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Gene expression profile analysis on different stages of hypertrophic scarring in a rabbit ear model.

ABSTRACT: Hypertrophic scarring (HS) is one of the most common skin disorders. The study aimed to investigate the gene expression profile at day 10 (Stage 1), 21 (Stage 2), and day 40 (Stage 3) post-wounding of HS using RNA-sequencing of a scar model from rabbit ears. A total of 17,386 unigenes were annotated using the eggNOG Functional Category database. The study identified significantly differentially expressed genes (DEGs) including 261, 141, and 247 upregulated ones as well as 253, 272, and 58 downregulated ones in three stages respectively. The DEGs varies among each stage measured by Gene Ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. DEGs were enriched in 'immune system process' and 'proteinaceous extracellular matrix' in Stage 1, 'anatomical structure development', 'cell differentiation', 'cell adhesion'and some other terms in Stage 2, 'cancers', 'proteinaceous extracellular matrix' and 'signal transduction' in Stage 3. Furthermore, the Wnt signaling pathway was found to play a pivotal role in regression of HS. In conclusion, we revealed comprehensively the gene expression profiles during HS formation providing probable targets in HS treatment.

SUBMITTER: Zhu J

PROVIDER: S-EPMC7388309 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature

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Gene expression profile analysis on different stages of hypertrophic scarring in a rabbit ear model.

Zhu Ji J Sun Mengyan M Wang Yuchong Y Bi Hongda H Xue Chunyu C

Experimental and therapeutic medicine 20200611 2

Hypertrophic scarring (HS) is one of the most common skin disorders. The study aimed to investigate the gene expression profile at day 10 (Stage 1), 21 (Stage 2), and day 40 (Stage 3) post-wounding of HS using RNA-sequencing of a scar model from rabbit ears. A total of 17,386 unigenes were annotated using the eggNOG Functional Category database. The study identified significantly differentially expressed genes (DEGs) including 261, 141, and 247 upregulated ones as well as 253, 272, and 58 downre ...[more]

PMID: 32742383

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Project description:BackgroundHypertrophic scars cause impaired skin appearance and function, seriously affecting physical and mental health. Due to medical ethics and clinical accessibility, the collection of human scar specimens is frequently restricted, and the establishment of scar experimental animal models for scientific research is urgently needed. The four most commonly used animal models of hypertrophic scars have the following drawbacks: the rabbit ear model takes a long time to construct; the immunodeficient mouse hypertrophic scar model necessitates careful feeding and experimental operations; female Duroc pigs are expensive to purchase and maintain, and their large size makes it difficult to produce a significant number of models; and mouse scar models that rely on tension require special skin stretch devices, which are often damaged and shed, resulting in unstable model establishment. Our group overcame the shortcomings of previous scar animal models and created a new mouse model of hypertrophic scarring induced by suture anchoring at the wound edge.MethodsWe utilized suture anchoring of incisional wounds to impose directional tension throughout the healing process, restrain wound contraction, and generate granulation tissue, thus inducing scar formation. Dorsal paired incisions were generated in mice, with wound edges on the upper back sutured to the rib cage and the wound edges on the lower back relaxed as a control. Macroscopic manifestation, microscopic histological analysis, mRNA sequencing, bioinformatics, and in vitro cell assays were also conducted to verify the reliability of this method.ResultsCompared with those in relaxed controls, the fibrotic changes in stretched wounds were more profound. Histologically, the stretched scars were hypercellular, hypervascular, and hyperproliferative with disorganized extracellular matrix deposition, and displayed molecular hallmarks of hypertrophic fibrosis. In addition, the stretched scars exhibited transcriptional overlap with mechanically stretched scars, and human hypertrophic and keloid scars. Phosphatidylinositol 3-kinase-serine/threonine-protein kinase B signaling was implicated as a profibrotic mediator of apoptosis resistance under suture-induced tension.ConclusionsThis straightforward murine model successfully induces cardinal molecular and histological features of pathological hypertrophic scarring through localized suture tension to inhibit wound contraction. The model enables us to interrogate the mechanisms of tension-induced fibrosis and evaluate anti-scarring therapies.

Project description:BackgroundThe clinical pathologic stages (stage I, II, III-IV) of hepatocellular carcinoma (HCC) are closely linked to the clinical prognosis of patients. This study aims at investigating the gene expression and mutational profile in different clinical pathologic stages of HCC.MethodsBased on the TCGA-LIHC cohort, we utilized a series of analytical approaches, such as statistical analysis, random forest, decision tree, principal component analysis (PCA), to identify the differential gene expression and mutational profiles. The expression patterns of several targeting genes were also verified by analyzing the Chinese HLivH060PG02 HCC cohort, several GEO datasets, HPA database, and diethylnitrosamine-induced HCC mouse model.ResultsWe identified a series of targeting genes with copy number variation, which is statistically associated with gene expression. Non-synonymous mutations mainly existed in some genes (e.g.,TTN, TP53, CTNNB1). Nevertheless, no association between gene mutation frequency and pathologic stage distribution was detected. The random forest and decision tree modeling analysis data showed a group of genes related to different HCC pathologic stages, including GAS2L3 and SEMA3F. Additionally, our PCA data indicated several genes associated with different pathologic stages, including SNRPA and SNRPD2. Compared with adjacent normal tissues, we observed a highly expressed level of GAS2L3, SNRPA, and SNRPD2 (P = 0.002) genes in HCC tissues of our HLivH060PG02 cohort. We also detected the high expression pattern of GAS2L3, SEMA3F, SNRPA, and SNRPD2 in the datasets of GSE102079, GSE76427, GSE64041, GSE121248, GSE84005, and the qPCR assay using diethylnitrosamine-induced HCC mouse model. Moreover, SEMA3F and SNRPD2 protein were highly stained in the HCC tissues of the HPA database. The high expression level of these four genes was associated with the poor survival prognosis of HCC cases.ConclusionsOur study provides evidence regarding the gene expression and mutational profile in different clinical pathologic stages of TCGA HCC cases. Identifying four targeting genes, including GAS2L3, SNRPA, SNRPD2, and SEMA3F, offers insight into the molecular mechanisms associated with different prognoses of HCC.

Dataset Information

Gene expression profile analysis on different stages of hypertrophic scarring in a rabbit ear model.

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Gene expression profile analysis on different stages of hypertrophic scarring in a rabbit ear model.

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