Hypoxia Upregulates VEGF Production in Keloid Fibroblasts

Steinbrech, Douglas S.; Mehrara, Babak J.; Chau, Dorothy; Rowe, Norman M.; Chin, Gyu S.; Lee, Tom; Saadeh, Pierre B.; Gittes, George K.; Longaker, Michael T.

doi:10.1097/00000637-199905000-00009

Cited by 61 publications

(45 citation statements)

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“…Vascular endothelial growth factor (VEGF), a positive regulator of angiogenesis, is produced in large amounts by epidermal cells during wound healing 8 . The over expression of VEGF has been demonstrated in early stages of pathological scar formation 9,10 .…”

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confidence: 99%

Recombinant human endostatin reduces hypertrophic scar formation in rabbit ear model through down-regulation of VEGF and TIMP-1

2016

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Background: Recombinant human endostatin (Endostar) has been widely used to suppress angiogenesis in carcinoma patients. Hypertrophic scar (HS) tissue, much like a carcinoma, is often associated with angiogenesis. However, there have been few studies conducted on the effects of Endostar on HS or its mechanism. Objective: This paper investigated the effects Endostar on the HS of rabbit ears and studied the effects of Endostar on VEGF and TIMP-1 expression. Methods: Sixteen New Zealand white rabbits were used to establish HS models. Then, rabbit ears containing HS were randomly assigned to either the Endostar group or the control group. The changes of appearance and histology were evaluated using the naked eye, hematoxylin eosin staining, and a scar elevation index. The VEGF and TIMP-1 expressions were detected by immunohistochemical staining, RT-PCR, and western blot. Results: The thickness of the connective tissue in the Endostar group were thinner, the numbers of micro vessels and fibroblasts were fewer, and the collagen fibers were smoother. Moreover, the mRNA and protein expressions of VEGF and TIMP-1 in the Endostar group were significantly lower than those in the control group. Conclusion:The results suggested that Endostar reduced the formation of HS by down-regulation of VEGF and TIMP-1 expressions.

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confidence: 99%

Recombinant human endostatin reduces hypertrophic scar formation in rabbit ear model through down-regulation of VEGF and TIMP-1

2016

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“…Both keloids and hypertrophic scars exhibit features of microvascular occlusion from an excess of endothelial cells, suggesting that a hypoxic microenvironment within a keloid may promote excess collagen production by fibroblasts (15,16). In addition, this hypoxic microenvironment may stimulate an increased production of growth factors such as vascular endothelial growth factor (34). More accurate differentiation is obtained by electron microscopy, where the ultrastructure of collagen fibrillar organization may separate keloids from hypertrophic scars (18).…”

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confidence: 99%

Fibroblasts cocultured with keloid keratinocytes: normal fibroblasts secrete collagen in a keloidlike manner

Lim

Phan

Bay

et al. 2002

American Journal of Physiology-Cell Physiology

120

111

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Keloid scars represent a pathological response to cutaneous injury, reflecting a new set point between synthesis and degradation biased toward extracellular matrix (ECM) collagen accumulation. Using a serum-free two-chamber coculture model, we recently demonstrated a significant increase in normal fibroblast proliferation when cocultured with keloid-derived keratinocytes. We hypothesized that similar keratinocytefibroblast interactions might influence fibroblast collagen production and examined conditioned media and cell lysate from coculture for collagen I and III production by Western blot, allied with Northern analysis for procollagen I and III mRNA. Normal fibroblasts cocultured with keloid keratinocytes produced increased soluble collagen I and III with a corresponding increase in procollagen I and III mRNA transcript levels. This was associated with decreased insoluble collagen from cell lysate. When keloid fibroblasts were cocultured with keloid keratinocytes, both soluble and insoluble collagen were increased with associated procollagen III mRNA upregulation. Transmission electron microscopy of normal fibroblasts cocultured with keloid keratinocytes showed an ECM appearance similar to in vivo keloid tissue, an appearance not seen when normal fibroblasts were cocultured with normal keratinocytes. keloids; epithelial-mesenchymal interactions; keratinocyte induction; serum-free coculture

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“…29 Moreover, Steinbrech found that hypoxia could stimulate upregulating of VEGF expression in KFs. 30 Interestingly, Ryoma Touchi's study showed that there is no significant difference in VEGF expression between central and marginal areas. 3 VEGF was not only highly expressed in local keloid tissues, but also elevated in serum in patients with keloids scars compared with normal population.…”

Section: Vascular Endothelial Growth Factor (Vegf)mentioning

confidence: 97%

病理性瘢痕血供及组织缺氧的研究进展

李梓菲¹,

Li²,

刘清亮³

et al. 2017

cmsj

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Blood supply is believed to be an important aspect in the development of pathological scars. However, there are controversies about vascular distribution, vascular structure and blood flow in pathological scars. Additionally, hypoxic microenvironment plays an important role in the vascularization of pathological scar tissues, and hypoxic conditions can be reflected by metabolic indexes and some cytokines. Furthermore, the correlation between blood supply and tissue hypoxia is controversial. The aim of this article is to review the literature on the characteristics of blood supply and tissue hypoxia in pathological scars, from which we can see pathological scars have unique characteristics of blood supply that are closely associated with tissue hypoxia. Moreover, development in the treatment of pathological scars is herein reviewed.Chin Med Sci J 2017; 32(2):113-118. DOI:10.24920/J1001-9294.2017.014 ATHOLOGICAL scars include hypertrophic scar and keloid. They influence appearance and even cause functional disturbance, and place tremendous physiological and psychological burdens on patients. Therefore, pathological scars have been a challenge in plastic surgery and the focus of research.Blood supply is believed to be an important aspect in the development of pathological scars, and has thus attracted more attentions in recent years. However, there are controversies about blood supply in pathological scars.Hereby we summarized the advances of research on the blood supply in pathological scars, and explored future research directions. The vascular structure of pathological scars has different manifestations between hypertrophic scars and keloids. In terms of spatial vascular structure, blood vessels within hypertrophic scar tissues have a structure perpendicular to the skin surface, whereas those within keloid tissues present a typical dispersed, extended vascular structure. VASCULARITY OF PATHOLOGICAL SCARS 5,6The diameter or patency of the blood vessels of pathological scar remains controversial. Thaís et al used stereological methods to obtain information on pathological scar tissues with a microscope, and proposed that the blood vessels within the pathological scars were dilated compared with those in normal skin and normal scars.

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Hypoxia Upregulates VEGF Production in Keloid Fibroblasts

Cited by 61 publications

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Recombinant human endostatin reduces hypertrophic scar formation in rabbit ear model through down-regulation of VEGF and TIMP-1

Recombinant human endostatin reduces hypertrophic scar formation in rabbit ear model through down-regulation of VEGF and TIMP-1

Fibroblasts cocultured with keloid keratinocytes: normal fibroblasts secrete collagen in a keloidlike manner

病理性瘢痕血供及组织缺氧的研究进展

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