Methanobrevibacter mediated accumulation of L-3-aminoisobutyrate alleviates mastitis via the HSPA1B-p65 signaling pathway
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ABSTRACT:
ORGANISM(S): Bos Taurus
SUBMITTER: 
Yulin Chen
PROVIDER: PXD068458 | iProX | Tue Sep 16 00:00:00 GMT+01:00 2025
REPOSITORIES: iProX
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Project description:The mammary gland redeveloped to the pre-pregnancy state during involution, which shows that the mammary cells have the characteristics of remodeling. The rapidity and degree of mammary gland involution are different between mice and dairy livestock (dairy cows and dairy goats). However, the molecular genetic mechanism of involution and remodeling of goat mammary gland has not yet been clarified. Therefore, this study carried out the RNA-sequencing of nonlactating mammary gland tissue of dairy goats in order to reveal the transcriptome characteristics of nonlactating mammary tissues and clarify the molecular genetic mechanism of mammary cell involution and remodeling.
2021-10-22 | GSE185981 | GEO
Project description:ObjectiveTo reveal the molecular mechanism of the antagonistic effect of traditional Chinese medicine Tianma formula (TF) on dementia including vascular dementia (VaD) and Alzheimer's disease (AD) and to provide a scientific basis for the study of traditional Chinese medicine for prevention and treatment of dementia.MethodThe TF was derived from the concerted application of traditional Chinese medicine. We detected the pharmacological effect of TF in VaD rats. The molecular mechanism of TF was examined by APP/PS1 mice in vivo, Caenorhabditis elegans (C. elegans) in vitro, ELISA, pathological assay via HE staining, and transcriptome. Based on RNA-seq analysis in VaD rats, the differentially expressed genes (DEGs) were identified and then verified by quantitative PCR (qPCR) and ELISA. The molecular mechanisms of TF on dementia were further confirmed by network pharmacology and molecular docking finally.ResultsThe Morris water maze showed that TF could improve the cognitive memory function of the VaD rats. The ELISA and histological analysis suggested that TF could protect the hippocampus via reducing tau and IL-6 levels and increasing SYN expression. Meanwhile, it could protect the neurological function by alleviating Aβ deposition in APP/PS1 mice and C. elegans. In the RNA-seq analysis, 3 sphingolipid metabolism pathway-related genes, ADORA3, FCER1G, and ACER2, and another 5 nerve-related genes in 45 key DEGs were identified, so it indicated that the protection mechanism of TF was mainly associated with the sphingolipid metabolism pathway. In the qPCR assay, compared with the model group, the mRNA expressions of the 8 genes mentioned above were upregulated, and these results were consistent with RNA-seq. The protein and mRNA levels of ACER2 were also upregulated. Also, the results of network pharmacology analysis and molecular docking were consistent with those of RNA-seq analysis.ConclusionTF alleviates dementia by reducing Aβ deposition via the ACER2-mediated sphingolipid signaling pathway.
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Project description:The mammary gland redeveloped to the pre-pregnancy state during involution, which shows that the mammary cells have the characteristics of remodeling. The rapidity and degree of mammary gland involution are different between mice and dairy livestock (dairy cows and dairy goats). However, the molecular genetic mechanism of miRNA in involution and remodeling of goat mammary gland has not yet been clarified. Therefore, this study carried out the RNA-sequencing of nonlactating mammary gland tissue of dairy goats in order to reveal the transcriptome characteristics of miRNA in nonlactating mammary tissues and clarify the molecular genetic mechanism of miRNA in mammary cell involution and remodeling.
2023-10-01 | GSE243232 | GEO
Project description:Staphylococcus aureus is recognized worldwide as a major pathogen causing clinical or subclinical intramammary infections in all the dairy species (sheep, goats and cows). The present study was designed to comparatively investigate 65 S. aureus isolates recovered from dairy sheep and S. aureus suclinical mastitis from cows (n=21) and goats (n=22), for the presence of 190 putative virulence determinants with a single-dye DNA microarray and PCR. The probes (65 mer) were mainly designed from the S. aureus Mu50. The extracted DNA of each strain was labelled with Cy5. The microarray results were validated with PCR.The genomic comparative study with the DNA microarrays showed lineage and species specificity genes leading to the host-specific pathogenic traits of S. aureus in dairy species.
