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      Menstrual fluid factors facilitate tissue repair: identification and functional action in endometrial and skin repair

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          Summary

          Repair after damage is essential for tissue homeostasis. Postmenstrual endometrial repair is a cyclical manifestation of rapid, scar-free, tissue repair taking ∼ 3– 5 d. Skin repair after wounding is slower (∼ 2 wk). In the case of chronic wounds, it takes months to years to restore integrity.Herein, the unique " rapid-repair" endometrial environment is translated to the " slower repair" skin environment. Menstrual fluid (MF), the milieu of postmenstrual endometrial repair, facilitates healing of endometrial and keratinocyte " wounds" in vitro , promoting cellular adhesion and migration, stimulates keratinocyte migration inan ex vivo human skin reconstruct model, and promotes re-epithelialization in an in vivo porcine wound model. Proteomic analysis of MF identified a large number of proteins: migration inhibitory factor, neutrophil gelatinase– associated lipocalin, follistatin like-1, chemokine ligand-20, and secretory leukocyte protease inhibitor were selected for further investigation. Functionally, they promote repair of endometrial and keratinocyte wounds by promoting migration. Translation of these and other MF factors into a migration-inducing treatment paradigm could provide novel treatments for tissue repair.

          Abstract

          Repair after damage is essential for tissue homeostasis. Postmenstrual endometrial repair is a cyclical manifestation of rapid, scar-free, tissue repair taking ∼3-5 d. Skin repair after wounding is slower (∼2 wk). In the case of chronic wounds, it takes months to years to restore integrity. Herein, the unique "rapid-repair" endometrial environment is translated to the "slower repair" skin environment. Menstrual fluid (MF), the milieu of postmenstrual endometrial repair, facilitates healing of endometrial and keratinocyte "wounds" in vitro, promoting cellular adhesion and migration, stimulates keratinocyte migration in an ex vivo human skin reconstruct model, and promotes re-epithelialization in an in vivo porcine wound model. Proteomic analysis of MF identified a large number of proteins: migration inhibitory factor, neutrophil gelatinase-associated lipocalin, follistatin like-1, chemokine ligand-20, and secretory leukocyte protease inhibitor were selected for further investigation. Functionally, they promote repair of endometrial and keratinocyte wounds by promoting migration. Translation of these and other MF factors into a migration-inducing treatment paradigm could provide novel treatments for tissue repair.-Evans, J., Infusini, G., McGovern, J., Cuttle, L., Webb, A., Nebl, T., Milla, L., Kimble, R., Kempf, M., Andrews, C. J., Leavesley, D., Salamonsen, L. A. Menstrual fluid factors facilitate tissue repair: identification and functional action in endometrial and skin repair.

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          Author and article information

          Journal
          The FASEB Journal
          The FASEB Journal
          FASEB
          0892-6638
          1530-6860
          July 23 2018
          July 23 2018
          : fj.201800086R
          Affiliations
          [1 ]The Hudson Institute of Medical Research, Clayton, Victoria, Australia;
          [2 ]Department of Molecular and Translational Medicine, Monash University, Clayton, Victoria, Australia;
          [3 ]Walter and Eliza Hall Institute, Parkville, Victoria, Australia;
          [4 ]Institute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, Queensland, Australia;
          [5 ]Centre for Children’s Burns and Trauma Research, School of Biomedical Sciences, Institute of Health and Biomedical Innovation at Centre for Children’s Health Research, Queensland University of Technology, Brisbane, Queensland, Australia;
          [6 ]Centre for Children’s Burns and Trauma Research, Centre for Children’s Health Research, The University of Queensland, South Brisbane, Queensland, Australia; and
          [7 ]Skin Research Institute of Singapore, Singapore
          Article
          10.1096/fj.201800086R
          30036086
          a5f22534-c420-429c-ab02-7e6f5bca015f
          © 2018
          History

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