Wharton’s jelly-derived mesenchymal stem cells (WJ-MSCs) are a novel and promising strategy for tissue engineering because of their ability to differentiate into many cell types. We characterized the differentiation of WJ-MSCs into endometrial epithelial cell (EEC)-like and endometrial stromal cell (ESC)-like cells and assessed the effect of 17β-estradiol and 8-Br-cAMP on the differentiation system. WJ-MSCs were treated in two ways to differentiate into EEC-like and ESC-like cells respectively: cocultured with ESCs in control/differentiation medium (17β-estradiol, growth factors); and cultured in control/differentiation medium (8-Br-cAMP alone or 8-Br-cAMP plus 17β-estrogen and growth factors). Three signaling pathway inhibitors (SB203580, PD98059, H89) were used to investigate the mechanism of WJ-MSC differentiation into ESC-like cells. Immunofluorescence, western blot and flow cytometry analyses were used to analyze expression of epithelial markers and stromal cell markers. Enzyme-linked immunosorbent assays were used to test the production of secretory proteins associated with the differentiation of ESC-like cells. 17β-estradiol at 1 μM downregulated vimentin and CD13 and upregulated cytokeratin and CD9 proteins, promoting the differentiation of WJ-MSCs into EEC-like cells in the coculture system. 8-Br-cAMP at 0.5 mM upregulated vimentin and CD13 and downregulated CK and CD9, promoting the differentiation of WJ-MSCs into ESC-like cells. Prolactin (PRL) and insulin-like growth factor-binding protein 1 (IGFBP1) were upregulated and the protein kinase A (PKA) signaling pathway was activated, whereas extracellular signal-regulated (ERK)1/2 and p38 mitogen-activated protein kinase (MAPK) were not affected. 17β-estradiol at 1 μM is a good inducer for facilitating the differentiation of WJ-MSCs into EEC-like cells. 8-Br-cAMP plus estrogen and growth factors can induce the differentiation of WJ-MSCs into ESC-like cells. During the differentiation of WJ-MSCs into ESC-like cells, PRL and IGFBP1 were upregulated by the treatment and the PKA signaling pathway was activated, whereas ERK1/2 and p38 MAPK were not affected. These findings suggest a promising approach to the treatment of endometrial damage and other endometrial diseases and suggest new applications for WJ-MSCs in clinical practice.

Introduction: Acute promyelocytic leukemia (APL) is a distinct subtype of acute myeloid leukemia (AML) with unique clinical features. Flow cytometry (FCM) immunophenotyping analysis is crucial for accurate diagnosis and prognostic stratification. This study aims to explore the association between specific immune phenotype markers in APL patients and overall survival (OS). Methods: In this retrospective cohort study, immunophenotypic data from 72 APL patients were analyzed by FCM. Continuous and categorical variables are presented as mean ± standard deviation and frequency (percentage), respectively. Group comparisons were performed using ANOVA and Chi-square tests. Cox proportional hazards models were used to identify prognostic factors for OS, with results expressed as hazard ratios (HRs) and 95% confidence intervals (CIs). Kaplan-Meier survival analysis was employed to assess the impact of CD56, CD2, CD34, and CD200 expression on OS. Subgroup analyses were conducted based on age, gender, white blood cell count (WBC), and disseminated intravascular coagulation (DIC). Results: The baseline age (p = 0.513) and gender (p = 0.881) were comparable across different PML-RARα isoform groups. Compared to non-APL AML, APL blasts were characterized by significantly higher expression of CD33, CD13, CD9, and MPO (all p < 0.05), and lower expression of CD7, CD34, CD56, CD38, CD200, and HLA-DR (all p < 0.001). The PML-RARα (S-type) group showed relatively higher expression of CD34, CD2, and CD200 than the L-type group. Univariate Cox analysis revealed that expression of CD34, CD2, CD56, and CD200 were all significantly associated with poorer OS. After multivariate adjustment, CD2 (adjusted HR = 1.04, 95% CI: 1.01–1.07, p = 0.004) and CD200 (adjusted HR = 1.04, 95% CI: 1.01–1.06, p = 0.009) remained independent adverse prognostic factors. Subgroup analysis confirmed that the negative prognostic impact of CD2 and CD200 expression was consistent across different patient subgroups. Conclusion: Compared with non-APL-AML patients, APL patients (PML-RARα (S-type) and PML-RARα (L-type)) exhibit unique immunophenotypic changes. The expression frequencies of CD56, CD2, CD34, and CD200 in leukemia cells are significantly correlated with the OS of APL patients, and the high expression of these indicators before treatment may be an adverse prognostic factor for APL patients.

