Project description:Objective: To Explore the mechanism of autophagy in mice with immune premature ovarian failure (POF) and the effect of Bushen Huoxue Fang (BSHXF) Method: POF mice were treated with BSHXF, and estradiol valerate. Then, the ovaries were used for transcriptome sequencing.
Project description:Premature ovarian insufficiency (POI) has become a focus of many reproductive studies recently due to its long-life menopause-like symptoms in young women. It may affect up to three of a hundred women under 40 years. The possible causes include genetic diseases, infections, autoimmune disorders and iatrogenic events such as radiotherapy and chemotherapy. Recent studies investigating the regenerative dynamic potential of the ovaries demonstrate that follicular growth could be stimulated when an adequate ovarian environment is restored. This restoration can be achieved employing factors of known regenerative potential such as stem cells, or growth factors of platelet rich plasma (PRP), artificial ovary, ovarian transplantation, and mitochondrial replacement therapy. The emergence of autologous platelet-rich plasma (PRP) therapy reflects a break-through for POI patients, since the approach is the most ethical-friendly, the cheapest, the least invasive and limited adverse effects. Therefore, it has the highest potential to be applied in clinical routine practice. Nevertheless, the complex mechanism of PRP components’ on the ovary, especially in term of folliculogenesis, remains to be deciphered. Furthermore, it is necessary to clarify to what extent they impact the gene or protein targets that play important role in ovarian rejuvenation after POI. We report raw fastq data of Sprague Dawley rat models of POI in four treatment groups and one control to evaluate the effect of intraovarian injection of PRP on POI rat models. This report is a part of animal study regarding the effect of intraovarian injection of PRP on ovarian function recovery in POI rat models (unpublished study). The data collected from this study will be used to investigate how PRP induce the ovarian rejuvenation and to analyse transcriptomic changes after PRP treatment on chemotherapy-induced POI animal models.
Project description:Microarray analysis of HT-29 cells co-cultured with tumor necrosis factor (TNF-a) in the presence or absence of polymeric formula as used for Exclusive Enteral Nutrition (EEN) therapy. Results provide insights into the molecular mechanisms underlying the anti-inflammatory effect of polymeric formula on intestinal epithelium.
Project description:Advanced ovarian cancer is the most lethal gynecologic malignancy in the United States. Ovarian cancer cells are known to have diminished response to TGF-beta, but it remains unclear whether TGF-beta can modulate ovarian cancer cell growth in an indirect manner through cancer-associated fibroblasts (CAFs). Using transcriptome profiling analyses on TGF-beta-treated ovarian fibroblasts, we identified a TGF-beta-responsive gene signature in ovarian fibroblasts. Identifying TGF-beta-regulated genes in the ovarian microenvironment helps in understanding the role of TGF-beta in ovarian cancer progression.
Project description:Microarray analysis of HT-29 cells co-cultured with tumor necrosis factor (TNF-a) in the presence or absence of polymeric formula as used for Exclusive Enteral Nutrition (EEN) therapy. Results provide insights into the molecular mechanisms underlying the anti-inflammatory effect of polymeric formula on intestinal epithelium. Total RNA obtained from 9 samples of HT-29 cells. Six samples were treated with TNF-a in the presence (3 samples) or absence (3 samples) of Polymeric Formula. Three samples were untreated and used as a control.
Project description:Polycystic ovarian syndrome (PCOS) is an endocrine disorder of the reproductive and metabolic axis in women during the reproductive age. In this study, we used a rat model exhibiting reproductive and metabolic abnormalities similar to human PCOS to unravel the molecular mechanisms underlining this complex syndrome.
Project description:Major risk factors for necrotizing enterocolitis (NEC) are formula feeding and prematurity, however, their pathogenic mechanisms are unknown. We found that insufficient arginine/nitric oxide synthesis limits blood flow in the intestinal microvasculature, leading to hypoxia, mucosa damage and NEC in the premature intestine after formula feeding. Formula feeding led to increased intestinal hypoxia in pups at postnatal day 1(P1) and P5, but not in more mature pups at P9. Accordingly, blood flow in the intestinal microvasculature increased after formula feeding only in P9 pups. mRNA profiling revealed that regulators of arginine/nitric oxide synthesis are at higher levels in endothelial cells of the intestine of P9 than P1 pups. Importantly, arginine supplementation increased intestinal microvasculature blood flow, and prevented NEC, whereas an arginine antagonist exacerbated NEC. Our results suggest that balancing intestinal oxygen demand and supply in the premature intestine by modulating arginine/nitric oxide could be used to prevent NEC.