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  • 1
    Digitale Medien
    Digitale Medien
    Age-dependent response of primary human dermal fibroblasts to oxidative stress: cell survival, pro-survival kinases, and entrance into cellular senescence (2005)
    Malden, USA : Blackwell Science Inc
    Wound repair and regeneration 13 (2005), S. 0 
    Details
    ISSN: 1524-475X
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: A central question in cell biology is how cells become senescent. After a finite number of cell divisions, normal cultured human cells enter a state of irreversible growth arrest, termed “replicative senescence.” Alternatively, oxidative stress in the form of hydrogen peroxide (H2O2) can render human dermal fibroblasts (HDFs) nonproliferative and quiescent, a phenomenon known as stress-induced premature senescence (SIPS). Although critical to the understanding of the pathophysiological basis of many diseases, there is no research to date that has simultaneously examined the interactions between age, oxidative stress, and SIPS. Therefore, the goals of this study were to examine in concert the interactions between these three factors in primary HDFs, and to test our central hypothesis that aging lowers the ability of primary HDFs to respond to oxidative stress. Our data provide, for the first time, evidence that aging dramatically reduces the capacity of primary HDFs to respond to the challenge of hydrogen peroxide. Specifically, aged HDFs showed decreased cell viability, decreased phosphorylation (activation) of pro-survival kinases (Akt and ERK 1/2), and increased entrance into a senescent state when compared with their younger counterparts. Another important conclusion of this study is that blockade of transforming growth factor-β1 had a pronounced “rescue effect” in the aged, preventing entrance of HDFs into cellular senescence.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1111/j.1524-475X.2005.00079.x
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  • 2
    Digitale Medien
    Digitale Medien
    048
Retroviral Delivery of A Dominant Negative TGF-beta Receptor II Mitigates Scar in a Rabbit Model of Scar Hypertrophy (2004)
    Oxford, UK; Malden, USA : Blackwell Science Ltd/Inc.
    Wound repair and regeneration 12 (2004), S. 0 
    Details
    ISSN: 1524-475X
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: Effective blockade of the pluripotent cytokine TGF-beta as a means of cutaneous scar reduction is a strategy with great potential. This desired effect may be achieved through the overexpression of mutant TGF beta receptors within the wound milieu. Our goal was to examine the effects of dominant negative mutant TGF-beta receptor II (dnTGFRII) protein expression in a well-established rabbit ear model of hypertrophic scarring. Serial injections of a retroviral construct encoding a truncated TGFβRII and the marker green fusion protein (pMSCV-rIIdn-GFP) were performed in 7mm punch wounds at day 10 and day 14 (two-day injection group) or day 8, 10, 12 (three-day injection group) post wounding. Delivery of a null vector (pMSCV-GFP) at the same time points served as a negative control. Histomorphometric analysis of wounds harvested at day 28 revealed a statistically significant reduction (33%) in the scar elevation index in 2-day treated and a more modest reduction in SEI (17.5%) in the 3-day treated arm compared to null-treated controls. Confocal microscopy confirmed stable transfection of the construct in both peri-wound tissue as well as rabbit dermal fibroblasts transfected in vitro. Optimization of this novel application in retroviral gene therapy could lead to effective anti-scarring strategies.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1111/j.1067-1927.2004.0abstractau.x
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  • 3
    Digitale Medien
    Digitale Medien
    045
Adenoviral HTERT Transfection Results in Altered Phospho-erk Activity in Human Dermal Fibroblasts (2004)
    Oxford, UK; Malden, USA : Blackwell Science Ltd/Inc.
    Wound repair and regeneration 12 (2004), S. 0 
    Details
    ISSN: 1524-475X
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: Introduction: Telomeres are nucleoprotein structures at the ends of each chromosome. Due to the inability of DNA polymerase to replicate the full length of the chromosome, up to 50–200 base pairs of the telomere are lost during each successive round of cell division. In adult human somatic cells, telomerase is not active resulting in progressive loss of telomere length and entry into replicative senescence as observed in cell culture. hTERT is the catalytic subunit of telomerase, an enzyme which maintains telomere length. Transfection of human dermal fibroblasts (HDFs) by hTERT has been shown to reverse the senescent phenotype seen in aging HDFs in vitro. ERK (p44/42) is a MAP kinase which functions as a critical intermediary in the determination of cell growth and differentiation. Activation of ERK occurs through phosphorylation of threonine and tyrosine residues. 
