Unidentified
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA605946 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11070300_1.fastq.gz | Fastqsanger.gz | |||
| SRR11070300_2.fastq.gz | Fastqsanger.gz | |||
| SRR11070301_1.fastq.gz | Fastqsanger.gz | |||
| SRR11070301_2.fastq.gz | Fastqsanger.gz | |||
| SRR11070302_1.fastq.gz | Fastqsanger.gz |
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Project description:To determine te lncRNA expression profile in collagen-induced arthritis rats and normal rats, we uesed lncRNA microArray analysis form Arraystar to examine the expression of lncRNAs in CIA and normal rats' synovial tissues.
2022-11-16 | GSE206097 | GEO
Project description:Liver fibrosis (LF), driven primarily by activated hepatic stellate cells (aHSCs), progresses to life-threatening end-stage diseases such as cirrhosis, hepatocellular carcinoma. As the only effective treatment, liver transplantation remains limited by donor scarcity. While mesenchymal stem cells (MSCs) exert anti-fibrotic effects via immunomodulation, autophagy regulation, and tissue regeneration, their clinical application is hindered by poor survival, short residence time, and inefficient homing after systemic administration. Recent advances indicate that 3D MSCs spheroids enhance cell viability and paracrine function compared to monodispersed cells. Human umbilical cord MSCs (HUMSCs) are ideal due to low immunogenicity and minimal ethical concerns. Injectable decellularized extracellular matrix (dECM) hydrogels, particularly liver-derived ECM (LdECM), offer a bioactive microenvironment to support cell retention and sustained release.HUMSCs spheroids (HUMSCs sph) were engineered using AggreWell™ plates. An injectable hydrogel was fabricated from decellularized Sprague-Dawley (SD) rat liver scaffolds (LdECM). A novel therapeutic strategy for LF was developed by encapsulating HUMSCs sph within LdECM hydrogels. The structure and characteristics of HUMSCs sph/sus and LdECM were assessed. The efficacy of localized high-density HUMSCs sph delivery was evaluated in a C57BL/6 mouse model of bile duct ligation/carbon tetrachloride (BDL/CCL4)-induced LF, comparing outcomes against equivalent doses of HUMSCs suspension (HUMSCs sus). HSCs autophagy and activation were detected while co-cultured with HUMSCs sph/sus.
2025-12-31 | GSE311083 | GEO
Project description:The inflammation of articular cartilage in RA is caused by pro-inflammatory factors secreted by the synovium. However, a recent study has shown that chondrocytes in RA patients can spontaneously secrete pro-inflammatory cytokines and MMPs, which undoubtedly provided new thinking for the treatment of RA diseases. We built a CIA model in rats, took the knee cartilage for single-cell sequencing, and sought to verify whether the contribution of chondrocytes to the inflammatory response in CIA rats was consistent with that of cartilage in RA patients. Our present work is the first to show the genome-wide gene expression of CIA rats cartilage and its assciation with chondrocytes in inflammation response by single-cell RNA sequencing. It was the first time to verify that cartilage destruction in RA disease was involved in the spontaneous inflammation of chondrocytes through CIA model animals. Moreover, the specific pro-inflammatory response cell subtypes have also been identified, which was marked as effector chondrocytes (EC) in the CIA rats cartilage. This not only proved that the cartilage of the CIA rat model can well simulate the inflammatory manifestations of RA patients in vitro, but also provided detailed and complete genomic data for the future study of RA cartilage in vitro.
2025-12-31 | GSE230500 | GEO
Project description:Wound healing is a complex process regulated by various cell types and a plethora of mediators. While interactions between wounded skin and the hair follicles (HFs) could induce HF neogenesis or promote wound healing, it remains unknown whether the wound healing-associated signaling milieu can be manipulated to protect against alopecia, such as chemotherapy-induced alopecia (CIA). Utilizing a well-established neonatal rat model of CIA, we show here that skin wounding protects from alopecia caused by several clinically relevant chemotherapeutic regimens, and that protection is dependent on the time of wounding and hair cycle stage. Gene expression profiling unveiled a significant increase in interleukin-1 beta (IL-1β) mediated signaling by skin wounding. Subsequently, we showed that IL-1β is sufficient and indispensable for mediating the CIA-protective effect. Administration of IL-1β alone to unwounded rats exhibited local CIA protection while IL-1β neutralization abrogated CIA protection by wounding. Mechanistically, IL-1β retarded postnatal HF morphogenesis, making HFs at the wound sites or IL-1β treated areas damage-resistant while the rats developed total alopecia elsewhere. We conclude that wound healing switches the cutaneous cytokine milieu to an IL-1β-dominated state thus retarding HF growth progression and rendering the HFs resistant to chemotherapy agents. In the future, manipulation of HF progression through interfering with the IL-1β signaling milieu may provide therapeutic benefits to a variety of conditions, from prevention of CIA to inhibition of hair growth and treatment of hirsutism. In this experiment, we used the Rat MI-Ready array comprised of over 34,000 transcript probes for gene and alternative splice products in ENSEMBL release 37 to profile gene expression changes during acute wound healing in rat skin. 16,198 Selected rat probes were above threshold in at least one group. 3,239 significant genes were found (FDR < 0.1).
2017-06-29 | GSE98105 | GEO
Project description:Aim: Synovial fibroblasts (SFs) undergo a rewiring of their DNA methylation landscape that is associated with their development of an aggressive pathogenic phenotype during Rheumatoid Arthritis (RA), both in humans and in CIA, a mouse model of this chronic inflammatory disease. The helminth-derived immunomodulator, ES-62 acts to prevent joint destruction in CIA by suppressing pathogenic SF responses. We therefore investigated whether ES-62 suppressed the changes in DNA methylation observed in SFs from CIA, relative to those from healthy, mice. Methods: The DNA methylation status of SFs from naïve (no induction of CIA), CIA and ES-62-treated mice undergoing CIA (CIA_ES-62) was compared by Reduced Representation Bilsulphite Sequencing (RRBS) analysis performed by the Active Motif service. Results: Synovial fibroblasts from naive, CIA and CIA_ES-62 mice exhibit differential genomic methylation profiles. Conclusion: ES-62 protection against joint protection in CIA is not associated with prevention of the changes in DNA methylation occurring during rewiring of naive SFs to aggressively pathogenic CIA SFs but rather, reflects generation of a distinct ES-62 phenotype of SF genomic methylation.
2021-03-01 | GSE158185 | GEO
Project description:Transitional Gene Expression Profiling of Ovarian Follicle in Rats Treated with Indomethacin and RU486 (CBX258)
| PRJDB20139 | ENA
Project description:Pathological bone changes differ considerably between inflammatory arthritic diseases, and most studies have focused on bone erosion. Collagen Induced Arthritis (CIA) is a model for Rheumatoid Arthritis, which, in addition to bone erosion, demonstrates bone formation at the time for clinical manifestations. The objective of this study was to use the CIA model to study bone remodelling by performing a gene expression profiling time-course study on the CIA model.
2015-03-01 | GSE61140 | GEO
Project description:Chemotherapy-induced hair loss (alopecia; CIA) is a highly distressing adverse effect that many cancer patients endure. Yet the molecular pathobiology of CIA remains largely unknown. We analysis the changes of mRNA profiles at different time points after cyclophosphamide treatment using Next-generation Sequencing in a mouse model of CIA. Our result revealed that Shh signaling is an evolutionarily conserved key target in CIA pathobiology.
2018-08-29 | GSE119118 | GEO