Pulsed Heat Shocks to Enhance Collagen Production of Human Dermal Fibroblasts in Ex-Vivo Skin

2010 ◽  
Author(s):  
S. D. Dams ◽  
M. de Liefde ◽  
A. M. Nuijs ◽  
C. W. J. Oomens ◽  
F. P. T. Baaijens
Keyword(s):  
Ex Vivo ◽  
Contemporary Literature ◽  
Collagen Matrix ◽  
Dermal Fibroblasts ◽  
Human Dermal Fibroblasts ◽  
Procollagen Type ◽  
Different Temperatures ◽  
Heat Shocks ◽  
Ablative Techniques ◽  
Type 3

Well-known characteristics of aging skin are the development of fine lines and wrinkles, but also changes in skin tone, skin texture, thickness and moisture content [1, 2]. Rejuvenation of the skin aims at reversing the signs of aging and can be established in the epidermis as well as in the dermis. Aged dermis for that matter has a degenerated collagen matrix. To regenerate this matrix, fibroblasts need to be stimulated into synthesizing new collagen. Among the rejuvenation methods used the non-ablative techniques are gaining popularity. These methods produce dermal remodeling without obvious epidermal injury using a thermal approach. The generation of heat would cause collagen injury and contraction followed by collagen synthesis [2, 3]. However, little research on physiological evidence can be found in contemporary literature. In this study, the effects of heat shocks of different temperatures on the expression of procollagen type 1and type 3 of human dermal fibroblasts in ex-vivo skin are investigated.

Interleukin-1 Beta Promotes the Expression of Prox-1 and Vascular Endothelial Growth Factor Receptor Type-3 in Adult Human Dermal Fibroblasts

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 4738-4738
Author(s):  
Matsuo Takuji ◽  
Ryosuke Shirasaki ◽  
Haruko Tashiro ◽  
Yoko Oka ◽  
Tadashi Yamamoto ◽  
...  
Keyword(s):  
Morphological Changes ◽  
Interleukin 1 ◽  
Growth Factor Receptor ◽  
Dermal Fibroblasts ◽  
Vascular Endothelial ◽  
Human Dermal Fibroblasts ◽  
Interleukin 1 Beta ◽  
Lymphatic Duct ◽  
Type 3 ◽  
Endothelial Growth Factor

Abstract Abstract 4738 Background and Aims: We recently reported that human interleukin 1 beta (IL-1 beta) stimulates bone-marrow stromal myofibroblasts to express a hematopoietic stem cell marker, CD34 (16th EHA, and 53rdASH meeting). To characterize precisely the effects of IL-1 beta to the stromal cells, adult human dermal fibroblasts (HDF) were cultured with IL-1 beta, and the morphological changes and molecular expressions were observed. Materials and Methods: HDF were purchased, and cultured in knockout DMEM medium with 15% KSR with or without recombinant human IL-1 beta for 3 weeks. The morphological changes and the expression of specific hematopoiesis-related genes were analyzed time-dependently. The concentration of hematopoietic growth factors in the culturing supernatants was also measured. Results: When HDF were cultured with human IL-1 beta for 3 weeks, the cellular morphology changed to the filamentous appearance. RT-PCR analyses revealed that cells expressed Prox-1, a master molecule for lymphatic duct neogenesis, and also vascular endothelial growth factor receptor (VEGFR) type-3. Smad7 and PAI1 were also expressed; however, LYVE1, a marker for lymphatic vascular endothelial cell, was not induced. VEGF-C production was also demonstrated at RNA and protein levels, and VEGF-C and VEGFR type-3 system played an important role in morphological changes and cell-proliferation. Discussion: We previously reported that when HDF were cultured in DMEM/F12 medium with IL-1 beta and EPO, hematopoietic markers were induced. When HDF were cultured in knockout DMEM, a condition for immature cell-growth at ES cell levels, and IL-1 beta, lymphatic duct neogenesis-related genes were activated, and HDF converted their morphology without an introduction of any genes externally. We are now making clear the precise action of IL-1 beta to HDF using microarray analysis. Disclosures: No relevant conflicts of interest to declare.

