Self-polymerization silica nanoparticles based molecularly imprinted polymers for selective recognition of protein.

Molecularly imprinted polymers (MIPs) are promising for precise protein separation and purification. However, challenges persist due to their large size, variable configuration, and instability during preparation. Here, a simple silicon self-assembly program was designed to synthesize MIPs without any organic reagents and acid-base catalysis, avoiding the structural damage of protein under severe conditions. In this method, employing hemoglobin (Hb) as a model protein, with tween-20 in emulsification, and tetraethyl orthosilicate (TEOS) as the cross-linking agent, along with co-functional monomers 3-aminopropyltriethoxysilane (APTES) and benzyl(triethoxy)silane (BnTES), enhanced binding efficacy was achieved. Successful imprinting was evidenced through surface morphology observation and physical/chemical property evaluations of the synthesized MIPs. A series of adsorption experiments were performed to investigate the recognition performance of Hb-MIPs. The Hb-MIPs not only exhibited large adsorption capacity (400 µg/mg) and good imprinting factor (6.09) toward template protein, but also showed satisfactory selectivity for reference proteins. Five cycles of adsorption proved that the Hb-MIPs had good reusability. In addition, the successful isolation of HB from bovine blood indicated that Hb-MIPs were an excellent separation and purification material. The mild preparation conditions and good adsorption capacity demonstrated the potential value of this method in separation and purification research.

Substance P aggravates ligature-induced periodontitis in mice.

Periodontitis is one of the most common oral diseases in humans, affecting over 40% of adult Americans. Pain-sensing nerves, or nociceptors, sense local environmental changes and often contain neuropeptides. Recent studies have suggested that nociceptors magnify host response and regulate bone loss in the periodontium. A subset of nociceptors projected to periodontium contains neuropeptides, such as calcitonin gene-related peptide (CGRP) or substance P (SP). However, the specific roles of neuropeptides from nociceptive neural terminals in periodontitis remain to be determined. In this study, we investigated the roles of neuropeptides on host responses and bone loss in ligature-induced periodontitis. Deletion of tachykinin precursor 1 (Tac1), a gene that encodes SP, or treatment of gingiva with SP antagonist significantly reduced bone loss in ligature-induced periodontitis, whereas deletion of calcitonin related polypeptide alpha (Calca), a gene that encodes CGRP, showed a marginal role on bone loss. Ligature-induced recruitment of leukocytes, including neutrophils, and increase in cytokines leading to bone loss in periodontium was significantly less in Tac1 knockout mice. Furthermore, intra-gingival injection of SP, but not neurokinin A, induced a vigorous inflammatory response and osteoclast activation in alveolar bone and facilitated bone loss in ligature-induced periodontitis. Altogether, our data suggest that SP plays significant roles in regulating host responses and bone resorption in ligature-induced periodontitis.