Search Results (6)

Gestational diabetes mellitus (GDM) poses significant health risks to both mothers and infants, emphasizing the need for early detection strategies to mitigate its impact. However, the existing diagnostic methods, particularly the oral glucose tolerance test (OGTT) administered in the second or third trimester, show limitations in the detection of GDM during its early stages. This study aimed to explore the potential of the genes Protein Tyrosine Phosphatase Receptor-type Gamma (PTPRG) and Immunoglobulin Kappa Variable 2D-28 (IGKV2D-28) as early indicators for GDM among Filipino pregnant women. Utilizing reverse transcription–quantitative polymerase chain reaction (RT-qPCR), the gene expressions were analyzed in first-trimester blood samples obtained from 24 GDM and 36 non-GDM patients. The diagnostic performance of PTPRG and IGKV2D-28 was analyzed and evaluated using receiver operating characteristic (ROC) curves. The findings revealed elevated expression levels of PTPRG and IGKV2D-28 within the GDM cohort. Remarkably, PTPRG exhibited a sensitivity of 83%, while IGKV2D-28 demonstrated a specificity of 94% at determined cut-off values. Combining both genes yielded an improved but limited diagnostic accuracy with an area under the curve (AUC) of 0.63. This preliminary investigation of PTPRG and IGKV2D-28 sheds light on novel avenues for early GDM detection. While these findings are promising, further validation studies in larger cohorts are necessary to confirm these results and explore additional biomarkers to enhance diagnostic precision in GDM pregnancies and, ultimately, to improve maternal and fetal outcomes. Full article

This study concerns the analysis of the modulation of Chronic Myeloid Leukemia (CML) cell model K562 transcriptome following transfection with the tumor suppressor gene encoding for Protein Tyrosine Phosphatase Receptor Type G (PTPRG) and treatment with the tyrosine kinase inhibitor (TKI) Imatinib. Specifically, we aimed at identifying genes whose level of expression is altered by PTPRG modulation and Imatinib concentration. Statistical tests as differential expression analysis (DEA) supported by gene set enrichment analysis (GSEA) and modern methods of ontological term analysis are presented along with some results of current interest for forthcoming experimental research in the field of the transcriptomic landscape of CML. In particular, we present two methods that differ in the order of the analysis steps. After a gene selection based on fold-change value thresholding, we applied statistical tests to select differentially expressed genes. Therefore, we applied two different methods on the set of differentially expressed genes. With the first method (Method 1), we implemented GSEA, followed by the identification of transcription factors. With the second method (Method 2), we first selected the transcription factors from the set of differentially expressed genes and implemented GSEA on this set. Method 1 is a standard method commonly used in this type of analysis, while Method 2 is unconventional and is motivated by the intention to identify transcription factors more specifically involved in biological processes relevant to the CML condition. Both methods have been equipped in ontological knowledge mining and word cloud analysis, as elements of novelty in our analytical procedure. Data analysis identified RARG and CD36 as a potential PTPRG up-regulated genes, suggesting a possible induction of cell differentiation toward an erithromyeloid phenotype. The prediction was confirmed at the mRNA and protein level, further validating the approach and identifying a new molecular mechanism of tumor suppression governed by PTPRG in a CML context. Full article

In the current study, the genetic architecture of growth and linear type traits were investigated in Akkaraman sheep. Estimations of genomic heritability, genetic correlations, and phenotypic correlations were implemented for 17 growth and linear type traits of 473 Akkaraman lambs by the univariate and multivariate analysis of animal mixed models. Correspondingly, moderate heritability estimates, as well as high and positive genetic/phenotypic correlations were found between growth and type traits. On the other hand, 2 genome-wide and 19 chromosome-wide significant single nucleotide polymorphisms were found to be associated with the traits as a result of animal mixed model-based genome-wide association analyses. Accordingly, we propose several genes located on different chromosomes (e.g., PRDM2, PTGDR, PTPRG, KCND2, ZNF260, CPE, GRID2, SCD5, SPIDR, ZNF407, HCN3, TMEM50A, FKBP1A, TLE4, SP1, SLC44A1, and MYOM3) as putative quantitative trait loci for the 22 growth and linear type traits studied. In our study, specific genes (e.g., TLE4, PTGDR, and SCD5) were found common between the traits studied, suggesting an interplay between the genetic backgrounds of these traits. The fact that four of the proposed genes (TLE4, MYOM3, SLC44A1, and TMEM50A) are located on sheep chromosome 2 confirms the importance of these genomic regions for growth and morphological structure in sheep. The results of our study are therefore of great importance for the development of efficient selection indices and marker-assisted selection programs, as well as for the understanding of the genetic architecture of growth and linear traits in sheep. Full article