2008-07-01 | E-TABM-288 | biostudies-arrayexpress
Project description:Hepatic ischemia-reperfusion injury (IRI) is a common complication occurs during hepatic resection and transplantation. However, the mechanisms underlying hepatic IRI have not been fully elucidated. Here, we aim to explore the role of fibroblast growth factor 18 (FGF18) in hepatic IRI. In this work, we find that Hepatic stellate cells (HSCs) secrete FGF18 and alleviates hepatocytes injury. HSCs-specific FGF18 deletion largely aggravates hepatic IRI. Mechanistically, FGF18 treatment reduces the levels of ubiquitin carboxyl-terminal hydrolase 16 (USP16), leading to increased ubiquitination levels of Kelch Like ECH Associated Protein 1 (KEAP1) and the activation of nuclear factor erythroid 2-related factor 2 (Nrf2). Furthermore, USP16 interacts and deubiquitinates KEAP1. More importantly, Nrf2 directly binds to the promoter of USP16 and forms a negative feedback loop with USP16. Collectively, our results show FGF18 alleviates hepatic IRI by USP16/KEAP1/Nrf2 signaling pathway in male mice, suggesting that FGF18 represents a promising therapeutic approach for hepatic IRI.
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Project description:BackgroundIdiopathic pulmonary fibrosis (IPF) is a chronically progressive fibrotic pulmonary disease characterized by an uncertain etiology, a poor prognosis, and a paucity of efficacious treatment options. Dexmedetomidine (Dex), an anesthetic-sparing alpha-2 adrenoceptor (α2AR) agonist, plays a crucial role in organ injury and fibrosis. However, the underlying mechanisms of IPF remain unknown.MethodsIn our study, the role of Dex in murine pulmonary fibrosis models was determined by Dex injection intraperitoneally in vivo. Fibroblast activation and myofibroblast differentiation were assessed after Dex treatment in vitro. The activation of MAPK pathway and the expression of Adenosine A2B receptor (ADORA2B) were examined in lung myofibroblasts. Moreover, the role of ADORA2B in Dex suppressing myofibroblast differentiation and pulmonary fibrosis was determined using the ADORA2B agonist BAY60-6583.ResultsThe results revealed that Dex could inhibit Bleo-induced pulmonary fibrosis in mice. In vitro studies revealed that Dex suppressed TGF-β-mediated MAPK pathway activation and myofibroblast differentiation. Furthermore, Dex inhibits myofibroblast differentiation and pulmonary fibrosis via downregulating ADORA2B expression.ConclusionsOur findings suggest Dex as a potential therapeutic agent for pulmonary fibrosis. Dex may alleviate lung fibrosis and myofibroblast differentiation through the ADORA2B-mediated MAPK signaling pathway.
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Project description:This study explored the mechanism by which metformin (Met) inhibits osteoclast activation and determined its effects on osteoarthritis (OA) mice. Bone marrow-derived macrophages were isolated. Osteoclastogenesis was detected using tartrate-resistant acid phosphatase (TRAP) staining. Cell proliferation was evaluated using CCK-8, F-actin rings were detected by immunofluorescence staining, and bone resorption was detected using bone slices. Nuclear factor kappa-B (NF-κB) and nuclear factor of activated T-cell cytoplasmic 1 (NFATc1) were detected using luciferase assays, and the adenosine monophosphate-activated protein kinase (AMPK), NF-κB, and mitogen-activated protein kinase (MAPK) signaling pathways were detected using western blotting. Finally, expression of genes involved in osteoclastogenesis was measured using quantitative polymerase chain reaction. A knee OA mouse model was established by destabilization of the medial meniscus (DMM). Male C57BL/6J mice were assigned to sham-operated, DMM+vehicle, and DMM+Met groups. Met (100 mg/kg/d) or vehicle was administered from the first day postoperative until sacrifice. At 4- and 8-week post OA induction, micro-computed tomography was performed to analyze microstructural changes in the subchondral bone, hematoxylin and eosin staining and Safranin-O/Fast Green staining were performed to evaluate the degenerated cartilage, TRAP-stained osteoclasts were enumerated, and receptor activator of nuclear factor κB ligand (RANKL), AMPK, and NF-κB were detected using immunohistochemistry. BMM proliferation was not affected by Met treatment below 2 mM. Met inhibited osteoclast formation and bone resorption in a dose-dependent manner in vitro. Met suppressed RANKL-induced activation of p-AMPK, NF-κB, phosphorylated extracellular regulated protein kinases (p-ERK) and up-regulation of genes involved in osteoclastogenesis. Met reversed decreases in BV/TV, Tb.Th, Tb.N, and CD, and an increase in Tb.Sp at 4 weeks postoperatively. The number of osteoclasts and OARSI score were decreased by Met without effect on body weight or blood glucose levels. Met inhibited RANKL, p-AMPK, and NF-κB expression in early OA. The mechanism by which Met inhibits osteoclast activation may be associated with AMPK/NF-κB/ERK signaling pathway, indicating a novel strategy for OA treatment.