Heat shocks enhance procollagen type I and III expression in fibroblasts in ex vivo human skin

2011 ◽  
Vol 17 (2) ◽  
pp. 167-180 ◽  
Author(s):  
S. D. Dams ◽  
M. de Liefde-van Beest ◽  
A. M. Nuijs ◽  
C. W. J. Oomens ◽  
F. P. T. Baaijens
Keyword(s):  
Human Skin ◽  
Ex Vivo ◽  
Type I ◽  
Procollagen Type ◽  
Procollagen Type I ◽  
Heat Shocks

Adhesion and Proliferation of Human Dermal Fibroblasts on Collagen Matrix

2004 ◽  
Vol 18 (3) ◽  
pp. 209-222 ◽  
Author(s):  
Maria Antonietta Croce ◽  
Chiara Silvestri ◽  
Deanna Guerra ◽  
Elena Carnevali ◽  
Federica Boraldi ◽  
...  
Keyword(s):  
Collagen Matrix ◽  
Dermal Fibroblasts ◽  
Human Dermal Fibroblasts

scholarly journals Elucidating the Cellular Mechanism for E2-induced Dermal Fibrosis

2021 ◽  
Author(s):  
DeAnna Baker Frost ◽  
Alisa Savchenko ◽  
Adeyemi Ogunleye ◽  
Milton Armstrong ◽  
Carol Feghali-Bostwick
Keyword(s):  
Human Skin ◽  
Ex Vivo ◽  
Mapk Pathway ◽  
Dermal Fibroblasts ◽  
Skin Tissue ◽  
Human Dermal Fibroblasts ◽  
Ici 182,780 ◽  
Dermal Fibrosis ◽  
Human Skin Tissue

Abstract Background: Both TGFb and estradiol (E2), a form of estrogen, are pro-fibrotic in the skin. In the connective tissue disease, systemic sclerosis (SSc), both TGFb and E2 are likely pathogenic. Yet, the regulation of TGFb in E2-induced dermal fibrosis remains ill-defined. Elucidating those regulatory mechanisms will improve the understanding of fibrotic disease pathogenesis and set the stage for developing potential therapeutics. Using E2-stimulated primary human dermal fibroblasts in vitro and human skin tissue ex vivo, we identified the important regulatory proteins for TGFb and investigated the extracellular matrix (ECM) components that are directly stimulated by E2-induced TGFb signaling.Methods: We used primary human dermal fibroblasts in vitro and human skin tissue ex vivo stimulated with E2 or vehicle (ethanol) to measure TGFb1, TGFb2 levels using quantitative PCR (qPCR). To identify the necessary cell signaling proteins in E2-induced TGFb1 and TGFb2 transcription, human dermal fibroblasts were pre-treated with an inhibitor of the extracellular signal-regulated kinase/ mitogen-activated protein kinase (ERK/MAPK) pathway, U0126. Finally, human skin tissue ex vivo was pre-treated with SB-431542, a TGFb receptor inhibitor, and ICI 182,780, an estrogen receptor α (ER α) inhibitor, to establish the effects of TGFb and ER α signaling on E2-induced collagen 22A1 (Col22A1) transcription. Results: We found that expression of TGFb1, TGFb2, and Col22A1, a TGFb-responsive gene, are induced in response to E2 stimulation. Mechanistically, Col22A1 induction was blocked by SB-431542 and ICI 182,780 despite E2 stimulation. Additionally, inhibiting E2-induced ERK/MAPK activation and early growth response 1 (EGR1) transcription prevents the E2-induced increase in TGFb1 and TGFb2 transcription and translation. Conclusions: We conclude that E2-induced dermal fibrosis occurs in part through induction of TGFb1, 2 and Col22A1, which is regulated through EGR1 and the MAPK pathway. Thus, blocking estrogen signaling and/or production may be a novel therapeutic option in pro-fibrotic diseases.

Fibrin-Reinforced Collagen Matrix Enhances Tissue Regeneration and Angiogenesis

2005 ◽  
Vol 288-289 ◽  
pp. 257-260
Author(s):  
Dong Lim Seol ◽  
Won Hee Jang ◽  
Sung Jae Lee ◽  
Young Il Yang
Keyword(s):  
Tissue Regeneration ◽  
Nude Mice ◽  
Functional Integration ◽  
Collagen Matrix ◽  
Dermal Fibroblasts ◽  
Surrounding Tissue ◽  
Human Dermal Fibroblasts ◽  
Collagen Matrices

The goal of this study was to investigate effects of fibrin reinforcement of collagen sponges on fibroblasts-mediated contraction and in vivo tissue regeneration, especially angiogenesis. Human dermal fibroblasts (HDFs)-populated collagen sponges reinforced with or without fibrin were cultivated via the free-floating method in vitro. They were then evaluated using xenogeneic implantation into nude mice. The HDFs-populated collagen sponges reinforced with fibrin exhibited significantly decreased HDFs-mediated contraction in vitro (p<0.05). Microvascular and cellular densities of the collagen sponges were significantly higher with fibrin than without (p<0.01). Cell ingrowths, neovascularization, and deposition of ECM matrix were more evenly distributed in the fibrin-reinforced collagen matrices. The results demonstrated that fibrin reinforcement of porous collagen sponges can reduce cell-mediated contraction in vitro while enhancing functional integration with surrounding tissue in vivo.

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