The YAP signaling pathway promotes the progression of lymphatic malformations through the activation of lymphatic endothelial cells

Zhong, Wenqun; Jiang, Hao; Zou, Yanping; Ren, Jian‐Gang; Li, Zhizheng; He, Kefei; Zhao, Jianhua; Zhou, Xiaoshun; Mou, Dongsheng; Cai, Yu

doi:10.1038/s41390-020-0863-0

Cited by 7 publications

(11 citation statements)

References 40 publications

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“…The inactivation of Hippo pathway promotes YAP translocation to the nucleus ( 40 ). After entering the nucleus, YAP interacts with TEA domain transcription factors to activate the transcription of target genes and promote chondrocyte differentiation ( 18 ). Silencing SETD7 using a lentiviral vector system demonstrated that SETD7 prevented YAP from entering the nucleus and inhibited the chondrogenic differentiation ability of ATDC5 cells.…”

Section: Discussionmentioning

confidence: 99%

“…When Hippo signaling is activated, a series of phosphorylation events occur via mammalian STE20-like T cells (MST) and the linker for activation of T cells (LAT) kinases, ultimately leading to phosphorylation of Yes-associated Protein (YAP) ( 17 ). Phosphorylated (p-)YAP is sequestered in the cytoplasm, which decreases transcription of downstream genes in the nucleus ( 18 ). By contrast, inactivation of the Hippo pathway increases nuclear translocation of YAP, where YAP interacts with other transcription factors, such as tafazzin ( 19 ), to activate the transcription of target genes ( 18 ).…”

Section: Introductionmentioning

confidence: 99%

“…Phosphorylated (p-)YAP is sequestered in the cytoplasm, which decreases transcription of downstream genes in the nucleus ( 18 ). By contrast, inactivation of the Hippo pathway increases nuclear translocation of YAP, where YAP interacts with other transcription factors, such as tafazzin ( 19 ), to activate the transcription of target genes ( 18 ). Recently, YAP was found to be associated with chondrocyte differentiation.…”

Section: Introductionmentioning

confidence: 99%

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SETD7 regulates chondrocyte differentiation and glycolysis via the Hippo signaling pathway and HIF‑1α

Ning

Wang

et al. 2021

Int J Mol Med

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Chondrocytes are well adapted to hypoxia and produce more functional extracellular matrix in low oxygen environments in vitro . In our previous study, methyltransferase SET domain containing (SETD)7 regulated chondrocyte activity in hypoxic conditions. However, the precise association between SETD7 and chondrocyte differentiation under low oxygen partial pressure remains unclear. The association between SETD7 and chondrocyte differentiation was studied by silencing SETD7 in chondrocytes in vitro . The results showed that the silencing of SETD7 in ATDC5 cells inhibited the Hippo signaling pathway, decreased Yes-associated protein (YAP) phosphorylation and increased the levels of YAP and hypoxia inducible factor-1α (HIF-1α) in the nucleus. YAP combined with HIF-1α to form a complex that promoted the expression of genes involved in chondrogenic differentiation and the glycolytic pathway. Thus, SETD7 inhibited chondrocyte differentiation and glycolysis via the Hippo signaling pathway. The present study demonstrated that SETD7 was a potential molecular target that maintained the chondrocyte phenotype during cartilage tissue engineering and cartilage-associated disease.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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SETD7 regulates chondrocyte differentiation and glycolysis via the Hippo signaling pathway and HIF‑1α

Ning

Wang

et al. 2021

Int J Mol Med

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“…It has previously been reported that TAK1 could be participated in multiple inflammations [18,19]. On the other hand, YAP and TAZ proteins have been confirmed to be transcriptional coactivators encoded by paralogous genes, which shuttle between the cytoplasm and the nucleus in response to multiple inputs [20]. In addition, YAP/TAZ has been confirmed to be a promoter during the activation of fibroblasts [21].…”

Section: Introductionmentioning

confidence: 94%

LncRNA TUG1 exhibits pro-fibrosis activity in hypertrophic scar through TAK1/YAP/TAZ pathway via miR-27b-3p

Chen

et al. 2021

Mol Cell Biochem

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Hypertrophic Scar (HS) is a complicated fibrotic disease. In addition, its pathogenesis is still to be further explored. Long non-coding RNAs (lncRNAs) have been proved to be participated in multiple diseases, including HS. However, the role of lncRNA TUG1 in HS remains unclear. The expression level of RNA and protein in cells were detected by q-PCR and western blot, respectively. MTT assay was performed to test the cell proliferation. Cell migration was detected by transwell assay. Cell apoptosis was measured by flow cytometry. Dual luciferase report assay and RNA pull down were used to verify the relationship between TUG1, miR-27b-3p and TAK1.TUG1 and TAK1 were upregulated in HS, while miR-27b-3p was downregulated. Knockdown of TUG1 significantly suppressed the proliferation and migration and induced the apoptosis of HS fibroblasts (HSF). In addition, silencing of TUG1 notably inhibited the extracellular matrix (ECM) biosynthesis in HSF. Overexpression of miR-27b-3p has the same effect on HS as that of TUG1 knockdown. Meanwhile, TUG1 could sponge miR-27b-3p, and TAK1 was the direct target of miR-27b-3p. Furthermore, knockdown of TUG1 significantly suppressed the fibrosis in HS via miR-27b-3p/TAK1/YAP/TAZ axis mediation. LncRNA TUG1 promotes the fibrosis in HS via sponging miR-27b-3p and then activates TAK1/YAP/TAZ pathway, which may serve as a potential target for treatment of HS.

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“…Human dermal lymphatic endothelial cells (HDLECs) (catalog number 2010; ScienCell, Carlsbad, CA) and human umbilical vein endothelial cells (HUVECs) were cultured according to a previous study. 10,11 Glucose Uptake, Lactate, and ATP Production After treatment for 24 hours, lactate in the culture media, intracellular glucose, and ATP were measured using the Lactic Acid Assay Kit (catalog number A019-2-1; Nanjing Jiancheng Bioengineering Institute, Nanjing, China), Glucose Uptake Cell-Based Assay Kit (catalog number 600470; Cayman Chemical, Ann Arbor, MI), and the ATP Assay Kit (catalog number A095-1-1; Nanjing Jiancheng Bioengineering Institute), respectively, according to the manufacturers' instructions.…”

Section: Cell Culturementioning

confidence: 99%

Pyruvate Kinase M2 Mediates Glycolysis in the Lymphatic Endothelial Cells and Promotes the Progression of Lymphatic Malformations

Jiang

Zou

Zhao

et al. 2021

The American Journal of Pathology

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The YAP signaling pathway promotes the progression of lymphatic malformations through the activation of lymphatic endothelial cells

Cited by 7 publications

References 40 publications

SETD7 regulates chondrocyte differentiation and glycolysis via the Hippo signaling pathway and HIF‑1α

SETD7 regulates chondrocyte differentiation and glycolysis via the Hippo signaling pathway and HIF‑1α

LncRNA TUG1 exhibits pro-fibrosis activity in hypertrophic scar through TAK1/YAP/TAZ pathway via miR-27b-3p

Pyruvate Kinase M2 Mediates Glycolysis in the Lymphatic Endothelial Cells and Promotes the Progression of Lymphatic Malformations

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