Ji Li Similar Datasets
Project description:Background: Recent studies have shown that platelets actively contribute to most inflammatory reactions and neural signaling, yet the involvement of platelets in the cutaneous inflammation and pruritus in skin is largely unknown. Methods: Optogenetic platelet activation, platelet depletion, serotonin depletion and TRPV1+ neuron specific deletion of HTR2B were used to determine the functional relevance of platelets in cutaneous inflammation and itch. Results: Upon optogenetic stimulation, activated platelets were attracted to the inflamed lesion, which elicits erythema, edema and pruritus in mice. Then a characteristic transcriptomics of photostimulated lesion showed a pathogenetic resemblance to skin disorders, especially atopic dermatitis (AD). Platelet depletion alleviated scratching behaviors and skin pathology in AD, whereas platelet activation exacerbated both. Subsequently, depletion of serotonin (5-HT) released from platelets reduced the spontaneous scratching and cutaneous inflammation by C-fiber excitability and suppressing macrophage infiltration. For itch transmission, genetic approaches reveal that platelet-derived serotonin activates TRPV1⁺ pruriceptors through HTR2B receptors in AD. Conclusions: These data showed the sufficiency of platelet activation for cutaneous inflammation and itch, which uncovered a novel platelet-immune-neuron axis as a promising therapeutic target for AD and potentially other skin disorders.
2026-06-01 | GSE314731 | GEO
Project description:Background: Mechanical forces play a crucial role in regulating cellular communication during tissue repair, yet how mechanical stimulation modulates endothelial exosome secretion and their effects on fibroblast activation remains unclear. Methods: In this study, endothelial cells were incorporated into 3D bioprinted tissue-engineered dermal constructs and cultured under static or mechanically stretched conditions. Exosomes were isolated, characterized, and applied to human dermal fibroblasts to assess their influence on proliferation, migration, and extracellular matrix formation. Data-independent acquisition proteomics was performed to analyze exosomal protein cargo and associated signaling pathways. Results: Mechanical loading increased exosome secretion by approximately 2.5-fold without altering vesicle morphology. Functionally, mechanically stimulated exosomes significantly enhanced fibroblast migration and type I collagen synthesis compared with controls. Proteomic profiling identified 4,476 proteins, of which 677 were differentially expressed. Enrichment analysis revealed activation of VEGF, HIF-1, Relaxin, and AGE–RAGE pathways, implicating roles in angiogenesis, metabolic regulation, and extracellular matrix remodeling. Conclusion: These findings demonstrate that 3D mechanical stimulation not only augments the quantity of endothelial exosomes but also reshapes their molecular cargo, thereby enhancing biomechanical communication between endothelial cells and fibroblasts. Together with prior evidence of fibroblast-derived exosomes promoting endothelial angiogenesis, this study proposes a bidirectional “mechanical stimulation–exosome–communication–tissue reconstruction” loop, providing a theoretical foundation for optimizing exosome-based strategies in skin tissue engineering.
2025-12-25 | PXD072415 |
Project description:Transcriptomic studies of human tumor xenografts are complicated by the presence of murine cellular mRNA. As such, it is useful to know the extent to which mouse mRNA cross-hybridizes to any given array platform. In this study, murine cDNA samples from diverse sources were hybridized to Affymetrix Human Genome U133 Plus 2.0 Arrays. In this regard it is possible to identify specific probes that are potential targets of cross-species interference. Array data was generated for 5 different mouse cDNAs and 5 different human cDNAs hybridized to human Affymetrix U133 Plus 2 arrays [3 replicates for each biological sample]. Samples included A) mouse and B) human universal RNA (Strategene, La Jolla, CA), C) B16F10 murine melanoma tumor and D) skin from same model [C57BL/6 mice] E) COLON-26 murine tumor xenograft and F) skin from same model [Balb/C mice] G) NCI-H522 human lung carcinoma xenograft and H) skin from same model (nude mice) I) LOX-IMVI human melanoma xenograft and J) skin from same model (nude mice).
