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A transcriptional analysis of normotrophic scar and control fibroblasts

ABSTRACT: 3mm punch biopsies were taken from a healed normotrophic scar and a contralateral matched control site in burn patients with a scar at least 1 year old. Fibroblasts were cultured from explants to passage 2 and RNA was extracted and run on expression arrays to examine differences in scar and control fibroblast gene expression Normotrophic scar maintains its abnormal scar phenotype for the rest of the patients life, long after the injury has healed. Differences in gene expression may reaveal target genes that can be modulated to improve scar appearance

ORGANISM(S): Homo sapiens

PROVIDER: GSE136906 | GEO | 2019/09/06

REPOSITORIES: GEO

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A methylation analysis of human normotrophic scar dermal fibroblasts

Project description:3mm punch biopsies were taken from a healed normotrophic scar and a contralateral matched control site in burn patients with a scar at least 1 year old. Fibroblasts were cultured from explants to passage 2 and DNA was extracted and run on methylation arrays to examine differences in scar and control fibroblast gene expression Normotrophic scar maintains its abnormal scar phenotype for the rest of the patients life, long after the injury has healed. Differences in gene expression may reaveal target genes that can be modulated to improve scar appearance

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RNAseq analysis comparing siRNA knocked down FOXF2 in and MKX in human normotrophic scar dermal fibroblasts

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A transcriptional analysis of normotrophic scar and control fibroblasts

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A methylation analysis of human normotrophic scar dermal fibroblasts

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Microarray profiling analysis of microRNAs expression in Hypertrophic scar

Project description:Excessive repair after burn or trauma will lead to the formation of pathological scar. TGF-β1 is a powerful growth factor after wound healing. It is considered to be a key regulator of HS and various fibrotic diseases. MicroRNAs (miRNAs) can widely participate in the pathophysiological processes of various diseases by participating in post transcriptional gene regulation. At present, there is no research report on miR-361 and hypertrophic scar. This study found that miR-361 in HS is down-regulated. MiR-361 can inhibit the proliferation of HS fibroblasts and promote their apoptosis by inhibiting TGF-β1. Moreover, miR-361 can inhibit the formation of rabbit ear scar by inhibiting the expression of TGF-β1.

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Project description:The mammalian heart possesses a poor ability to regenerate after acute ischemic cardiac injury and lost cardiac muscle is replaced by scar tissue. Multiple clinical studies demonstrate that the size of scar tissue following myocardial infarction is an independent predictor of cardiovascular outcomes, yet little is known about factors that regulate the size of scar after ischemic cardiac injury. In this report, we demonstrate that collagen V, a fibrillar collagen and a minor constituent of heart scars regulates the size of heart scars after ischemic cardiac injury. Depletion of collagen V in heart scars in two independent animal models led to a significant and paradoxical increase in post infarction scar tissue size with worsening of heart function. A systems genetics approach analyzing genes versus traits across 100 in-bred strains of mice independently demonstrated that collagen V is a critical driver of post injury heart function. We show that collagen V deficiency alters the ultra-structure and mechanical properties of scar tissue that make it more vulnerable to expansion. There is altered reciprocal feedback between matrix and cells that induce expression of specific mechanosensitive integrins which drive fibroblast activation and increased ECM gene expression. Scar size increases. Administration of cilengitide, an inhibitor of specific integrins, completely rescues the phenotype of increased post injury scarring, myofibroblast formation and cardiac dysfunction in collagen V deficient mice. These observations demonstrate that collagen V, a structural constituent of heart scar tissue regulates scar size in an integrin dependent manner.

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Type V collagen in scar tissue regulates the size of scar after heart injury

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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:CNS injury results in chronic scar formation that interferes with function and inhibits repair. Extracellular matrix (ECM) is prominent in the scar and potently regulates cell behavior. However, comprehensive information about the ECM proteome is largely lacking, and region- as well as injury-specific differences are often not taken into account. These aspects are the focus of our perspective on injury and scar formation. To highlight the importance of such comprehensive proteome analysis we include data obtained with novel analysis tools of the ECM composition in the scar and show the contribution of monocytes to the ECM composition after traumatic brain injury (TBI). Monocyte invasion was reduced using the CCR2-/- mouse line and step-wise de-cellularization and proteomics allowed determining monocyte-dependent ECM composition and architecture of the glial scar. We find significant reduction in the ECM proteins Tgm1, Itih (1,2, and 3), and Ftl in the absence of monocyte invasion. We also describe the scar ECM comprising zones with distinctive composition and show a subacute signature upon comparison to proteome obtained at earlier times after TBI. These results are discussed in light of injury-, region- and time-specific regulation of scar formation highlighting the urgent need to differentiate injury conditions and CNS-regions using comprehensive ECM analysis.

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