Abstract

Decellularization is a process that has gained importance in the newly emerging field of tissue engineering and regenerative medicine. The extracellular matrix (ECM) derived from the decellularized liver acts as a bioscaffold to provide a microarchitectural environment for the regeneration of cells. Although regenerative approaches using artificially generated and/or de novo generated ECMs have been used to test their ability in supporting such regenerative process, a deeper understanding of the role of tissue injury on the ECM and its effect in organ regeneration has been poorly explored. The present study was carried out to assess the effect of the liver toxin D-galactosamine (D-GalN)-induced acute liver injury on the mouse liver ECM. ALI (acute liver injury) was developed in mice by administering D-GalN intraperitoneally at a dose of 800 mg/kg body weight, and the mice were sacrificed after 24 h. The whole liver was decellularized using a combination of detergents, namely, sodium dodecyl sulphate (SDS) and Triton-X 100, perfused through the portal vein. The matrices obtained from both normal and injured liver were analysed to look for differences in their network architecture and biochemical composition by employing scanning electron microscopy (SEM) and biochemical quantification of DNA content, glycosaminoglycans (GAG) and collagen levels post-decellularization. The ECM components such as collagen, fibronectin and laminin were studied immunohistochemically. Our study reveals that ALI of the mouse liver does not negatively alter the general architecture or basic components of the ECM. The burden of acute liver injury (ALI) in the ECM is seldom studied. In light of the recent evidence, it is clear that there is a dynamic communication between the ECM and the respective cells in order to maintain homoeostasis and enable regeneration of a given organ. Therefore, understanding liver ECM microarchitecture in injured conditions may help us to advance the field of regenerative medicine. Here, we did a comparative study of acute liver injured and normal liver ECMs after decellularization. Our results suggest that the basic architecture of the ECM matrix and their components are well maintained in both liver scaffolds.

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