Browsing by Subject "Keloid"
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Item Analysis of Association Between Keloids and Other Medical Conditions(2016-01-19) Rutherford, Audrey; Glass, Donald A., IIBACKGROUND: Keloids are an exaggerated response to cutaneous wound healing. Keloids negatively affect patients' quality of life and there is no 100% effective treatment to prevent occurrence or recurrence. Previous results from the Genetic Causes of Keloid Formation Study (GCKFS), an IRB-approved keloid registry, showed that hypertension and obesity may be more prevalent in African-Americans with keloids versus the general African-American population. This suggests that there are possible common mechanisms between keloids and these comorbidities. OBJECTIVE: The aim was to assess for an association between hypertension and/or obesity with keloid-affected patients, and to evaluate various subcategories of keloid-affected patients. METHODS: Seventy-nine GCKFS participants with diagnosed keloids were matched to controls from the Dallas Heart Study (at a 1 GCKFS:7 DHS ratio). Participants were categorized into hypertensive and obese cohorts using objective recorded measurements and calculations made using Fisher's exact test (significance P < 0.05). Sub-analyses were assessed among the GCKFS cohort using number of keloids, location, and number of anatomic sites involved. RESULTS: There were 504 total keloids distributed among six designated anatomical sites (ears, neck up, extremities, trunk, abdomen, other). Thirty (37.97%) GCKFS participants were hypertensive, and thirty-six (45.57%) were obese. The GCKFS participants showed an association with hypertension (p=0.045) but not with obesity (p=0.903). On subanalyses, keloid-affected individuals under age 30 had a higher prevalence of hypertension (p=0.042) and participants with multiple keloid sites had a higher prevalence of obesity (p=0.024). CONCLUSIONS: The results are consistent with hypertensive associations with keloids found in the literature. Data collection will continue by increasing the GCKFS cohort to determine if the trending data will reach statistical significance. Further research is encouraged to delve into the mechanisms between the association between hypertension and/or obesity and keloids.Item Upregulation of Cytokines Midkine and Pleiotrophin in Keloids(2020-01-21) Marella, Pooja; Tran, An; Glass, Donald A., IIKeloids are benign proliferative scars that are exaggerated responses to cutaneous wound healing. They can be painful and/or pruritic, and commonly affect the chest, upper back, shoulders, and earlobes. Keloids often affect skin of color; most keloid patients are of African, Hispanic, or Asian descent. Although keloids are heavily implicated in fibrosis, there remain gaps in our understanding of keloid pathogenesis and our elucidation of potential biomarkers. The goal of this project was to identify novel molecules upregulated in keloids in order to identify uncharacterized mechanisms underlying keloid pathogenesis. Matched sets of keloid tissue and perilesional normal tissue were obtained from three keloid patients recruited from the outpatient dermatology clinics of Parkland Hospital and UT Southwestern Medical Center. Whole transcriptome sequencing comparing keloid tissue to perilesional normal tissue showed 344 genes with differential expression across the three sample pairings. Of note were Midkine (MDK) and Pleiotrophin (PTN), which were upregulated 30 fold and 10 fold respectively. MDK and PTN are cytokine signaling molecules known to play a role in wound healing, mitogenicity, and inflammation. They are upregulated in several cancers, and higher expression generally indicates poor prognosis. Keloids have been implicated in cancer pathogenesis, and prior research has shown that human skin keloid fibroblasts display bioenergetics of cancer cells (Vincent AS, 2008). Because MDK and PTN were upregulated in whole keloid tissue, we hypothesized that MDK and PTN would be upregulated in primary keloid fibroblasts in vitro versus primary normal skin fibroblasts in vitro. We performed RT-PCR on RNA obtained from keloid fibroblasts and normal fibroblasts grown in vitro, using MDK, PTN, and GAPDH (positive control) primers, and water serving as a negative control. Results showed that keloid fibroblasts did not have significant increased expression of MDK and PTN at the RNA level compared to normal skin fibroblasts grown in vitro. It is possible that some other component of the keloid microenvironment, such as keratinocytes, endothelial cells, or inflammatory cells may be inducing upregulation of MDK and PTN in whole keloid tissue in vivo. Further work on this project involves performing Western blots on keloid fibroblasts and normal fibroblasts grown in vitro to determine whether MDK and PTN are upregulated at the protein level. In addition, in situ hybridization experiments for MDK and PTN on keloid sections will enable us to determine which cell type(s) are making MDK and PTN in keloid tissue.