Cutting-edge collagen biocomposite reinforced with 2D nano-talc for bone tissue engineering.

The advancement of nanobiocomposites reinforced with 2D nano-materials plays a pivotal role in enhancing bone tissue engineering. In this study, we introduce a nanobiocomposite that reinforces bovine collagen with 2D nano-talc, a recently exfoliated nano-mineral. These nanobiocomposites were prepared by blending collagen with varying concentrations of 2D nano-talc, encompassing mono- and few-layers talc from soapstone nanomaterial. Extensive characterization techniques including AFM, XPS, nano-FTIR, s-SNOM nanoimaging, Force Spectroscopy, and PeakForce QNM® were employed. The incorporation of 2D nano-talc significantly enhanced the mechanical properties of the nanobiocomposites, resulting in increased stiffness compared to pristine collagen. In vitro studies supported the growth and proliferation of osteoblasts onto 2D nano-talc-reinforced nanobiocomposites, as well as showed the highest mineralization potential. These findings highlight the substantial potential of the developed nanobiocomposite as a scaffold material for bone tissue engineering applications.

Efficacy of collagen-only scaffolds compared to polymer-associated collagen and nanomaterials in skin wound repair ­ a review

Wound healing remains a clinical problem, with cases of atrophic, hypertrophic, or keloid scars. Three-dimensional scaffolds have been used to restore skin function, facilitating cell migration, adhesion, and proliferation. Collagen is the most common, presenting low antigenicity, decreased inflammation, and replacement by autologous tissue. It is used as sheets/films, sponges, membranes, sprays, and hydrogels of various origins. This integrative literature review aimed to evaluate the application of unassociated collagen scaffolds for skin wound healing and compare them to collagen associations with nanomaterials and polymers. Properties such as applications in humans and other unconventional models cause burns, partial and full-thickness wounds, and others. Scaffold, biomaterials, collagen, wound, injury, repair, and healing were among the descriptors. We found 3,098 articles published between 1995 and 2022 (Mendeley platform), including clinical/experimental trials. After exclusion, 26 studies were identified and analyzed. Autologous and heterologous collagens are the most used in the clinic and favor wound closure by improving re-epithelialization and reducing inflammation but may present challenges in aesthetic acceptance and loss of repair function in the wound site. Furthermore, collagen integration with other nanomaterials improved wound repair and experimental models.

Angiotensin Converting Enzyme Regulates Cell Proliferation and Migration.

BACKGROUND: The angiotensin-I converting enzyme (ACE) plays a central role in the renin-angiotensin system, acting by converting the hormone angiotensin-I to the active peptide angiotensin-II (Ang-II). More recently, ACE was shown to act as a receptor for Ang-II, and its expression level was demonstrated to be higher in melanoma cells compared to their normal counterparts. However, the function that ACE plays as an Ang-II receptor in melanoma cells has not been defined yet. AIM: Therefore, our aim was to examine the role of ACE in tumor cell proliferation and migration. RESULTS: We found that upon binding to ACE, Ang-II internalizes with a faster onset compared to the binding of Ang-II to its classical AT1 receptor. We also found that the complex Ang-II/ACE translocates to the nucleus, through a clathrin-mediated process, triggering a transient nuclear Ca2+ signal. In silico studies revealed a possible interaction site between ACE and phospholipase C (PLC), and experimental results in CHO cells, demonstrated that the ß3 isoform of PLC is the one involved in the Ca2+ signals induced by Ang-II/ACE interaction. Further studies in melanoma cells (TM-5) showed that Ang-II induced cell proliferation through ACE activation, an event that could be inhibited either by ACE inhibitor (Lisinopril) or by the silencing of ACE. In addition, we found that stimulation of ACE by Ang-II caused the melanoma cells to migrate, at least in part due to decreased vinculin expression, a focal adhesion structural protein. CONCLUSION: ACE activation regulates melanoma cell proliferation and migration.