Methods: In order to delineate some of the cellular mechanisms by which hTERT functions, we treated adenoviral hTERT (Ad-hTERT) transfected HDFs with TGFB1, and assayed phosphorylated ERK activity by Western blotting.
Results: Ad-hTERT treated HDFs demonstrated a 2–3 fold increase in phospho-ERK activity. In addition, our preliminary findings show that Ad-hTERT transfected HDFs have increased TGFB1, TGFB1-Receptor I and II, and COL1A1 gene expression by real-time rtPCR. 
Conclusions: Increased phosphor-ERK activity as well as increased TGFB1, TGFB1-Receptor I and II, and COL1A1 gene expression is seen in hTERT transfected HDF’s. Further studies will focus on defining other intermediary changes resulting from Ad-hTERT tranfection.Funding source: Geron Corporation
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1111/j.1067-1927.2004.0abstractar.x
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  • 4
    Digitale Medien
    Digitale Medien
    Use of hypoxia-inducible factor signal transduction pathway to measure O2 levels and modulate growth factor pathways (2003)
    Malden, USA : Blackwell Science Inc
    Wound repair and regeneration 11 (2003), S. 0 
    Details
    ISSN: 1524-475X
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: Tissue PO2 levels are known to directly modulate numerous processes involved in the reparative response to cutaneous tissue injury, including cell differentiation and migration, extracellular matrix synthesis and maturation, and effectiveness of endogenous and exogenous growth factors. Oxygen is therefore likely the critical variable determining the healing capabilities of any tissue. Significant advances in the understanding of cutaneous wound healing progressed with advances in the measurement of tissue PO2, which has advanced over the past several decades from implantable probes to now include molecular tools such as the transcription factor hypoxia inducible factor-1 (HIF-1). HIF-1 modulates the expression of genes that drive the cellular adaptive response to hypoxia and possess the HIF-1 binding sequence named hypoxia response element within their promoter sequence. Molecular biology techniques are now allowing exploitation of the HIF-1/hypoxia response element pathway to drive the expression of potential vulnerary ectopic genes. Here we show the utility of the hypoxia response element for hypoxia-driven expression of the transforming growth factor-β–signaling component Smad3 in vitro and the in vivo detection of ischemic hypoxia using luciferase. Smad3 is a positive effector of transforming growth factor-β superfamily signal transduction. Such approaches are the latest evolution of work championed by Hunt and colleagues over the past 4 decades. (WOUND REP REG 2003;11:496–503)
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1046/j.1524-475X.2003.11620.x
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  • 5
    Digitale Medien
    Digitale Medien
    015
Impact of Hydration on MMP-Activity (2004)
    Oxford, UK; Malden, USA : Blackwell Science Ltd/Inc.
