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| Status |
Public on Nov 26, 2007 |
| Title |
Gene profiling of keloid fibroblasts shows altered expression in multiple fibrosis-associated pathways |
| Organism |
Homo sapiens |
| Experiment type |
Expression profiling by array
|
| Summary |
Keloids are benign tumors of the dermis that form during a protracted wound healing process. Susceptibility to keloid formation occurs predominantly in people of African and Asian descent. The key alteration(s) responsible for keloid formation has not been identified and there is no satisfactory treatment for this disorder. The altered regulatory mechanism is limited to dermal wound healing, although several diseases characterized by an exaggerated response to injury are prevalent in individuals of African ancestry. We have observed a complex pattern of phenotypic differences in keloid fibroblasts grown in standard culture medium or induced by hydrocortisone. In this study Affymetrix-based microarray was performed on RNA obtained from fibroblasts cultured from normal scars and keloids grown in the absence and presence of hydrocortisone. We observed differential regulation of approximately 500 genes of the 38,000 represented on the Affymetrix chip. Of particular interest was increased expression of several IGF-binding and IGF-binding related proteins and decreased expression of a subset of Wnt pathway inhibitors and multiple IL-1-inducible genes. Increased expression of CTGF and IGFBP-3 was observed in keloid fibroblasts only in the presence of hydrocortisone. These findings support a role for multiple fibrosis-related pathways in the pathogenesis of keloids
Keywords: cell-type comparison, drug treatment comparison
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| Overall design |
Cell cultures were initiated from human biopsy material from normal dermal scars and keloids of adult males and females. Experimental cultures were derived from the first passage of cells thawed from liquid nitrogen. Cultures of fibroblasts from samples were grown with or without 1.5 micromolar hydrocortisone. RNA from each cell strain was isolated from three independent cell cultures and pooled, then run on an Affymetrix Human Genome U133 Plus 2.0 GeneChip.
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| Contributor(s) |
Smith J, Boone B, Opalenik S, Williams S, Russell S |
| Citation(s) |
17989729 |
| Submission date |
May 24, 2007 |
| Last update date |
Mar 25, 2019 |
| Contact name |
Shirley Brody Russell |
| E-mail(s) |
shirley.b.russell@vanderbilt.edu
|
| Phone |
615-343-5853
|
| Fax |
615-343-8619
|
| Organization name |
Vanderbilt University
|
| Department |
Medicine
|
| Street address |
519 Light Hall
|
| City |
Nashville |
| State/province |
TN |
| ZIP/Postal code |
37232-0700 |
| Country |
USA |
| |
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| Platforms (1) |
| GPL570 |
[HG-U133_Plus_2] Affymetrix Human Genome U133 Plus 2.0 Array |
|
| Samples (19)
|
| GSM194104 |
keloid treated with hydrocortisone-1 |
| GSM194105 |
keloid treated with hydrocortisone-2 |
| GSM194106 |
keloid treated with hydrocortisone-3 |
| GSM194107 |
keloid treated with hydrocortisone-4 |
| GSM194108 |
keloid treated with hydrocortisone-5 |
| GSM194109 |
keloid with no hydrocortisone treatment-1 |
| GSM194110 |
keloid with no hydrocortisone treatment-2 |
| GSM194111 |
keloid with no hydrocortisone treatment-3 |
| GSM194112 |
keloid with no hydrocortisone treatment-4 |
| GSM194113 |
keloid with no hydrocortisone treatment-5 |
| GSM194114 |
normal scar treated with hydrocortisone-1 |
| GSM194115 |
normal scar treated with hydrocortisone-2 |
| GSM194116 |
normal scar treated with hydrocortisone-3 |
| GSM194117 |
normal scar treated with hydrocortisone-4 |
| GSM194118 |
normal with no hydrocortisone treatment-1 |
| GSM194119 |
normal with no hydrocortisone treatment-2 |
| GSM194120 |
normal with no hydrocortisone treatment-3 |
| GSM194121 |
normal with no hydrocortisone treatment-4 |
| GSM194122 |
normal with no hydrocortisone treatment-5 |
|
| Relations |
| BioProject |
PRJNA99931 |
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