Journal of Tissue Science and Engineering

Progress in tissue engineering clinically useful replacements for soft, elastic tissues is presently constrained by poor elastogenicity of most adult cell types, and difficulties in replicating the biocomplexity of elastic matrix assembly that occurs primarily in the fetal and neonatal stages. With recent progress in being able to enhance elastin precursor (tropoelastin) synthesis by adult cell types, the present emphasis in the field has shifted to developing strategies to address the other, equally important, if not more critical issues such as extremely poor recruitment and crosslinking of tropoelastin, and the need to direct the organization of crosslinked elastin deposits into matrix structures (e.g., aligned, spatially-oriented fibers) so as to be able to replicate the mechanical anisotropy of native tissues. This editorial provides insight into potential strategies to address these challenges and the key factors that are likely to influence their outcomes.

The development of a clinically translatable method of engineering with adipose-derived adult stem (ADAS) for reconstruction requires investigation of several components. The differentiation of ADAS cells into neuronal cells has been reported by several groups. The stringent maintenance of genomic stability in adult stem cells via anti-stress defenses and DNA repair mechanisms is particularly important because any genetic alteration can compromise the genomic stability and functionality of the cell. The main objective of this data was to examine some parameters related to DNA damage in cells submitted to the neural differentiation protocol and to understand if DNA damage can be associated to cell differentiation. The comet assay, micronucleus tests, and the cell viability assay were utilized to observe ADAS cells treated with neural induction medium. The results of our genotoxicity assays suggest that increased DNA damage observable by the comet assay was induced by neural differentiation. Emerging findings suggest that DNA damage; telomerase and DNA repair proteins play important roles in neurogenesis developing. Surprisingly we obtain evidence for an association between DNA damage and neuronal-like differentiation and hypothesize that during neural differentiation DNA damage will recruit telomerase TIP60 and MCM3, where they may function in DNA repair, chromatin remodeling and limiting DNA replication.

The objective of this study was to evaluate the ability of a collagen membrane (CM) as a carrier to successfully deliver platelet-derived growth factor (PDGF) and to observe the subsequent effects of the factor on preosteoblasts in vitro. MC3T3-E1 mouse preosteoblasts were cultured with a commercially available CM containing PDGF. After a two-day cell culture, cell viability was investigated by the MTT assay and cell proliferation was assessed by the crystal violet proliferation assay. Expression levels of the following osteoblastic differentiation marker genes were measured by real-time PCR: runt-related transcription factor 2 (RUNX2), osteopontin (OPN), bone sialoprotein (BSP), and osteocalcin (OCN). A cell proliferation assay was conducted, and osteoblastogenesis was determined by alkaline phosphatase (ALP) activity. A sustained release of PDGF from a CM was observed for ~3 weeks. Gene expression of all RUNX2, OPN, BSP, and OCN in CM with PDGF was significantly upregulated compared to those in CM without PDGF (all p < 0.05). Interestingly, CM without PDGF also significantly increased gene expression of RUNX2 and OPN in MC3T3-E1 cells compared to the cell control (both p < 0.05). Furthermore, it was observed that the PDGF released from CM significantly promoted ALP activity and cell proliferation with little cytotoxicity. These results suggest that a CM can be utilized for sustained delivery of PDGF. Also, released PDGF can promote MC3T3-E1 cell activities. This strategy may lead to an improvement in the current clinical treatment of bone defects in periodontal and implant therapy.