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Deficiency of liver...
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Botusan, I. R.Karolinska Institutet
(författare)
Deficiency of liver-derived insulin-like growth factor-I (IGF-I) does not interfere with the skin wound healing rate
- Artikel/kapitelEngelska2018
Förlag, utgivningsår, omfång ...
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2018-03-13
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Public Library of Science (PLoS),2018
Nummerbeteckningar
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LIBRIS-ID:oai:gup.ub.gu.se/266188
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https://gup.ub.gu.se/publication/266188URI
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https://doi.org/10.1371/journal.pone.0193084DOI
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http://kipublications.ki.se/Default.aspx?queryparsed=id:137848237URI
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Ämneskategori:art swepub-publicationtype
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Objective: IGF-I is a growth factor, which is expressed in virtually all tissues. The circulating IGF-I is however derived mainly from the liver. IGF-I promotes wound healing and its levels are decreased in wounds with low regenerative potential such as diabetic wounds. However, the contribution of circulating IGF-I to wound healing is unknown. Here we investigated the role of systemic IGF-I on wound healing rate in mice with deficiency of liver-derived IGF-I (LI-IGF-I-/- mice) during normal (normoglycemic) and impaired wound healing (diabetes). Methods: LI-IGF-I-/- mice with complete inactivation of the IGF-I gene in the hepatocytes were generated using the Cre/loxP recombination system. This resulted in a 75% reduction of circulating IGF-I. Diabetes was induced with streptozocin in both LI-IGF-I-/- and control mice. Wounds were made on the dorsum of the mice, and the wound healing rate and histology were evaluated. Serum IGF-I and GH were measured by RIA and ELISA respectively. The expression of IGF-I, IGF-II and the IGF-I receptor in the skin were evaluated by qRT-PCR. The local IGF-I protein expression in different cell types of the wounds during wound healing process was analyzed using immunohistochemistry. Results: The wound healing rate was similar in LI-IGF-I-/- mice to that in controls. Diabetes significantly delayed the wound healing rate in both LI-IGF-I-/- and control mice. However, no significant difference was observed between diabetic animals with normal or reduced hepatic IGF-I production. The gene expression of IGF-I, IGF-II and IGF-I receptor in skin was not different between any group of animals tested. Local IGF-I levels in the wounds were similar between of LI-IGF-I-/- and WT mice although a transient reduction of IGF-I expression in leukocytes in the wounds of LI-IGF-I-/- was observed seven days post wounding. Conclusion: Deficiency in the liver-derived IGF-I does not affect wound healing in mice, neither in normo-glycemic conditions nor in diabetes.
Ämnesord och genrebeteckningar
Biuppslag (personer, institutioner, konferenser, titlar ...)
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Zheng, X.Karolinska Institutet
(författare)
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Narayanan, S.
(författare)
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Grünler, J.Karolinska Institutet
(författare)
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Sunkari, V. G.
(författare)
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Calissendorff, F. S.
(författare)
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Ansurudeen, I.
(författare)
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Illies, C.
(författare)
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Svensson, Johan,1964Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för invärtesmedicin och klinisk nutrition,Centre for Bone and Arthritis Research,Institute of Medicine, Department of Internal Medicine and Clinical Nutrition(Swepub:gu)xsjohc
(författare)
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Jansson, John-Olov,1954Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology(Swepub:gu)xjanjo
(författare)
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Ohlsson, Claes,1965Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för invärtesmedicin och klinisk nutrition,Centre for Bone and Arthritis Research,Institute of Medicine, Department of Internal Medicine and Clinical Nutrition(Swepub:gu)xohlcl
(författare)
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Brismar, K.Karolinska Institutet
(författare)
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Catrina, S. B.Karolinska Institutet
(författare)
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Karolinska InstitutetInstitutionen för medicin, avdelningen för invärtesmedicin och klinisk nutrition
(creator_code:org_t)
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Ingår i:PLoS ONE: Public Library of Science (PLoS)13:31932-6203
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Botusan, I. R.
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Zheng, X.
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Narayanan, S.
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Grünler, J.
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Sunkari, V. G.
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Calissendorff, F ...
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Ansurudeen, I.
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Illies, C.
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Svensson, Johan, ...
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Jansson, John-Ol ...
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Ohlsson, Claes, ...
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Brismar, K.
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Catrina, S. B.
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