Ontology highlight
ABSTRACT:
PROVIDER: PRJNA905476 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22411706.fastq.gz | Fastqsanger.gz | |||
| SRR22411707.fastq.gz | Fastqsanger.gz | |||
| SRR22411708.fastq.gz | Fastqsanger.gz | |||
| SRR22411709.fastq.gz | Fastqsanger.gz | |||
| SRR22411710.fastq.gz | Fastqsanger.gz |
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Project description:Scars are a heterogeneous disease including normotrophic scars, hypertrophic scars, and keloids. Of these lesions, keloids are a distinct subtype from any other type of scar because clinically, it causes pain, itching, or tenderness, causing life discomfort and characteristically irreversible. Therefore, for accurate diagnosis and treatment of keloids, it is essential to identify keloid-specific genes. However, in previous studies, keloids were compared with controls such as scar-free normal skin. In these studies, general scar-related genes were likely to be chosen rather than keloid-specific genes. In this study, we acquired transcriptomic profiles of normotrophic scars, hypertrophic scars, and keloids from formalin-fixed paraffin-embedded human skin samples using high-throughput RNA-sequencing techniques. We compared the transcriptome profile of keloids with those of other scar lesions to select for highly accurate keloid-specific genes and pathways. The results revealed that genes related with several biological processes such as sensory/visual perception are upregulated strongly in keloids, whereas genes related with activation of immune response were downregulated remarkably in keloids. Furthermore, the biological process of extracellular matrix organization was highlighted in both hypertrophic scars and keloids. In conclusion, our study provides insight into the pathogenesis of keloids distinct from other scar lesions as well as potential keloid-specific biomarkers.
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Project description:Primary outcome(s): The clinical significance of immune and gene-expression profile in colorectal cancer
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Project description:Keloids are scar tissue that can develop under tensile stress and manifest the tactile itch called alloknesis due to the heterogeneous course. But the molecular and cellular mechanisms underlying the pathology of keloid have been still unknown. Here, we found that unique fibroblast subpopulation that have dense-core granules with enhanced expression of PIEZO2 in the dermal layer of keloid tissue with alloknesis, a pressure-tactile itch. PIEZO2-expressed fibroblasts showed enhanced expression of COL1A1, COL1A2 and COL3A1. Gene expression profile analysis of fibrous disease tissues could distinguish the keloid cases by higher PIEZO2, which correlated with collagen COL1A1, COL1A2, and COL3A1 gene expression, not only from the keloid cases with lower PIEZO2 expression but also from the lymphedema cases where massive fibroblast proliferation appears. Notably, patients with the keloid accompanied by higher expression of PIEZO2 showed a significantly shorter time to recurrence after keloidectomy in patients with the keloids (4/5 vs. 0/5, p = 0.047). Thus, a unique subset of PIEZO2-positive fibroblasts may be involved in a keloid pathology and be a potent therapeutic target for the intractable keloids.
2025-06-20 | GSE266338 | GEO
Project description:Keloids are scar tissue that can develop under tensile stress and manifest the tactile itch called alloknesis due to the heterogeneous course. But the molecular and cellular mechanisms underlying the pathology of keloid have been still unknown. Here, we found that unique fibroblast subpopulation that have dense-core granules with enhanced expression of PIEZO2 in the dermal layer of keloid tissue with alloknesis, a pressure-tactile itch. PIEZO2-expressed fibroblasts showed enhanced expression of COL1A1, COL1A2 and COL3A1. Gene expression profile analysis of fibrous disease tissues could distinguish the keloid cases by higher PIEZO2, which correlated with collagen COL1A1, COL1A2, and COL3A1 gene expression, not only from the keloid cases with lower PIEZO2 expression but also from the lymphedema cases where massive fibroblast proliferation appears. Notably, patients with the keloid accompanied by higher expression of PIEZO2 showed a significantly shorter time to recurrence after keloidectomy in patients with the keloids (4/5 vs. 0/5, p = 0.047). Thus, a unique subset of PIEZO2-positive fibroblasts may be involved in a keloid pathology and be a potent therapeutic target for the intractable keloids.
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Project description:Keloids are characterized by abnormal wound healing with excessive accumulation of extracellular matrix. Myofibroblasts are the primary contributor to extracellular matrix secretion, playing an essential role in the wound healing process. However, the differences between myofibroblasts involved in keloid formation and normal wound healing remain unclear. To identify the specific characteristics of keloid myofibroblasts, we initially assessed the expression levels of well-established myofibroblast markers, α-smooth muscle actin (α-SMA) and transgelin (TAGLN), in scar and keloid tissues (n = 63 and 51, respectively). The objective was to evaluate the enrichment of myofibroblasts in these tissues. Although myofibroblasts were present in significant quantities in keloids and immature scars, they were absent in mature scars. Next, we conducted RNA sequencing using myofibroblast-rich areas from keloids and immature scars to investigate the difference in RNA expression profiles among myofibroblasts. Comparison of the results with publicly available RNA-sequencing datasets revealed that 112 genes were significantly upregulated and 108 genes were downregulated in keloid samples compared with immature scar samples. Among them, KN motif and ankyrin repeat domains 4 (KANK4) was identified as a specifically upregulated gene in keloids. Immunohistochemical analysis showed that KANK4 protein was expressed in myofibroblasts in keloid tissues; however, it was not expressed in any myofibroblasts in immature scar tissues. There are two main isoforms of KANK4 transcripts, with short isoforms being dominantly expressed in keloid tissue. Overexpression of the short isoform of KANK4 enhanced cell mobility in keloid myofibroblasts. Our results suggest that the KANK4-mediated increase in myofibroblast mobility contributes to keloid pathogenesis.
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Project description:Background: The pathophysiology of keloid formation is not yet understood, so the identification of biomarkers for kelod can be one step towards designing new targeting therapies which will improve outcomes for patients with keloids or at risk of developing keloids. Methods: In this study, we performed single-cell RNA sequencing analysis, weighted co-expression network analysis, and differential expression analysis of keloids based on public databases. And 3 RNA sequencing data from keloid patients in our center were used for validation. Besides, we performed QRT-PCR on keloid tissue and adjacent normal tissues from 16 patients for further verification. Results: We identified the sensitive biomarker of keloid: Tenascin-C (TNC). Then, Pseudotime analysis found that the expression level of TNC decreased first, then stabilized and finally increased with fibroblast differentiation, suggesting that TNC may play an potential role in fibroblast differentiation. In addition, there were differences in the infiltration level of macrophages M0 between the TNC-high group and the TNC-low group. Macrophages M0 had a higher infiltration level in low TNC- group (P<0.05). Conclusion: Our results can provide a new idea for the diagnosis and treatment of keloid.
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