Protein tyrosine phosphatase receptor gamma (PTPRG) is known to interact with and regulate several tyrosine kinases, exerting a tumor suppressor role in several type of cancers. Its wide expression in human tissues compared to the other component of group 5 of receptor phosphatases, PTPRZ expressed as a chondroitin sulfate proteoglycan in the central nervous system, has raised interest in its role as a possible regulatory switch of cell signaling processes. Indeed, a carbonic anhydrase-like domain (CAH) and a fibronectin type III domain are present in the N-terminal portion and were found to be associated with its role as [HCO₃⁻] sensor in vascular and renal tissues and a possible interaction domain for cell adhesion, respectively. Studies on PTPRG ligands revealed the contactins family (CNTN) as possible interactors. Furthermore, the correlation of PTPRG phosphatase with inflammatory processes in different normal tissues, including cancer, and the increasing amount of its soluble form (sPTPRG) in plasma, suggest a possible role as inflammatory marker. PTPRG has important roles in human diseases; for example, neuropsychiatric and behavioral disorders and various types of cancer such as colon, ovary, lung, breast, central nervous system, and inflammatory disorders. In this review, we sum up our knowledge regarding the latest discoveries in order to appreciate PTPRG function in the various tissues and diseases, along with an interactome map of its relationship with a group of validated molecular interactors. Full article

Aging is associated with metabolic changes and low-grade inflammation in several organs, which may be due to NLRP3 inflammasome activation. Methods: Here, we asked whether age-related liver changes such as lipid metabolism and fibrosis are reduced in aged mice lacking the NLRP3 inflammasome. We report reduced protein levels of lipid markers (MTP, FASN, DGAT1), SOD activity, oxidative stress marker PTPRG, and the fibrotic markers TPM2β, COL1-α1 associated with increased GATA4, in NLRP3 deficient mice. Fibrotic, lipid, and oxidative reduction in liver tissues of mice was more pronounced in those old KO NLRP3 mice than in the younger ones, despite their greater liver damage. These results suggest that absence of the NLRP3 inflammasome attenuates age-related liver fibrotic pathology in mice, suggesting that pharmacological targeting may be beneficial. Full article

Protein tyrosine phosphatase receptor type γ (PTPRG) is a tumor suppressor gene, down-regulated in Chronic Myeloid Leukemia (CML) cells by the hypermethylation of its promoter region. β-catenin (CTNNB1) is a critical regulator of Leukemic Stem Cells (LSC) maintenance and CML proliferation. This study aims to demonstrate the antagonistic regulation between β-catenin and PTPRG in CML cells. The specific inhibition of PTPRG increases the activation state of BCR-ABL1 and modulates the expression of the BCR-ABL1- downstream gene β-Catenin. PTPRG was found to be capable of dephosphorylating β-catenin, eventually causing its cytosolic destabilization and degradation in cells expressing PTPRG. Furthermore, we demonstrated that the increased expression of β-catenin in PTPRG-negative CML cell lines correlates with DNA (cytosine-5)-methyl transferase 1 (DNMT1) over-expression, which is responsible for PTPRG promoter hypermethylation, while its inhibition or down-regulation correlates with PTPRG re-expression. We finally confirmed the role of PTPRG in regulating BCR-ABL1 and β-catenin phosphorylation in primary human CML samples. We describe here, for the first time, the existence of a regulative loop occurring between PTPRG and β-catenin, whose reciprocal imbalance affects the proliferation kinetics of CML cells. Full article