Differential Gene Expression of Fibroblasts: Keloid versus Normal

Cohly, Hari H. P.; Heath, Scott; Ndebele, Kenneth; Jenkins, John K.; Angel, Michael

doi:10.3390/i3111162

Cited by 4 publications

(2 citation statements)

References 43 publications

(32 reference statements)

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“…It also plays a role in signal transduction. HSPB1 protects against ischemic and reoxygenationmediated injury and inhibits apoptosis induction [20]. Our experimental findings support the literature results.…”

Section: Discussionsupporting

confidence: 91%

Proteomic Analysis of Differential Protein Expression of Achilles Tendon in a Rabbit Model by Two-Dimensional Polyacrylamide Gel Electrophoresis at 21 Days Postoperation

Jielile

Jialili

Sabirhazi

et al. 2011

Appl Biochem Biotechnol

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Postoperative early kinesitherapy has been advocated as an optimal method for treating Achilles tendon rupture. However, an insight into the rationale of how early kinesitherapy contributes to healing of Achilles tendon remains to be achieved, and research in the area of proteomic analysis of Achilles tendon has so far been lacking. Forty-two rabbits were randomized into control group, immobilization group, and early motion group, and received postoperative cast immobilization and early motion treatments. Achilles tendon samples were prepared 21 days following microsurgery, and the proteins were separated with two-dimensional polyacrylamide gel electrophoresis. Differentially expressed proteins were first recognized by PDQuest software, and then identified using peptide mass fingerprinting, tandem mass spectrometry, and database searching. A total of 463 ± 12, 511 ± 39, and 513 ± 80 protein spots were successfully detected in the two-dimensional polyacrylamide gels for the Achilles tendon samples of rabbits in the control group, immobilization group, and early motion group, respectively. There were 15, 8, and 9 unique proteins in these three groups, respectively, and some differentially expressed proteins were also identified in each group. It was indicated that some of the differentially expressed proteins were involved in various metabolism pathways and may play an important role in healing of Achilles tendon rupture. Postoperative early kinesitherapy resulted in differentially expressed proteins in ruptured Achilles tendon compared with those treated with postoperative cast immobilization. These differentially expressed proteins may contribute to healing of Achilles tendon rupture through a mechanobiological mechanism due to the application of postoperative early kinesitherapy.

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Section: Discussionsupporting

confidence: 91%

Proteomic Analysis of Differential Protein Expression of Achilles Tendon in a Rabbit Model by Two-Dimensional Polyacrylamide Gel Electrophoresis at 21 Days Postoperation

Jielile

Jialili

Sabirhazi

et al. 2011

Appl Biochem Biotechnol

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“…Table 8.1). The specific genes and their differentially regulated expression may have direct implications toward understanding the keloid development [25].…”

Section: Gene Expressionmentioning

confidence: 99%

Genetics of Keloid Scarring

Sadiq¹,

Khumalo²

2020

Textbook on Scar Management

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Keloid disease is a benign fibro-proliferative reticular dermal tumor that develops in response to dysregulated cutaneous wound-healing process. The key alterations result in keloid formation have not been fully understood yet.Extensive literature review suggests that there is a strong genetic predisposition for keloid formation as keloid cases have appeared in twins, families, Asian and African descendant ethnic groups predominantly. Thus, there have been several attempts to investigate the genetic variations that may act as contributing factors in keloid pathogenesis, but no single genetic cause has been identified so far. Gene expression studies have shown highly variable results in linkage analysis of keloid families and in keloid fibroblasts. These findings provide clues that keloids arise from heterogeneous genetic events in coordination with immune-related components for example, the Major Histocompatibility Complex genes, consequently that may contributing towards dermal fibrosis. In addition, it is likely that multiple genetic and epigenetic factors are responsible for the development of the disease pathology. In summary, keloid disease is a disorder in which the exact genetic contribution to pathogenesis is yet to be elucidated. Understanding the genetic basis of keloid disease would help to identify targeted therapies as well as accurately assess individual genetic susceptibility to keloids, in order to provide a more personalized approach to their management.

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microRNA-7 down-regulation mediates excessive collagen expression in localized scleroderma

et al. 2012

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Localized scleroderma (LSc), a connective tissue disorder restricted to the skin and subcutaneous tissue, is characterized by skin fibrosis due to an excessive deposition of types I collagen. The mechanism of such fibrosis is still unknown, but epigenetics may play some roles in the excessive collagen expression. In the present study, we investigated the mechanism of fibrosis seen in LSc, focusing on microRNA (miRNA). miRNA expression was determined by PCR array, real-time PCR, and in situ hybridization. The function of miRNA was evaluated using specific inhibitor. Immunoblotting was performed to detect α2(I) collagen protein. PCR array analysis using tissue miRNA demonstrated miR-7 level was significantly decreased in LSc skin as well as keloid tissue compared to normal skin in vivo. In situ hybridization also showed miR-7 expression in dermal fibroblasts was decreased in LSc dermis. The transfection of specific inhibitor for miR-7 into cultured normal dermal fibroblasts resulted in the up-regulation of α2(I) collagen protein in vitro. Also, the serum levels of miR-7 were significantly decreased in LSc patients compared with healthy controls, but serum miR-29a levels not. Systemic or local down-regulation of miR-7 may contribute to the pathogenesis of LSc via the overexpression of α2(I) collagen, and serum miR-7 may be useful as a disease marker. Investigation of the regulatory mechanisms of LSc by miRNA may lead to new treatments by the transfection into the lesional skin of this disease.

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Differential Gene Expression of Fibroblasts: Keloid versus Normal

Cited by 4 publications

References 43 publications

Proteomic Analysis of Differential Protein Expression of Achilles Tendon in a Rabbit Model by Two-Dimensional Polyacrylamide Gel Electrophoresis at 21 Days Postoperation

Proteomic Analysis of Differential Protein Expression of Achilles Tendon in a Rabbit Model by Two-Dimensional Polyacrylamide Gel Electrophoresis at 21 Days Postoperation

Genetics of Keloid Scarring

microRNA-7 down-regulation mediates excessive collagen expression in localized scleroderma

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