TBX20 Regulates Angiogenesis Through the Prokineticin 2–Prokineticin Receptor 1 Pathway

Meng, Shu; Gu, Qilin; Yang, Xiaojie; Lv, Jie; Owusu, Iris; Matrone, Gianfranco; Chen, Kaifu; Cooke, John P.; Fang, Longhou

doi:10.1161/circulationaha.118.033939

Cited by 33 publications

(32 citation statements)

References 60 publications

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“… 119 – 121 Besides, Tbx20 participated in the signaling cascade of Tbx20-PROK2-PROKR1 and regulated angiogenesis. 122 The above findings provide further mechanistic insights into the link between cardiomyocyte proliferation and cardiac regeneration.…”

Section: Proliferation and Mitosis Of Pre-existing Cardiomyocytesmentioning

confidence: 78%

Regulation of cardiomyocyte fate plasticity: a key strategy for cardiac regeneration

Gong

Jiang

Загидуллин

et al. 2021

Sig Transduct Target Ther

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With the high morbidity and mortality rates, cardiovascular diseases have become one of the most concerning diseases worldwide. The heart of adult mammals can hardly regenerate naturally after injury because adult cardiomyocytes have already exited the cell cycle, which subseqently triggers cardiac remodeling and heart failure. Although a series of pharmacological treatments and surgical methods have been utilized to improve heart functions, they cannot replenish the massive loss of beating cardiomyocytes after injury. Here, we summarize the latest research progress in cardiac regeneration and heart repair through altering cardiomyocyte fate plasticity, which is emerging as an effective strategy to compensate for the loss of functional cardiomyocytes and improve the impaired heart functions. First, residual cardiomyocytes in damaged hearts re-enter the cell cycle to acquire the proliferative capacity by the modifications of cell cycle-related genes or regulation of growth-related signals. Additionally, non-cardiomyocytes such as cardiac fibroblasts, were shown to be reprogrammed into cardiomyocytes and thus favor the repair of damaged hearts. Moreover, pluripotent stem cells have been shown to transform into cardiomyocytes to promote heart healing after myocardial infarction (MI). Furthermore, in vitro and in vivo studies demonstrated that environmental oxygen, energy metabolism, extracellular factors, nerves, non-coding RNAs, etc. play the key regulatory functions in cardiac regeneration. These findings provide the theoretical basis of targeting cellular fate plasticity to induce cardiomyocyte proliferation or formation, and also provide the clues for stimulating heart repair after injury.

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Section: Proliferation and Mitosis Of Pre-existing Cardiomyocytesmentioning

confidence: 78%

Regulation of cardiomyocyte fate plasticity: a key strategy for cardiac regeneration

Gong

Jiang

Загидуллин

et al. 2021

Sig Transduct Target Ther

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“…PROK2, also named Bv8, is a ligand for a G protein-coupled receptor, PROKR2. Recently, it has been found that the PROK2-PROKR2 pathway is crucial for angiogenesis in embryonic development and that the expression of PROK2 is regulated by the TBX20 transcription factor 51 . Considering that the products of genes causative of KS contribute to embryonic angiogenesis, abnormality in the angiogenic process appears to be important for the pathogenesis of KS.…”

Section: Discussionmentioning

confidence: 99%

Anosmin-1 activates vascular endothelial growth factor receptor and its related signaling pathway for olfactory bulb angiogenesis

Matsushima

Shimizu

Kondo

et al. 2020

Sci Rep

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Anosmin-1 is a secreted glycoprotein encoded by the ANOS1 gene, and its loss of function causes Kallmann syndrome (KS), which is characterized by anosmia and hypogonadism due to olfactory bulb (OB) dysfunction. However, the physiological function of anosmin-1 remains to be elucidated. In KS, disordered angiogenesis is observed in OB, resulting in its hypoplasia. In this study, we examined the involvement of anosmin-1 in angiogenic processes. Anosmin-1 was detected on the vessel-like structure in OB of chick embryos, and promoted the outgrowth of vascular sprouts as shown by assays of OB tissue culture. Cell migration, proliferation, and tube formation of endothelial cells were induced by treatment with anosmin-1 as well as vascular endothelial growth factor-A (VEGF-A), and further enhanced by treatment with both of them. We newly identified that anosmin-1 activated VEGF receptor-2 (VEGFR2) by binding directly to it, and its downstream signaling molecules, phospholipase cγ1 (PLCγ1) and protein kinase C (PKC). These results suggest that anosmin-1 plays a key role in the angiogenesis of developing OB through the VEGFR2-PLCγ1-PKC axis by enhancing the VEGF function.

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“…In the recently published study by Meng et al, the authors sought to analyse the function of the key transcription factor T-box 20 (TBX20) and the signaling pathway which is activated during angiogenesis (7). TBX20 is considered a pivotal transcription factor during embryogenesis.…”

Section: The Study By Meng Et Almentioning

confidence: 99%

“…PROK2 that acts on its receptor PROKR1in an autocrine fashion. The authors presume that this mechanism might help to further sustain the pro-angiogenic signalling [adapted fromMeng et al(7)].…”

mentioning

confidence: 99%

TBX20 and the PROK2-PROKR1 pathway—new kid on the block in angiogenesis research

Lichtenauer

Jung

2018

Ann. Transl. Med

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TBX20 Regulates Angiogenesis Through the Prokineticin 2–Prokineticin Receptor 1 Pathway

Cited by 33 publications

References 60 publications

Regulation of cardiomyocyte fate plasticity: a key strategy for cardiac regeneration

Regulation of cardiomyocyte fate plasticity: a key strategy for cardiac regeneration

Anosmin-1 activates vascular endothelial growth factor receptor and its related signaling pathway for olfactory bulb angiogenesis

TBX20 and the PROK2-PROKR1 pathway—new kid on the block in angiogenesis research

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