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Project description:Diabetes could directly induce cardiac injury, leading to cardiomyopathy. However, treatment strategies for diabetic cardiomyopathy remain limited. ZNF593-AS knockout and cardiomyocyte-specific transgenic mice were constructed. In addition, high-fat diet (HFD)-induced diabetic mouse model and db/db mice, another classic diabetic mouse model, were employed. ZNF593-AS was silenced using GapmeR, a modified antisense oligonucleotide, while overexpressed using a recombinant adeno-associated virus serotype 9-mediated gene delivery system. Transcriptome sequencing, RNA pull-down assays, and RNA immunoprecipitation assays were also performed to investigate the underlying mechanisms. ZNF593-AS expression was decreased in diabetic hearts. ZNF593-AS attenuated the palmitic acid-induced apoptosis of cardiomyocytes in vitro. In HFD-induced diabetic mice, ZNF593-AS deletion aggravated cardiac dysfunction and enhanced cardiac apoptosis and inflammation. In contrast, HFD-induced cardiac dysfunction was improved in ZNF593-AS transgenic mice. Consistently, ZNF593-AS exerted the same cardioprotective effects in db/db mice. Mechanistically, ZNF593-AS directly interacted with the functional domain of interferon regulatory factor 3 (IRF3), and suppressed fatty acid-induced phosphorylation and activation of IRF3, contributing to the amelioration of cardiac cell death and inflammation. In conclusion, our results identified the protective role of ZNF593-AS in diabetic cardiomyopathy, suggesting a novel potential therapeutic target.
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Project description:Five healthy Laoshan dairy goats (four years old, third lactation) from Qingdao Laoshan dairy goat primary farm (Shandong Province, China) were used. The mammary gland samples were collected surgically after general anaesthesia using Xylazine Hydrochloride injection solution (Huamu Animal Health Products Co., Ltd. China) at corresponding lactation stage, including early, peak and late lactations.
2020-02-22 | GSE135930 | GEO
Project description:BackgroundDepression is one of the most common psychiatric disorders worldwide. Many antidepressant drugs are only effective for specific patients and their long-term use can lead to treatment resistance. There is an ongoing need for more effective antidepressant treatments.MethodsThe rats were exposed to chronic unpredictable mild stress (CUMS) to induce depression model. The glutamate level in the hippocampus was determined by high performance liquid chromatography (HPLC). Protein levels in the tissues were measured using western blotting. The fluid consumption test was performed to evaluate potential anhedonia. Open field test was conducted to evaluate locomotor activity. Forced swimming test was used to evaluate susceptibility to negative mood.ResultsIn the present study, the depressive-like behaviors induced by CUMS were alleviated in rats by treatments with Herba Rhodiolae (0.04 g/kg, 1 mL), venlafaxine (0.035 g/kg, 1 mL), and combination of Herba Rhodiolae and glycogen synthase kinase 3 beta (GSK-3β) inhibitor (10 µM, 1 mL). Among these treatments, the combination of Herba Rhodiolae and GSK-3β inhibitor was most effective. Abnormalities in the glutamate system and autophagy of the brain were decreased greatly in Herba Rhodiolae and GSK-3β inhibitor-treated CUMS rats. Herba Rhodiolae was more effective in promoting the brain derived neurotrophic factor/tropomyosin receptor kinase B (BDNF/TrkB) signaling. The expression of GSK-3β was remarkably suppressed by the GSK-3β inhibitor.ConclusionsThese findings indicated that the combined effects of Herba Rhodiolae and GSK-3β inhibitor contributed to the activation of BDNF/TrkB-GSK-3β signaling pathway.
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