    Wound repair and regeneration 12 (2004), S. 0 
    Details
    ISSN: 1524-475X
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: Hydration of keratinocytes modifies the levels of cytokines they secrete, which in turn impacts the secretory behaviour of dermal fibroblasts. In an in vitro coculture model, conditioned media (CM) collagen content was decreased 44% when keratinocytes were hydrated. We hypothesized that this is partly due to increased MMP-activity. We used the same coculture model to study changes in MMP-activity and TIMP secreted by keratinocytes as well as by fibroblasts in monoculture and in coculture in relation to air-treatment or hydration of keratinocytes. Stratified human epidermal keratinocytes (HEK) and confluent human dermal fibroblasts (HDF) were cocultured for 72 h under serum-free conditions. HEK were either kept at the air-interface or hydrated. CM was assayed for MMP-1, −2, −9, TIMP-1 and −2 were assayed using zymograms, western blotting, and ELISA. MMP-1, secreted by both cell types, increased significantly in cocultures compared to monocultures (4-fold in the air-treated group, 26-fold in the hydrated group). MMP-2, secreted mainly by HDFs, was significantly increased by coculture (hydration: 2.4-fold, air: 2.8-fold). MMP-9, predominantly secreted by air-treated HEKs and was significantly decreased in hydrated monoculture (76%) and coculture. HEK-monoculture hydration also significant decreased MMP-1 (86%) and MMP-2 (81%) activity. HDF-secreted TIMP-1 expression was significantly increased by coculture and was unaffected by hydration. Our findings demonstrate that paracrine interactions between HEK and HDF modify MMP activity and that HEK hydration significantly effects on MMP activity. The findings provide insight into the role of hydration on HEK and HDF ctivity during the wound healing process.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1111/j.1067-1927.2004.0abstractxp.x
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  • 6
    Digitale Medien
    Digitale Medien
    Inhibition of prolyl 4-hydroxylase reduces scar hypertrophy in a rabbit model of cutaneous scarring (2003)
    Malden, USA : Blackwell Science Inc
    Wound repair and regeneration 11 (2003), S. 0 
    Details
    ISSN: 1524-475X
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: Hypertrophic scars result from excessive collagen deposition at sights of healing dermal wounds and can be functionally and cosmetically problematic. Pharmacological regulation of collagen synthesis and deposition is a direct approach to the control of scar tissue formation. We tested the ability of the phenanthrolinone derivative FG-1648 (in 0.5% Carbopol 971 PNF gel, pH 6.5), a prolyl 4-hydroxylase inhibitor, to reduce hypertrophic scar formation in a rabbit ear hypertrophic scar model. New Zealand White rabbits were divided into two treatment groups (n = 12 wounds per group with an equal number of controls): low-dose group: 0.5% FG-1648; high-dose group: 1% FG-1648. Left ears were used for treatment and right ear for control. Four 7-mm dermal ulcer wounds were made on each ear. The inhibitor was topically applied to the wound at the time of wounding and once daily up to postoperative day 7. Wounds were harvested at postoperative day 28 and scar hypertrophy quantified by measurement of the scar elevation index. All wounds showed complete healing. Treatment of wounds with 1% prolyl 4-hydroxylase inhibitor decreased the scar elevation index by 26% compared to control wounds (p 〈 0.01). Wounds treated with 0.5% FG-1648 inhibitor showed no difference in scar elevation compared to control wounds. These results suggest that inhibition of prolyl 4-hydroxylase may be a suitable agent for topical treatment for the prevention of hypertrophic scar tissue. (WOUND REP REG 2003;11:368–372)
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1046/j.1524-475X.2003.11509.x
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  • 7
    Digitale Medien
    Digitale Medien
    Wound epithelialization deficits in the transforming growth factor-α knockout mouse (2001)
    Oxford, UK : Blackwell Science, Ltd.
    Wound repair and regeneration 9 (2001), S. 0 
    Details
    ISSN: 1524-475X
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: In vitro, transforming growth factor-α is an important factor controlling epithelial cell proliferation and migration. However, the transforming growth factor-α knockout mouse has shown no wound epithelialization defect in tail amputation and full-thickness back wounds. To resolve this disparity, we combined a full-thickness head wound and a partial-thickness ear wound on the transforming growth factor-α knockout mouse for analysis of wound epithelialization with or without granulation tissue formation. Three-millimeter ear wounds were made on the transforming growth factor-α knockout and heterozygous control mice. Full-thickness head wounds were made using a 6-mm trephine on the crown of the skull. In the ear model, transforming growth factor-α knockout mice had significantly larger epithelial gaps versus control at post-operative day 3 and 5. Epithelial thickness at the wound edge of transforming growth factor-α deficient mice was also depressed at post-operative day 3 and post-operative day 5 compared to control mice. On post-operative day 8, most wounds of both groups were epithelialized. In contrast, no difference in epithelial gap or new granulation tissue was found in the head model. The data support the concept that transforming growth factor-α plays a significant early role in wound epithelialization in vivo but its deficit is compensated if accompanied by granulation tissue formation. The data further show the importance of appropriate wound models to address the role of vulnerary factors.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1046/j.1524-475x.2001.00386.x
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