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Ahlskog, Nina
Publications (2 of 2) Show all publications
Sulniute, R., Shen, Y., Guo, Y.-Z., Fallah, M., Ahlskog, N., Ny, L., . . . Ny, T. (2016). Plasminogen is a critical regulator of cutaneous wound healing. Thrombosis and Haemostasis, 115(5), 1001-1009
Open this publication in new window or tab >>Plasminogen is a critical regulator of cutaneous wound healing
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2016 (English)In: Thrombosis and Haemostasis, ISSN 0340-6245, Vol. 115, no 5, p. 1001-1009Article in journal (Refereed) Published
Abstract [en]

Wound healing is a complicated biological process that consist of partially overlapping inflammatory, proliferation and tissue remodelling phases. A successful wound healing depends on a proper activation and subsequent termination of the inflammatory phase. The failure to terminate the inflammation halts the completion of wound healing and is a known reason for formation of chronic wounds. Previous studies have shown that wound closure is delayed in plasminogen deficient mice, and a role for plasminogen in dissection of extracellular matrix was suggested. However, our finding that plasminogen is transported to the wound by inflammatory cells early during the healing process, where it potentiates inflammation, indicates that plasminogen may also have other roles in the wound healing process. Here we report that plasminogen-deficient mice have extensive fibrin and neutrophil depositions in the wounded area long after re-epithelialisation, indicating inefficient debridement and chronic inflammation. Delayed formation of granulation tissue suggests that fibroblast function is impaired in the absence of plasminogen. Therefore, in addition to its role in the activation of inflammation, plasminogen is also crucial for subsequent steps, including resolution of inflammation and activation of the proliferation phase. Importantly, supplementation of plasminogen-deficient mice with human plasminogen leads to a restored healing process that is comparable to that in wild-type mice. Besides of being an activator of the inflammatory phase during wound healing, plasminogen is also required for the subsequent termination of inflammation. Based on these results, we propose that plasminogen may be an important future therapeutic agent for wound treatment.

Keywords
Plasminogen, wound healing, inflammation
National Category
Hematology
Identifiers
urn:nbn:se:umu:diva-121571 (URN)10.1160/TH15-08-0653 (DOI)000375372400015 ()
Available from: 2016-06-30 Created: 2016-06-03 Last updated: 2018-10-31Bibliographically approved
Johansson, S. M., Nilsson, E. C., Elofsson, M., Ahlskog, N., Kihlberg, J. & Arnberg, N. (2007). Multivalent sialic acid conjugates inhibit adenovirus type 37 from binding to and infecting human corneal epithelial cells. Antiviral Research, 73(2), 92-100
Open this publication in new window or tab >>Multivalent sialic acid conjugates inhibit adenovirus type 37 from binding to and infecting human corneal epithelial cells
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2007 (English)In: Antiviral Research, ISSN 0166-3542, E-ISSN 1872-9096, Vol. 73, no 2, p. 92-100Article in journal (Refereed) Published
Abstract [en]

Adenovirus type 37 is one of the main causative agents of epidemic keratoconjunctivitis. In a series of publications, we have reported that this virus uses sialic acid as a cellular receptor. Here we demonstrate in vitro that on a molar basis, multivalent sialic acid conjugated to human serum albumin prevents adenovirus type 37 from binding to and infecting human corneal epithelial cells 1000-fold more efficiently than monosaccharidic sialic acid. We also demonstrate that the extraordinary inhibitory effect of multivalent sialic acid is due to the ability of this compound to aggregate virions. We conclude that multivalent sialic acid may be a potential new antiviral drug, for use in the treatment of epidemic keratoconjunctivitis caused by the adenoviruses that use sialic acid as cellular receptor.

Keywords
Adenovirus, EKC, Sialic acid, Multivalent
National Category
Microbiology in the medical area
Identifiers
urn:nbn:se:umu:diva-12970 (URN)10.1016/j.antiviral.2006.08.004 (DOI)
Available from: 2007-05-11 Created: 2007-05-11 Last updated: 2018-06-09Bibliographically approved
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