OBJECTIVETo investigate the property of genipin-crosslinked silk fibroin(SF)/chitosan(CS) microspheres for slow releasing of bovine serum albumin (BSA).

METHODSBSA-loaded genipin-crosslinked SF/CS microspheres were prepared by emulsion cross-linking technique. The micropheres were observed for surface morphology and size distribution under scanning electron microscope (SEM), and X-ray diffractometry (XRD) and fourier transform infrared spectroscopy (FTIR) were used to analyze their structural characteristics. BCA method was used for determining the drug entrapment, loading rate and cumulative drug release in 21 days.

RESULTThe microspheres were spherical and showed a smooth surface with an average diameter of 7.84∓0.97 µm. The drug entrapment efficiency of the microspheres was (50.16∓4.32)% with a drug loading ratio of (1.25∓0.11)% and a cumulative release of the total drug of (75.2∓2.53)% in 21 days.

CONCLUSIONGenipin-crosslinked SF/CS microspheres have a high drug entrapment efficiency and possess good capacity of sustained drug release.

Chitosan ; chemistry ; Delayed-Action Preparations ; Emulsions ; Fibroins ; chemistry ; Iridoids ; chemistry ; Microscopy, Electron, Scanning ; Microspheres ; Particle Size ; Spectroscopy, Fourier Transform Infrared ; X-Ray Diffraction ; X-Rays

Hereditary gingival fibromatosis (HGF) is a rare inherited condition with fibromatoid hyperplasia of the gingival tissue that exhibits great genetic heterogeneity. Five distinct loci related to non-syndromic HGF have been identified; however, only two disease-causing genes, SOS1 and REST, inducing HGF have been identified at two loci, GINGF1 and GINGF5, respectively. Here, based on a family pedigree with 26 members, including nine patients with HGF, we identified double heterozygous pathogenic mutations in the ZNF513 (c.C748T, p.R250W) and KIF3C (c.G1229A, p.R410H) genes within the GINGF3 locus related to HGF. Functional studies demonstrated that the ZNF513 p.R250W and KIF3C p.R410H variants significantly increased the expression of ZNF513 and KIF3C in vitro and in vivo. ZNF513, a transcription factor, binds to KIF3C exon 1 and participates in the positive regulation of KIF3C expression in gingival fibroblasts. Furthermore, a knock-in mouse model confirmed that heterozygous or homozygous mutations within Zfp513 (p.R250W) or Kif3c (p.R412H) alone do not led to clear phenotypes with gingival fibromatosis, whereas the double mutations led to gingival hyperplasia phenotypes. In addition, we found that ZNF513 binds to the SOS1 promoter and plays an important positive role in regulating the expression of SOS1. Moreover, the KIF3C p.R410H mutation could activate the PI3K and KCNQ1 potassium channels. ZNF513 combined with KIF3C regulates gingival fibroblast proliferation, migration, and fibrosis response via the PI3K/AKT/mTOR and Ras/Raf/MEK/ERK pathways. In summary, these results demonstrate ZNF513 + KIF3C as an important genetic combination in HGF manifestation and suggest that ZNF513 mutation may be a major risk factor for HGF.
Animals ; Humans ; Mice ; Fibromatosis, Gingival/pathology* ; Gingiva ; Kinesins/genetics* ; Mutation/genetics* ; Phosphatidylinositol 3-Kinases/genetics*