Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    042
FGF-BP improves wound healing through the induction of more collagen in rats (2004)
    Oxford, UK; Malden, USA : Blackwell Science Ltd/Inc.
    Wound repair and regeneration 12 (2004), S. 0 
    Details
    ISSN: 1524-475X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The fibroblast growth factors are important regulators during wound healing. To quench their biological activities, secreted FGFs are tightly bound to heparan sulfate proteoglycans in the extracellular matrix (ECM). One of the approaches for releasing the active FGF from ECM involves the binding to an FGF binding protein (FGF-BP), which prevents FGF degradation and retains its activities. FGF-BP enhances the proliferation of fibroblasts through FGF-1 and -2 and of endothelial cells through FGF-2. To detect the biological function of FGF-BP in wound healing, we constructed an adenoviral vector containing murine FGF-BP cDNA (Ad-FGF-BP). Polyvinyl alcohol (PVA) sponges were implanted subcutaneously in rats. 107–108 PFU of either Ad-FGF-BP or Ad-LacZ (as local control) was injected into the sponges at d3 after implantation. At d4 after injection, Ad-FGF-BP infected sponges displayed much better organization of granulation tissue with the presence of more macroscopic hemorrhage than the local control. At d7 after injection, Ad-FGF-BP infected experimental granulation tissues in sponges showed more collagen deposition. The contents of collagen, protein and DNA in Ad-FGF-BP infected sponges increased 24.0%(p 〈 0.05), 11.3%(p 〈 0.05, d4) and 28.2%(p 〈 0.001, d7), respectively. Incisional wounding was performed in rats and 108 PFU Ad-FGF-BP or Ad-lacZ was intracutaneously injected along the wound margins. At 7d after injection, the tensile strength of Ad-FGF-BP infected wounds increased 41.1%(p 〈 0.05). Our data indicate that overexpression of FGF-BP can improve wound healing, and the inductionof more collagen in granulation tissue may be one of the mechanisms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1067-1927.2004.0abstractao.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    003
α1-Antichymotrypsin – A Human Serpin with the Potential to Heal Diabetic Ulcers (2004)
    Oxford, UK; Malden, USA : Blackwell Science Ltd/Inc.
    Wound repair and regeneration 12 (2004), S. 0 
    Details
    ISSN: 1524-475X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: α1-Antichymotrypsin (α1-ACT) is a secreted serine proteinase inhibitor of the serpin family. It is strongly upregulated during the inflammatory phase of wound repair to control the undesirable destructive side effects of cathepsin G which is released from infiltrating neutrophils. We have shown that α1-ACT and its mouse homologue spi2 exhibit a classic acute phase response after cutaneous injury in murine and human skin. The induction of spi2 gene expression following wounding is significantly less pronounced in diabetic mice. Transient overexpression of spi2 or α1-ACT significantly increased wound tensile strength in two independent diabetic models: in genetically diabetic mice, gene gun mediated delivery of spi2 or α1-ACT cDNA increased the average wound strength by 42%(P = 0.001) and 21%(P = 0.013) at d5 post-wounding respectively. In a STZ induced diabetic rat model the breaking strength of adenovirally spi2- or α1-ACT-infected wounds increased by 20%(P = 0.049) and 23%(P = 0.004) at d7 after injection respectively. Moreover, the topical application of human α1-ACT protein to wounds of diabetic mice had a significant and dose dependent effect on tensile strength at d5 post-wounding (21% increase, P = 0.003). Histological analyses of these wounds indicated less infiltration of neutrophils in the treated wounds. α1-ACT appears to be a key mediator between proteolysis and cytokine agonism and antagonism. Our data indicate that this balance is disturbed in diabetic wounds and that α1-ACT might act as a switch to initiate wound healing in diabetic ulcers.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1067-1927.2004.0abstractd.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    064
Adenoviral-Mediated Overexpression of Human Alpha1-Antichymotrypsin and Its Murine Homolog SPI2 Improve Wound Healing in Rats (2005)
    Oxford, UK; Malden, USA : Blackwell Publishing Ltd/Inc.
