On the role of pleiotrophin and its receptors in development and angiogenesis

Papadimitriou, Evangelia; Mourkogianni, Eleni; Ntenekou, Despoina; Christopoulou, Magdalini; Κουτσιούμπα, Μαρίνα; Lamprou, Margarita

doi:10.1387/ijdb.210122ep

Cited by 19 publications

(16 citation statements)

References 95 publications

(56 reference statements)

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“…Cardiac fibroblasts derive from both the endocardium and epicardium during embryonic development and are considered to significantly affect myocardial growth, whereas they seem to have little effect in the adult myocardium in health or disease ( 54 ). PTPRZ1 has been shown to be highly expressed during embryonic development ( 5 ) in line with our data in the present work showing increased expressed in the embryonic heart and is known to affect angiogenesis through downstream activation of numerous signaling molecules ( 5 , 10 , 22 ). The role of PTPRZ1 in fibroblasts functions has not been studied up to date.…”

Section: Discussionsupporting

confidence: 92%

“…Binding of these ligands on PTPRZ1 seems to affect the tyrosine phosphatase activity of the receptor and increase tyrosine phosphorylation of numerous downstream signaling molecules, such as c-Src and Fyn kinases, α ν β 3 -integrin, protein kinase C, and phosphoinositide 3-kinase, to control cell adhesion and cell migration (revised in Refs. 5 , 10 ).…”

Section: Introductionmentioning

confidence: 99%

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Protein tyrosine phosphatase receptor-ζ1 deletion triggers defective heart morphogenesis in mice and zebrafish

Katraki-Pavlou

Kastana

Bousis

et al. 2022

American Journal of Physiology-Heart and Circulatory Physiology

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Protein tyrosine phosphatase receptor zeta 1 (PTPRZ1) is a transmembrane tyrosine phosphatase receptor highly expressed in embryonic stem cells. In the present work, gene expression analyses of Ptprz1-/- and Ptprz1+/+ mice endothelial cells and hearts pointed to an unidentified role of PTPRZ1 in heart development through regulation of heart-specific transcription factor genes. Echocardiography analysis in mice identified that both systolic and diastolic functions are affected in Ptprz1-/- compared to Ptprz1+/+ hearts, based on a dilated LV cavity, decreased ejection fraction and fraction shortening, and increased angiogenesis in Ptprz1-/- hearts, with no signs of cardiac hypertrophy. A zebrafish ptprz1-/- knockout was also generated and exhibits mis-regulated expression of developmental cardiac markers, bradycardia and defective heart morphogenesis characterized by enlarged ventricles and defected contractility. A selective PTPRZ1 tyrosine phosphatase inhibitor affected zebrafish heart development and function in a way like what is observed in the ptprz1-/- zebrafish. The same inhibitor had no effect in the function of the adult zebrafish heart, suggesting that PTPRZ1 is not important for the adult heart function, in line with data from the human cell atlas showing very low to negligible PTPRZ1 expression in the adult human heart. However, in line with the animal models, Ptprz1 was expressed in many different cell types in the human fetal heart, such as valvar, fibroblast-like, cardiomyocytes and endothelial cells. Collectively, these data suggest that PTPRZ1 regulates cardiac morphogenesis in a way that subsequently affects heart function and warrant further studies for the involvement of PTPRZ1 in idiopathic congenital cardiac pathologies.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Protein tyrosine phosphatase receptor-ζ1 deletion triggers defective heart morphogenesis in mice and zebrafish

Katraki-Pavlou

Kastana

Bousis

et al. 2022

American Journal of Physiology-Heart and Circulatory Physiology

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“…Ptn is a ligand for several receptors in the brain, including protein tyrosine phosphatase receptor type Z1 (Ptprz1), anaplastic lymphoma kinase (Alk), and nucleolin (Ncl) 81,82 . We found increased Ptn to Ptprz1 signaling in OPCs, decreased Ptn to Alk signaling between SMC1 and InNs, as well as decreased Ptn to Ncl signaling between SMC1 and endothelial cells in the trisomic mouse brain (Figures 3F and 3G).…”

Section: Ligand-receptor Analysis Of the Ts65dn Cortex Identifies Cha...mentioning

confidence: 99%

Single-nucleus profiling identifies accelerated oligodendrocyte precursor cell senescence in a mouse model of Down Syndrome