2013-07-31 | E-GEOD-49353 | biostudies-arrayexpress
Project description:We demonstrated that a visceral immunosuppressive tumor can influence a distant, normally-responsive tumor, located in the skin and rend it resistant to a particular immunotherapy. Examination of the transcriptome of sub-cutaneous tumors that were growing in a mouse model, in the presence or in the absence of a concomitant intra-kidney immunosuppressive tumor
2014-05-31 | E-GEOD-56905 | biostudies-arrayexpress
Project description:Immune checkpoint inhibitors (ICIs) targeting PD-1 and CTLA-4 are essential components of the cancer therapeutic armamentarium. The remarkable responses seen with ICIs however, are also accompanied by immune-related adverse events (irAEs). These inflammatory side-effects impact virtually all organ systems, with the most common being the skin and gastrointestinal tract. Here, we establish a mouse model of commensal bacteria-driven skin irAEs and demonstrate that immune checkpoint blockade aberrantly unleashes commensal-specific T cell responses. Such responses caused widespread immune cell infiltration and inflammation throughout the skin, recapitulating the skin irAEs seen in patients treated with ICIs. This skin inflammation was dependent on production of the cytokine IL-17 by commensal-specific T cells, which in turn induced hyperactive responses from macrophages and myeloid cells. Importantly, these responses had long-term consequences, with commensal-specific T cells elicited in the context of ICIs being highly sensitive to re-activation by commensals months later. Together, our results establish a mouse model of skin irAEs and show that immune checkpoint blockade can potentiate aberrant immunity to skin commensals with long-lasting consequences.
2022-06-20 | GSE176030 | GEO
Project description:The peritoneal cavity contains a large population of GATA6-expressing large peritoneal macrophages (LPMs), known to support healing of intra-abdominal organs. In this study, we aimed to explore their full sphere of influence by examining their ability to perform wound healing at distant sites outside the cavity. In a mouse model combining a remote skin injury with peritoneal stimulation we observed a significant acceleration of skin wound healing in response to LPM activation. Tracking GATA6-expressing LPMs, we demonstrated that LPMs do not migrate to distant wound sites following peritoneal activation. Using parabiosis experiments and administration of activated peritoneal contents indicated an important role of molecules secreted by LPMs in remote skin wound healing. More specifically, proteomic and transcriptomic analyses identified fibronectin as a key factor produced by activated LPMs. In facts, depletion of LPMs or genetic knockout of fibronectin in myeloid cells eliminated the enhanced healing effect. These findings highlight the endocrine function of LPMs in systemic tissue repair, challenging the traditional perspective of plasma fibronectin being exclusively liver-derived. Our results suggest that LPMs, strategically positioned in the peritoneal cavity, serve as a source of circulating fibronectin, promoting matrix formation and accelerating wound healing at distant sites.
2026-02-12 | PXD066819 | Pride
Project description:To test gene expression changes of human cancer cells and mouse surrounding tissue cells during tumor progression, 4 different types of cancer cells (MDA-MB231Br3, PC14Br4, KM12M, A375SM) were injected into mouse brain, skin and orthotopic sites. RNAs containing human cancer cells and mouse surrounding tissue cells were extracted and hybridized into human and mouse arrays at the same times and it revealed the brain microenvironment induced complete reprogramming of metasized cancer cells, resulting in a gain of neuronal cell characteristic , mimicking neurogenesis during development.
2011-09-24 | GSE19184 | GEO
Project description:Atopic dermatitis (AD) typically starts in infancy or early childhood, showing spontaneous remission in a subset of patients, while others develop lifelong disease. Despite an increased understanding of AD, factors guiding its natural course are only insufficiently elucidated. We thus performed suction blistering in skin of adult patients with stable, spontaneous remission from previous moderate-to-severe AD during childhood. Samples were compared to healthy controls without personal or familial history of atopy, and to chronic, active AD lesions. Skin cells and tissue fluid obtained were used for single-cell RNA sequencing and proteomic multiplex assays, respectively. We found overall cell composition and proteomic profiles of spontaneously healed AD to be comparable to healthy control skin, without upregulation of typical AD activity markers (e.g., IL13, S100As, and KRT16). Among all cell types in spontaneously healed AD, melanocytes harbored the largest numbers of differentially expressed genes in comparison to healthy controls, with upregulation of potentially anti-inflammatory markers such as PLA2G7. Conventional T-cells also showed increases in regulatory markers, and a general skewing toward a more Th1-like phenotype. By contrast, gene expression of regulatory T-cells and keratinocytes was essentially indistinguishable from healthy skin. Melanocytes and conventional T-cells might thus contribute a specific regulatory milieu in spontaneously healed AD skin.
2021-02-15 | GSE162054 | GEO
Project description:Interventions: Others : Comparison of postoperative outcome between conventional skin stapling and tissue adhesive (2-octyl cyanoacrylate) for skin closure in colorectal cancer
Primary outcome(s): comparison of postoperative outcome between conventional skin stapling and tissue adhesive for skin closure in colorectal cancer
Primary Purpose : Treatment, Intervention Model : Parallel, Blinding/Masking : , Blinding Target : , Allocation : RCT
| 2738215 | ecrin-mdr-crc