Purpose: To evaluate the diagnostic value of serum hepatokines, leucocyte cell-derived chemotaxin 2 (LECT2) and pigment epithelium-derived factor (PEDF), for pediatric metabolic-associated fatty liver disease (MAFLD), and to assess their correlations with metabolic/liver injury indices and diagnostic utility. Patients and methods: A total of 198 patients were included in the study (78 in the MAFLD group, 60 in the obese non-MAFLD and 60 in the control group). Serum LECT2 and PEDF levels were measured in all three groups. Group comparisons were performed, and LECT2/PEDF levels were correlated with metabolic parameters, and liver injury markers. ROC curve analyses and logistic regression were also conducted. Results: Serum LECT2 and PEDF levels exhibited stepwise elevations (control < obese non-MAFLD < MAFLD; both P < 0.001), with significant correlations in MAFLD patients to BMI, insulin resistance (HOMA-IR), and liver injury markers (ALT/AST). For MAFLD versus controls, PEDF showed superior diagnostic accuracy (AUC = 0.804, 95% CI: 0.731– 0.877) to LECT2 (AUC = 0.734, 0.651– 0.817), while combined PEDF with LECT2 further improved discrimination (AUC = 0.849; sensitivity 79.5%, specificity 78.3%). For MAFLD versus obese non-MAFLD, both hepatokines had modest utility (LECT2 AUC = 0.623; PEDF AUC = 0.668), though their combination enhanced performance (AUC = 0.712; sensitivity 60.3%, specificity 73.9%). Multivariable analysis confirmed LECT2 and PEDF as independent MAFLD predictors. Conclusion: LECT2 and PEDF are elevated in pediatric MAFLD and correlate with metabolic dysfunction. While their combination effectively distinguishes MAFLD from healthy controls, it shows moderate efficacy in differentiating MAFLD from simple obesity. Nevertheless, the LECT2/PEDF panel represents a promising risk-stratification tool to identify high-risk obese children for further diagnostic evaluation.Plain Language Summary Metabolic-associated fatty liver disease (MAFLD) is the most common long-term liver problem in children, especially those who are obese. Diagnosing it can be hard—doctors usually need invasive tests like liver biopsies or expensive scans. So, researchers wanted to find simple blood tests that could help diagnose MAFLD in kids. The team studied 198 children, split into three groups: 78 with MAFLD, 60 who were obese but did not have MAFLD, and 60 healthy kids. They measured two substances in the children’s blood—LECT2 (a factor linked to inflammation) and PEDF (a factor linked to fat regulation). They found:Levels of both LECT2 and PEDF rose step by step: lowest in healthy kids, higher in obese kids without MAFLD, and highest in kids with MAFLD.Higher levels of these substances correlated with bigger weight problems, worse insulin resistance (when the body does not use insulin well), and more liver damage.PEDF was better at telling MAFLD apart from healthy kids than LECT2. Using both together worked even better—catching 79.5% of MAFLD cases and correctly ruling out 78.3% of healthy kids. These results mean LECT2 and PEDF could become simple, non-invasive blood markers to help doctors spot MAFLD in children early, especially before the disease gets serious.