by bicinchoninic acid assay and 10 µL aliquots containing 20 μg total cell proteins were separated by 10% sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and then transferred to nitrocellulose membranes as previously described [22]. The membranes were blocked at room temperature for 2 h in TBST and 0.1% Tween 20 containing 5% nonfat dry milk.…”

Section: Western Blot Assaymentioning

confidence: 99%

Galangin Alleviates Liver Ischemia-Reperfusion Injury in a Rat Model by Mediating the PI3K/AKT Pathway

Li¹,

Tong²,

Zhang³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Liver ischemia-reperfusion (I/R) injury is a pathological process that often occurs during liver and trauma surgery. There are numerous causes of liver I/R injury, but the mechanism is unknown. Galangin (GA) is a flavonoid, a polyphenolic compound widely distributed in medicinal herbs that has anti-inflammatory, antioxidant, and antitumor activity. This study evaluated the protective effect of GA on hepatic I/R injury. Methods: An I/R model was created in male Wistar rats by clamping the hepatoportal vein, hepatic artery and hepatic duct for 30 min followed by reperfusion for 2 h. A hypoxia/restoration (H/R) model was established in buffalo rat liver (BRL) cells by hypoxia for 4 h followed by normoxic conditions for 10 h. The extent of liver injury was assayed by serum ALT/AST, hepatic histology, and MPO activity. Oxidative stress was assayed by serum superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and malondialdehyde (MDA). Expression of apoptosis-related proteins in BRL cells was assayed in western blots. Expression of AKT and p-AKT proteins in vivo and vitro were assayed in western blots. Results: GA significantly decreased ALT/AST expression, reversed changes in oxidative stress markers induced by I/R, and mediated caspase-3 activity expression of apoptosis-related proteins in vivo and in vitro. Methylthiazol tetrazolium (MTT) assay, flow cytometry, and Hoechst 33258 staining confirmed that GA inhibited apoptosis of BRL cells. GA also increased the expression of phosphorylated AKT after H/R. Conclusion: GA reduced liver I/R injury both in vivo and vitro and inhibited BRL cell apoptosis. PI3K/AKT signaling have been involved. GA may protect against liver I/R and be a potential therapeutic candidate.

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Bone morphogenetic protein‐7 inhibits endothelial‐mesenchymal transition in pulmonary artery endothelial cell under hypoxia

Cited by 41 publications

References 42 publications

Transcriptome-wide map of m6A circRNAs identified in a rat model of hypoxia mediated pulmonary hypertension

Transcriptome-wide map of m6A circRNAs identified in a rat model of hypoxia mediated pulmonary hypertension

Endothelial-to-mesenchymal transition in anticancer therapy and normal tissue damage

Galangin Alleviates Liver Ischemia-Reperfusion Injury in a Rat Model by Mediating the PI3K/AKT Pathway

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