Investigation of diabetes-related molecular changes in embryo-endometrium crosstalk.

The primary aim of this study was to explore the impact of diabetes on matrix metalloproteases and tissue inhibitors, crucial factors for successful implantation, and to elucidate the molecular mechanisms that undergo changes in the endometrium and the embryo during diabetic pregnancies. In this investigation, we established a streptozotocin-induced diabetic pregnant rat model. Microarray analysis followed by RT-PCR was utilized to identify gene regions exhibiting expression alterations. Subsequently, we assessed the effects of MMPs and tissue inhibitors using ELISA and immunohistochemistry techniques, in addition to analyzing changes at the genetic level. Diabetes led to the upregulation of MMP3, MMP9, and MMP20 on the 6.5th day of pregnancy, while causing the downregulation of MMP3, MMP9, and MMP11 on the 8.5th day of pregnancy. TIMP1 expression was downregulated on the 8.5th day compared to the control group. No statistically significant differences were observed between the groups regarding other TIMP expressions. KEGG pathway analysis revealed that diabetes induced alterations in the expression of genes associated with certain microRNAs, as well as signaling pathways such as cAMP, calcium, BMP, p53, MAPK, PI3K-Akt, Jak-STAT, Hippo, Wnt, and TNF. Additionally, gene ontology analysis unveiled changes in membrane structures, extracellular matrix, signaling pathways, ion binding, protein binding, cell adhesion molecule binding, and receptor-ligand activity. This study serves as a valuable guide for investigating the mechanisms responsible for complications in diabetic pregnancies. By revealing the early-stage effects of diabetes, it offers insight into the development of new diagnostic and treatment approaches, ultimately contributing to improved patient care.

CD97 expression level and its effect on cell adhesion in Preeclampsia.

OBJECTIVES: Cellular interactions and cell adhesion underlie preeclampsia (PE). The aim of the current study is to investigate the role of cell adhesion molecules such as CD97, neural (N)-cadherin, epithelial (E) -cadherin and integrin beta-4 in PE. METHODS: This prospective study included 20 pregnant women with PE and a control group of 16 healthy pregnant women who were matched for age, gestational age, gravida and parity. Standard blood tests and placental cell adhesion molecule immunohistochemical staining were examined. RESULTS: The creatinine, uric acid and lactate dehydrogenase (LDH) levels from standard blood tests were found to be statistically higher in the PE group (p = 0.002, p = 0.000, p = 0.001; respectively). In the PE group, the CD97 maternal serum level was statistically significantly lower, as was its immunohistochemical expression in placental sections (p = 0.028, p = 0.000; respectively). The E-cadherin expression score was statistically higher in the PE group compared to the control group (3,65 ± 1,84 vs 2,06 ± 1,76 respectively; p = 0.003). The N-cadherin expression score was statistically lower in the PE group compared to the control group (1,50 ± 0,82 vs 2,43 ± 1,59 respectively; p = 0.049). Integrin beta-4 was not statistically different between groups. CONCLUSIONS: Cellular interaction may be responsible for PE as in cancer. A balance in intercellular communication, as researched in cancer therapy, may offer the solution in PE.

Adipose derived mesenchymal stem cell treatment in experimental asherman syndrome induced rats.

Asherman syndrome (AS) occurs due to fibrosis or uterine adhesions as a result of damage to the basal layer of the endometrium. The aim of this study is investigating the effects of adipose tissue-derived mesenchymal stem cell (ADMSC) application on the expression of vascular endothelial growth factor (VEGF), insulin-like growth factor (IGF-1), miRNA-98, miRNA199a in endometrial tissue in rats with AS. Study groups were designed as, control (C), Asherman syndrome (AS), AS + oral estrogen (ASO), AS + ADMSC (ASSC), AS + oral estrogen + ADMSC (ASSCO) with 7 samples in each group. Characterization and differentiation experiments were performed in ADMSC obtained. Two weeks after the development of the AS, ADMSC therapy was applied. BrdU (5-bromo-2'-deoxyuridine) labeling was performed to show the presence of ADMSC in the tissues. Rats were sacrificed after 8 weeks and bilateral uterine horn resection was performed. Tissues were fixed in formaldehyde. After routine tissue follow-up, sections were taken and evaluated with hematoxylin eosin staining. VEGF1 and IGF1 expressions were evaluated by immunohistochemical staining and western blot analysis. Expression changes of miR-98 and miR-199a were detected by RT-PCR. Our results showed that stem cells and estrogen giving together reduced inflammation and fibrosis in the endometrium. Immunohistochemistry and western blot results suggested that this effect was achieved especially through IGF-1. In our study, decreased miR-98 and miR-199a expressions were determined in Asherman syndrome. Furthermore, no changes of miRNA expressions were observed in treatment groups.

Tissue reaction to urogynecologic meshes: effect of steroid soaking in two different mesh models.

INTRODUCTION AND HYPOTHESIS: Steroid soaking may decrease mesh-triggered inflammatory reaction in tissue. We aimed to investigate the tissue reaction to a steroid-soaked mesh material and an unsoaked mesh material in the rat model. METHODS: Neutral and steroid-soaked type I macroporous polypropylene (PP) monofilament and polyvinylidene fluoride (PVF) mesh materials were implanted on the rectus abdominis muscle of 20 mature Wistar albino rats. Animals were divided into four groups: PP mesh with steroid (PP-S), PP mesh without steroid, PVF mesh with steroid (PVF-S), and PVF mesh without steroid. The rats were killed after 12 weeks, and histologic, immunohistochemical and electron microscopic examinations were performed. For immunohistochemical analysis, polyclonal rabbit anti-mouse CD3, rabbit anti-mouse CD68, rabbit anti-mouse CD15, and rabbit anti-mouse CD34 antibodies were used for the detection of lymphocytes, macrophages, polymorphonuclear leukocyte foreign body giant cells, and fibromyocyte stem cells, respectively. Samples were stained with hematoxylin and eosin for the histologic evaluation of inflammation and with Masson's trichrome stain for the evaluation of collagen deposition. Pore size and mesh ultrastructure were evaluated by electron microscopy. RESULTS: Expression of CD3 was lower in the PVF, PVF-S and PP-S groups, and expression of CD34 was higher in the PVF-S and PP-S groups than in the PP groups (p < 0.05). Collagen deposition was lower in the PVF, PVF-S and PP-S groups (p < 0.05). Histologically, the intensity of inflammation was lower in the PVF-S and PP-S groups than in the PP mesh group (p < 0.05). There were no significant differences among the groups in terms of pore size and mesh ultrastructure on electron microscopic examination (p > 0.05). CONCLUSIONS: PVF mesh induces less inflammation than PP mesh, and in both mesh types steroid soaking further decreases inflammation without changing the pore size.