Rusu

Kukreja

et al. 2023

Preprint

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Down Syndrome (DS), the most common genetic cause of intellectual disability, is associated with lifelong cognitive disability. However, the mechanisms by which triplication of human chromosome 21 genes drive neuroinflammation and cognitive dysfunction are poorly understood. Here, using the Ts65Dn mouse model of DS, we performed an integrated single-nucleus RNA- and ATAC-seq analysis of the cortex. We identify cell type-specific transcriptional and chromatin-associated changes in the Ts65Dn cortex, including regulators of neuroinflammation, transcription and translation, myelination, and mitochondrial function. We discover enrichment of a senescence-associated transcriptional signature in Ts65Dn oligodendrocyte precursor cells (OPCs) and epigenetic changes consistent with a loss of heterochromatin. We find that senescence is restricted to a subset of cortical OPCs concentrated in deep cortical layers. Treatment of Ts65Dn mice with a senescence-reducing flavonoid rescues cortical OPC proliferation, restores microglial homeostasis, and improves contextual fear memory. Together, these findings suggest that cortical OPC senescence may be an important driver of neuropathology in DS.

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“…In osteosarcoma cells, lncRNA OIP5-AS1 is capable of binding to miR-200b-3p or miR-137-3p, resulting in the overexpression of FN1 or PTN, respectively [ 152 , 153 ]. Since FN1 is well-known as a mesenchymal indicator that has been reported to be involved in PTN in angiogenesis [ 154 , 155 ], the induction of FN1 or PTN mediated by lncRNA OIP5-AS1 in response to doxorubicin might contribute to chemoresistance accompanied by EMT induction and tumor metastasis.…”

Section: Lncrnas Regulate Therapeutic Resistance Associated With Glut...mentioning

confidence: 99%

The Involvement of Long Non-Coding RNAs in Glutamine-Metabolic Reprogramming and Therapeutic Resistance in Cancer

Roh

Chae

et al. 2022

IJMS

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Metabolic alterations that support the supply of biosynthetic molecules necessary for rapid and sustained proliferation are characteristic of cancer. Some cancer cells rely on glutamine to maintain their energy requirements for growth. Glutamine is an important metabolite in cells because it not only links to the tricarboxylic acid cycle by producing α-ketoglutarate by glutaminase and glutamate dehydrogenase but also supplies other non-essential amino acids, fatty acids, and components of nucleotide synthesis. Altered glutamine metabolism is associated with cancer cell survival, proliferation, metastasis, and aggression. Furthermore, altered glutamine metabolism is known to be involved in therapeutic resistance. In recent studies, lncRNAs were shown to act on amino acid transporters and glutamine-metabolic enzymes, resulting in the regulation of glutamine metabolism. The lncRNAs involved in the expression of the transporters include the abhydrolase domain containing 11 antisense RNA 1, LINC00857, plasmacytoma variant translocation 1, Myc-induced long non-coding RNA, and opa interacting protein 5 antisense RNA 1, all of which play oncogenic roles. When it comes to the regulation of glutamine-metabolic enzymes, several lncRNAs, including nuclear paraspeckle assembly transcript 1, XLOC_006390, urothelial cancer associated 1, and thymopoietin antisense RNA 1, show oncogenic activities, and others such as antisense lncRNA of glutaminase, lincRNA-p21, and ataxin 8 opposite strand serve as tumor suppressors. In addition, glutamine-dependent cancer cells with lncRNA dysregulation promote cell survival, proliferation, and metastasis by increasing chemo- and radio-resistance. Therefore, understanding the roles of lncRNAs in glutamine metabolism will be helpful for the establishment of therapeutic strategies for glutamine-dependent cancer patients.

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On the role of pleiotrophin and its receptors in development and angiogenesis

Cited by 19 publications

References 95 publications

Protein tyrosine phosphatase receptor-ζ1 deletion triggers defective heart morphogenesis in mice and zebrafish

Protein tyrosine phosphatase receptor-ζ1 deletion triggers defective heart morphogenesis in mice and zebrafish

Single-nucleus profiling identifies accelerated oligodendrocyte precursor cell senescence in a mouse model of Down Syndrome

The Involvement of Long Non-Coding RNAs in Glutamine-Metabolic Reprogramming and Therapeutic Resistance in Cancer

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