Abstract: The present invention provides for methods for identifying modulators of extracellular matrix (ECM) movement towards a site requiring deposition of ECM. Such modulators can be applied for use in a method for the modulation of ECM movement towards a site requiring deposition of ECM, e.g. a wound, thereby allowing treatment of a condition involving ECM deposition. Since the modulator may either be an inhibitor or promoter, either excessive or insufficient ECM deposition could be dealt with by the means and methods of the present invention.

Abstract: The present invention relates to a compound for use in a method of reducing the formation of heliocytes causing adhesiogenesis. An in vitro assay for the formation of heliocyte and/or the formation of adhesions is also comprised herein, as well as methods comprising the use of said in vitro assay. It also relates to a pharmaceutical composition for use in a method of reducing the formation of heliocytes comprising the compound mentioned above.

Abstract: The present invention relates to a method for generating an ex vivo skin sample being capable of developing scar. Further, the present invention comprises a method for screening for a compound which modulates scar development. Additionally, a preparation comprising a scarred full thickness skin sample obtainable by the method of the present invention is also envisaged. Finally, the present invention also encompasses a preparation comprising a full thickness skin model comprising a full thickness skin sample immersed and unethered in liquid culture.

Abstract: Aspects of the present disclosure include methods of treating a subject to reduce adhesion formation, the method comprising administering to a subject in need of thereof an agent that that targets adhesion-formation by injured mesothelial cells. The agent can act at a variety of checkpoints in the development of adhesions by injured mesothelial cells, including: targeting the injured mesothelial cells for destruction, recruiting inflammatory macrophages to the site of adhesion, preventing neutrophil recruitment to the site of adhesion, and/or inhibiting the expression or activity of a gene product whose expression is induced in the injured mesothelial cells. Compositions and kits for performing the methods are also provided.

Abstract: Aspects of the present disclosure include methods of treating a subject to reduce adhesion formation, the method comprising administering to a subject in need of thereof an agent that that targets adhesion-formation by injured mesothelial cells. The agent can act at a variety of checkpoints in the development of adhesions by injured mesothelial cells, including: targeting the injured mesothelial cells for destruction, recruiting inflammatory macrophages to the site of adhesion, preventing neutrophil recruitment to the site of adhesion, and/or inhibiting the expression or activity of a gene product whose expression is induced in the injured mesothelial cells. Compositions and kits for performing the methods are also provided.

Abstract: Populations enriched for smooth muscle progenitors are obtained by selection on the basis of expression of specific cell surface markers.

Abstract: Populations enriched for smooth muscle progenitors are obtained by selection on the basis of expression of specific cell surface markers.