Thin endometrium (< 7 mm) could cause low clinical pregnancy, reduced live birth, increased spontaneous abortion, and decreased birth weight. However, the treatments for thin endometrium have not been well developed. In this study, we aim to determine the role of Pluronic F-127 (PF-127) encapsulation of human umbilical cord mesenchymal stem cells (hUC-MSCs) in the regeneration of thin endometrium and its underlying mechanism. Thin endometrium rat model was created by infusion of 95% ethanol. Thin endometrium modeled rat uterus were treated with saline, hUC-MSCs, PF-127, or hUC-MSCs plus PF-127 separately. Regenerated rat uterus was measured for gene expression levels of angiogenesis factors and histological morphology. Angiogenesis capacity of interleukin-1 beta (IL-1β)-primed hUC-MSCs was monitored via quantitative polymerase chain reaction (q-PCR), Luminex assay, and tube formation assay. Decreased endometrium thickness and gland number and increased inflammatory factor IL-1β were achieved in the thin endometrium rat model. Embedding of hUC-MSCs with PF-127 could prolong the hUC-MSCs retaining, which could further enhance endometrium thickness and gland number in the thin endometrium rat model via increasing angiogenesis capacity. Conditional medium derived from IL-1β-primed hUC-MSCs increased the concentration of angiogenesis factors (basic fibroblast growth factor (bFGF), vascular endothelial growth factors (VEGF), and hepatocyte growth factor (HGF)). Improvement in the thickness, number of glands, and newly generated blood vessels could be achieved by uterus endometrium treatment with PF-127 and hUC-MSCs transplantation. Local IL-1β stimulation-primed hUC-MSCs promoted the release of angiogenesis factors and may play a vital role on thin endometrium regeneration.

Long non-coding RNAs (lncRNAs) are known to play a major role in the epigenetic regulation of muscle development. Unfortunately there is little understanding of the mechanisms with which they regulate muscle growth in abalone. Therefore, we used RNA-seq to study the muscle transcriptomes of six Haliotis discus hannai specimens: three large (L_HD group) and three small (S_HD group). We identified 2463 lncRNAs in abalone muscle belonging to two subtypes: 160 anti-sense lncRNAs and 2303 intergenic lncRNAs (lincRNAs). In the L_HD group, we identified 204 significantly differentially expressed lncRNAs (55 upregulated and 149 downregulated), and 2268 significantly differentially expressed mRNAs (994 upregulated and 1274 downregulated), as compared to the S_HD group. The bioinformatics analysis indicated that lncRNAs were relate to cell growth, regulation of growth, MAPK signaling pathway, TGF-β signaling pathway, PI3K-Akt and insulin signaling pathway, which involved in regulating muscle growth. These findings contribute to understanding the possible regulatory mechanisms of muscle growth in Pacific abalone.

Hypertrophic ligamentum flavum (LF) is a main factor responsible for lumbar spinal stenosis (LSS); however, the exact mechanisms of the pathogenesis of these processes remain unknown. This study aimed to elucidate whether circular RNAs and microRNAs regulate the pathogenesis of LF and LSS, especially focusing on circPDK1 (hsa_circ_0057105), a circRNA targeting pyruvate dehydrogenase kinase 1 and differentially expressed in LF tissues between lumbar disk herniation and LSS patients. The circPDK1/miR-4731 and miR-4731/TNXB (Tenascin XB) interactions were predicted and validated by luciferase reporter assay. Colony formation, woundhealing, and MTT assays were used for estimating cell proliferation and migration.Protein expression levels were evaluated using Western blotting. TNXB expression was verified using immunohistochemistry (IHC). Overexpressing circPDK1 promoted the proliferation, migration, and expression of fibrosis-related protein (alpha smooth muscle actin (α-SMA), lysyl oxidase like 2 (LOXL2), Collagen I, matrix metalloproteinase-2 (MMP-2) and TNXB) in LF whereas miR-4731-5p showed opposite effects. The expression of TNXB was promoted by circPDK1; contrary results were observed with miR-4731-5p. Co-overexpression of miR-4731-5p partially reversed the proliferative and fibrosis-prompting effects of circPDK1 or TNXB. The circPDK1-miR-4731-TNXB pathway may be proposed as a regulatory axis in LF hypertrophy, which might shed light on in-depth research of LSS, as well as providing a novel therapeutic target for LF hypertrophy-induced LSS.

Background The current study aimed to investigate the association between sarcopenia and symptomatic knee osteoarthritis (KOA) in middle-aged and older adults using nationally representative data from the China Health and Retirement Longitudinal Study (CHARLS). However, no causal relationships (i.e., whether symptomatic KOA is a risk factor or direct consequence of sarcopenia) were established. Methods We conducted cross-sectional and longitudinal analyses using baseline (from 2011) and follow-up CHARLS data (from 2018). Sarcopenic status was defined according to the Asian Working Group for Sarcopenia 2019 (AWGS 2019) consensus. Symptomatic KOA was based on participant self-reports of physician diagnoses. Symptomatic KOA events were defined as participants without symptomatic KOA at baseline (2011) and diagnosed with symptomatic KOA at follow-up (2018). The cross-sectional analysis included CHARLS 2011 data from 7,071 participants aged > 45 years. The longitudinal analysis included CHARLS data from 4,785 participants without KOA recruited in 2011 and followed-up in 2018. A Cox proportional hazards regression model was performed to examine the effect of sarcopenia on KOA. Results The prevalence rates of symptomatic KOA in the general population and in individuals without sarcopenia, with probable sarcopenia, and with sarcopenia were 11.3% (798/7,071), 10.4% (524/5,031), 13.6% (191/1,403), and 13.0% (83/637), respectively. In the general population, probable sarcopenia [odds ratio (OR):1.33; 95% confidence interval (CI): 1.11–1.59] was associated with symptomatic KOA. In the cross-sectional analyses, age, sex, educational attainment, smoking status, alcohol consumption, and self-reported physician diagnoses of diabetes, hypertension, and other chronic diseases were associated with sarcopenic status. At follow-up, 451 (9.4%) KOA events were identified, but the longitudinal analysis did not identify possible sarcopenia, and sarcopenia increased KOA risk. Conclusion Possible sarcopenia, assessed using the AWGS 2019 criteria, was associated with the risk of symptomatic KOA among middle-aged and older Chinese adults, but no longitudinal association was detected between sarcopenia and the onset of KOA due to the small sample size and insufficient statistical power.