YAP1-TEAD1 signaling controls angiogenesis and mitochondrial biogenesis through PGC1α

Mammoto, Akiko; Muyleart, Megan; Kadlec, Andrew O.; Gutterman, David D.; Mammoto, Tadanori

doi:10.1016/j.mvr.2018.04.003

Cited by 47 publications

(51 citation statements)

References 88 publications

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“…Besides the VEGF signaling axis, YAP regulates angiogenesis via the peroxisome proliferator-activated receptor gamma co-activator 1-alpha (PGC1α) signaling pathway that controls glucose metabolism within the mitochondria of ECs ( Mammoto et al, 2018 ). Mammoto et al (2018) showed that PGC1α knockdown inhibits YAP-induced EC sprouting in vitro and vascular morphogenesis within fibrin gels subcutaneously implanted into mice, whereas overexpression of PGC1α had the reverse effect. Hence, YAP-TEAD1 signaling induces mitochondrial biogenesis in ECs and stimulates angiogenesis through PGC1α.…”

Section: Modulation Of Stem/progenitor Cell Lineage Fate By Yap/tazmentioning

confidence: 99%

Role of YAP/TAZ in Cell Lineage Fate Determination and Related Signaling Pathways

Heng

Zhang

Aubel

et al. 2020

Front. Cell Dev. Biol.

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The penultimate effectors of the Hippo signaling pathways YAP and TAZ, are transcriptional co-activator proteins that play key roles in many diverse biological processes, ranging from cell proliferation, tumorigenesis, mechanosensing and cell lineage fate determination, to wound healing and regeneration. In this review, we discuss the regulatory mechanisms by which YAP/TAZ control stem/progenitor cell differentiation into the various major lineages that are of interest to tissue engineering and regenerative medicine applications. Of particular interest is the key role of YAP/TAZ in maintaining the delicate balance between quiescence, self-renewal, proliferation and differentiation of endogenous adult stem cells within various tissues/organs during early development, normal homeostasis and regeneration/healing. Finally, we will consider how increasing knowledge of YAP/TAZ signaling might influence the trajectory of future progress in regenerative medicine.

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Section: Modulation Of Stem/progenitor Cell Lineage Fate By Yap/tazmentioning

confidence: 99%

Role of YAP/TAZ in Cell Lineage Fate Determination and Related Signaling Pathways

Heng

Zhang

Aubel

et al. 2020

Front. Cell Dev. Biol.

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“…A luciferase reporter assay revealed binding sites for miR-520d-5 on TEA domain transcription factor 1 (TEAD1) target gene [86]. It has been proven recently that knockdown of TEAD1 decreases the expression of PGC1α and suppresses mitochondrial biogenesis, glycolysis, and oxygen consumption in endothelial cells [87]. Reducing the number of active mitochondria and slowing down the rate of mitochondrial oxidation as a result of down-regulation of TEAD1 and PGC1-α may contribute to disturbed fatty acid catabolism, and consequently to the development of fatty liver in high GIP patients.…”

Section: Discussionmentioning

confidence: 99%

Enhanced GIP Secretion in Obesity Is Associated with Biochemical Alteration and miRNA Contribution to the Development of Liver Steatosis

et al. 2020

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Nutrient excess enhances glucose-dependent insulinotropic polypeptide (GIP) secretion, which may in turn contribute to the development of liver steatosis. We hypothesized that elevated GIP levels in obesity may affect markers of liver injury through microRNAs. The study involved 128 subjects (body mass index (BMI) 25–40). Fasting and postprandial GIP, glucose, insulin, and lipids, as well as fasting alanine aminotransferase (ALT), γ-glutamyltransferase (GGT), cytokeratin-18, fibroblast growth factor (FGF)-19, and FGF-21 were determined. TaqMan low density array was used for quantitative analysis of blood microRNAs. Fasting GIP was associated with ALT [β = 0.16 (confidence interval (CI): 0.01–0.32)], triglycerides [β = 0.21 (95% CI: 0.06–0.36], and FGF-21 [β = 0.20 (95%CI: 0.03–0.37)]; and postprandial GIP with GGT [β = 0.17 (95%CI: 0.03–0.32)]. The odds ratio for elevated fatty liver index (>73%) was 2.42 (95%CI: 1.02–5.72) for high GIP versus low GIP patients. The miRNAs profile related to a high GIP plasma level included upregulated miR-136-5p, miR-320a, miR-483-5p, miR-520d-5p, miR-520b, miR-30e-3p, and miR-571. Analysis of the interactions of these microRNAs with gene expression pathways suggests their potential contribution to the regulation of the activity of genes associated with insulin resistance, fatty acids metabolism, and adipocytokines signaling. Exaggerated fasting and postprandial secretion of GIP in obesity are associated with elevated liver damage markers as well as FGF-21 plasma levels. Differentially expressed microRNAs suggest additional, epigenetic factors contributing to the gut–liver cross-talk.

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“…Appropriate physical properties of lung tissue are necessary for physiological postnatal lung development and LRP5 signaling mediates ECM structure-dependent angiogenesis and alveolar morphogenesis in the neonatal mouse lung [17]. Other mechanosensitive transcription factors and co-activators (e.g., TFII-I, GATA2, Twist1, YAP1) also control angiogenesis [43,48,73,76], and contribute to lung diseases ( e.g., pulmonary fibrosis, pulmonary hypertension) [42,43,77]. Aged fibroblasts produce more collagen and less elastin, leading to increasing pulmonary stiffness and lowering compliance [78].…”

Section: Discussionmentioning

confidence: 99%

LRP5 in age-related changes in vascular and alveolar morphogenesis in the lung

Mammoto

Muyleart

Mammoto

2019

Aging

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Aging is associated with impaired angiogenesis and lung alveolar regeneration, which contributes to the increased susceptibility to chronic lung diseases (CLD). We have reported that the Wnt ligand co-receptor, low-density lipoprotein receptor-related protein 5 (LRP5), stimulates angiogenesis and lung alveolar regeneration. However, the role of LRP5 in age-related decline in vascular and alveolar morphogenesis remains unclear. In this report, we have demonstrated that vascular and alveolar structures are disrupted in the 24-month (24M) old mouse lungs. The expression of LRP5 and the major angiogenic factors, VEGFR2 and Tie2, is lower in endothelial cells (ECs) isolated from 24M old mouse lungs compared to those from 2M old mouse lungs. Vascular and alveolar formation is attenuated in the hydrogel implanted on the 24M old mouse lungs, while overexpression of LRP5, which restores angiogenic factor expression, reverses vascular and alveolar morphogenesis in the gel. Compensatory lung growth after unilateral pneumonectomy is inhibited in 24M old mice, which is reversed by overexpression of LRP5. These results suggest that LRP5 mediates age-related inhibition of angiogenesis and alveolar morphogenesis. Modulation of LRP5 may be a novel intervention to rejuvenate regenerative ability in aged lung and will lead to the development of efficient strategies for aging-associated CLD.

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YAP1-TEAD1 signaling controls angiogenesis and mitochondrial biogenesis through PGC1α

Cited by 47 publications

References 88 publications

Role of YAP/TAZ in Cell Lineage Fate Determination and Related Signaling Pathways

Role of YAP/TAZ in Cell Lineage Fate Determination and Related Signaling Pathways

Enhanced GIP Secretion in Obesity Is Associated with Biochemical Alteration and miRNA Contribution to the Development of Liver Steatosis

LRP5 in age-related changes in vascular and alveolar morphogenesis in the lung

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