Towards a sustainable chitosan-based composite scaffold derived from Scylla serrata crab chitosan for bone tissue engineering.

Bone tissue engineering offers a novel therapy for repairing bone defects or fractures. However, it is becoming increasingly challenging because an ideal scaffold should possess a similar porous structure, high biocompatibility, and mechanical properties that match those of natural bone. To fabricate such a scaffold, biodegradable polymers are often preferred due to their degradability and tailored structure. This study involved the isolation of chitosan from crab shells (Scylla serrata) waste to use as a biomaterial in combination with hydroxyapatite (HAP) and collagen I (COL I) to mimic the extracellular matrix (ECM) composition of bone. After being cast and freeze-dried, it resulted in an interconnected porous scaffold with a porosity of 51.44% ± 2.28% and a pore diameter of 109.88 µm ± 49.84 µm. The swelling ratio of the crab scaffold was measured at 358.31% ± 25.23%, 363.04% ± 1.56%, and 370.11% ± 3.7% at 1, 3, and 6 h, respectively. Consequently, the scaffold exhibited a degradation ratio of 8.17% ± 2.59%, 21.62% ± 5.43%, 22.59% ± 14.23%, and 23.12% ± 6.28% over the course of 1 to 4 weeks. It demonstrated excellent biocompatibility with MG-63 osteosarcoma cells. Although the compression strength was lower than 2-12 MPa, the crab scaffold can still be applied effectively for non-load-bearing bone defects. Crab shell waste emerges as a promising source of chitosan for tissue engineering applications.

Fabrication of a Tailored, Hybrid Extracellular Matrix Composite.

The extracellular matrix (ECM) is a network of connective fibers that supports cells living in their surroundings. Native ECM, generated by the secretory products of each tissue's resident cells, has a unique architecture with different protein composition depending on the tissue. Therefore, it is very difficult to artificially design in vivo architecture in tissue engineering. In this study, a hybrid ECM scaffold from the basic structure of fibroblast-derived cellular ECMs is fabricated by adding major ECM components of fibronectin (FN) and collagen (COL I) externally. It is confirmed that while maintaining the basic structure of the native ECM, major protein components can be regulated. Then, decellularization is performed to prepare hybrid ECM scaffolds with various protein compositions and it is demonstrated that a liver-mimicking fibronectin (FN)-rich hybrid ECM promoted successful settling of H4IIE rat hepatoma cells. The authors believe that their method holds promise for the fabrication of scaffolds that provide a tailored cellular microenvironment for specific organs and serve as novel pathways for the replacement or regeneration of specific organ tissues.

An Accelerated Wound-Healing Surgical Suture Engineered with an Extracellular Matrix.

A suture is a ubiquitous medical device to hold wounded tissues together and support the healing process after surgery. Surgical sutures, having incomplete biocompatibility, often cause unwanted infections or serious secondary trauma to soft or fragile tissue. In this research, UV/ozone (UVO) irradiation or polystyrene sulfonate acid (PSS) dip-coating is used to achieve a fibronectin (FN)-coated absorbable suture system, in which the negatively charged moieties produced on the suture cause fibronectin to change from a soluble plasma form into a fibrous form, mimicking the actions of cellular fibronectin upon binding. The fibrous fibronectin coated on the suture can be exploited as an engineered interface to improve cellular migration and adhesion in the region around the wounded tissue while preventing the binding of infectious bacteria, thereby facilitating wound healing. Furthermore, the FN-coated suture is found to be associated with a lower friction between the suture and the wounded tissue, thus minimizing the occurrence of secondary wounds during surgery. It is believed that this surface modification can be universally applied to most kinds of sutures currently in use, implying that it may be a novel way to develop a highly effective and safer suture system for clinical applications.

Celecoxib, a COX-2 Selective Inhibitor, Induces Cell Cycle Arrest at the G2/M Phase in HeLa Cervical Cancer Cells.

Celecoxib, a selective inhibitor of COX-2, showed cytotoxic effects in many cancer cell lines including cervical cancer cells. This study investigated the effect of celecoxib on cell cycle arrest in HeLa cervical cancer cells through p53 expression. In vitro anticancer activity was determined with the 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) method. A double staining method was applied to investigate the mechanism of cell death, cell cycling was analyzed by flow cytometryand immunocytochemistry was employed to stain p53 expression in cells. Celecoxib showed strong cytotoxic effects and induced apoptosis with an IC50 value of 40 µM. It induced cell cycle arrest at G2/M phase by increasing level of p53 expression on HeLa cells.