    Wound repair and regeneration 13 (2005), S. 0 
    Details
    ISSN: 1524-475X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: α1-antichymotrypsin (ACT) and its murine homolog spi2 are serine protease inhibitors present in plasma, that are locally up-regulated during wound healing. Ad-spi2 and Ad-ACT expression vectors were constructed to address the biological activity of locally expressed serpins. The condition medium of infected COS-1 cell at 2 d postinfection contained 1.23 ng/ml spi2 and 2.61 ng/ml ACT. Ad-LacZ or Ad-spi2 108 pfu was injected into the sponges after 3 d subcutaneous implantation in rats. Histological analysis showed that overexpression of spi2 improves granulation tissue organization and collagen deposition at d7 implantation. Moreover, overexpression of spi2 increases the contents of tissue DNA (23.8%, p 〈 0.05) and protein (25.3%, p 〈 0.05) in sponge implantation model in rats. In incisional wound models in both normal and STZ-induced diabetic rats, Ad-spi2 increases tensile strength by 26%(p = 0.011) and 29%(p = 0.022) as well as Ad-ACT increases by 10.3%(p = 0.037) and 32%(p = 0.004), respectively. In adriamycin-induced wound model in rats, histological analysis displayed less inflammatory cells infiltrating in Ad-ACT injected wound than in Ad-LacZ after 21 d injection of adriamycin. Inflammation enzymes MPO and elastase levels were decreased by 32.3% and 29.2% in Ad-ACT injected wound tissue. Our data concluded that overexpression of spi2 and ACT improves wound healing in rats probably via inflammatory resolution.(Supported by Switch Biotech and the Department of Veterans Affairs)
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1067-1927.2005.130215bl.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    038
Adenoviral overexpression of MCP-2 induces macrophages and improves wound healing in diabetic rats (2004)
    Oxford, UK; Malden, USA : Blackwell Science Ltd/Inc.
    Wound repair and regeneration 12 (2004), S. 0 
    Details
    ISSN: 1524-475X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The recruitment of leukocyte subsets is mainly driven by chemokines. Monocyte chemotactic protein-2 (MCP-2) belongs to the CC subfamily of chemokines, and it is especially a chemoattractant for monocytes. Of all CC subfamily members only MCP-2 interacts with multiple receptors, and its N-terminal truncated isoform is a natural chemokine inhibitor. Gene expression profiling in excisional wounds showed MCP-2 was down-regulated 40% in wild type mice and 69.2% in diabetic mice at 24 h after wounding. To determine the biological response to MCP-2 during wound healing, we constructed an adenoviral vector (Ad-MCP-2). Ad-MCP-2 infected cell conditioned medium contained 460 ng/ml secreted MCP-2 (ELISA) and had chemotactic activity similar to recombinant full-length MCP-2 but not to MCP-2 N-terminal 8–13aa peptides in a THP-1cell migration assay. In an incisional wound model in STZ induced diabetic rats, the breaking strength of Ad-MCP-2 infected skin wounds increased by 43%(108 PFU, p 〈 0.05) and 30%(107 PFU, p 〈 0.05) at 7d after Ad-MCP-2 injection compared with Ad-LacZ control. The wound closure strength of 107 PFU Ad-MCP-2 infected wounds still increased by 21%(p 〈 0.05) at 10d after injection. In normal rats, the breaking strength of Ad-MCP-2 and Ad-Lacz infected wounds was not significantly different. In rats, we injected either Ad-MCP-2 or Ad-LacZ (108 PFU) into each PVA sponge at 3d after implantation. Histological analyses revealed numerous ED-1 positive macrophages infiltrating in the experimental granulation tissue at 7d after Ad-MCP-2 injection. Our data provide evidence that MCP-2 improved wound healing in diabetic rats, and the recruitment of macrophages into the wound granulation tissues was the one of the mechanisms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1067-1927.2004.0abstractak.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...