Please use this identifier to cite or link to this item: http://repository.uinjkt.ac.id/dspace/handle/123456789/38242
Title: Expressions of EGF, FGF and VEGF in hipoxic fibrosis tissue with keloid as a model
Authors: Endah Wulandari
Sri Widia A Jusman
Yefta Moenadjat
Ahmad A Jusuf
Mohamad Sadikin
Keywords: fibrosis;HIF-1α;EGF;FGF;VEGF
Issue Date: 2-Nov-2017
Publisher: UIN Syarif Hidayatullah Jakarta: Fakultas Kedokteran dan Ilmu Kesehatan, 2017
Series/Report no.: Medika Islamika Vol 14
Abstract: Fibrosis, the result of mutations increased proliferation, migration of fibroblasts, followed by excessive collagen synthesis. Uncontrolled tissue growth is not matched by adequate tissue vascularization. Existing blood vessels become insufficient, so that excessive fibrogensis allegedly caused by the continous hypoxia, such as the formation of tumors. In hypoxia, HIF-1α becomes stable, a transcription factor that regulates gene target of various cellular processes, such as tissue growth factor, eritropoisis, metabolism, angiogenesis, vascularization, cell cycle, and apoptosis suppressor. Keloid is one of the fibrosis cases, due to the excessive tissue growth which is not in accordance with the severity of trauma and it still continues to be a clinical problem. It is assumed that the excessive fibrogenesis in keloid tissue is the caused by the resulting hypoxia in stable HIF-1α, the which leads to further stimulation of transcription factors that Regulate the expression of growth factor proteins such as EGF, FGF and VEGF. The results showed in the keloid: EGF expression lower in the cells of epidermis; FGF expression higher in the cells of the dermis; the expression of VEGF protein in endothelial cells is higher than the preputium (control), the overall was significantly different (unpaired-t, p <0.05). HIF-1α expression correlates strongly with a third of the growth factor protein. In these studies show the expression of EGF, FGF and VEGF that related to hypoxia in keloid fibrosis.
URI: http://repository.uinjkt.ac.id/dspace/handle/123456789/38242
ISSN: 2598-8239
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