ABSTRACT
Lectins are proteins responsible for recognizing the signals of sugar molecules in the body. Sialic acid-binding immunoglobulin-like lectins (Siglecs) regulate the innate and adaptive immune responses in the tumor microenvironment by recognizing the glycan structure containing sialic acid and mediating downstream signals through immune receptor tyrosine inhibitory motifs. In recent years, a variety of tumor treatment strategies targeting the sialic acid-Siglecs axis have been introduced, including sialoglycoprotein-mediated drug delivery and antibody mediated inhibition of Siglecs from recognizing tumor surface ligands. In the future, by combining with glycoprotein nanotherapy, antibody therapy and gene therapy, Siglecs can be used to accurately locate tumor targets and release the anti-tumor immunity, so as to achieve the purpose of effective cure of tumors.
Subject(s)
Sialic Acid Binding Immunoglobulin-like Lectins/metabolism , N-Acetylneuraminic Acid , Immunoglobulins/metabolism , Receptors, Immunologic , LigandsABSTRACT
Objeetive To investigate the optimized concentration,effectiveness and histological change of Pingyangmycin by local injection of keloids for two weeks.Methods The appropriate concentration was analyzed,based on the Vancouver scar scale.48 eases of keloids were randomly divided into 4 groups with different concentrations of Pingyangmycin (1,0.5,0.25,and 0.125 mg/ml).Each case was iniected for five times at two weeks intervals,and then the statistical results (pair t test) and the histological changes were evaluated.Results Statistically,0.5 mg/ml group was more effective (P=0.0026),and this group had significant differences from the others (SNK test).The rate of the recurrence for one year was 12.00% in the whole effective cases.The keloid tissue after treatments,histologically,showed the thicker epidermis and larger papillary layer of the dermis,more inflammatory cells.Conclusions 0.5 mg/ml Pingyangmycin is the most appropriate concentration in this study and 0.25 mg/ml is the effective one.This treatment for keloid is convenient,safe,effective,low recrudescence and few side effects.
ABSTRACT
The recombinant human Smad7 adenoviral vector was constructed by direct DNA cloning protocol and then transfected into 293 cells for virus packaging. After amplification and purification, the recombinant adenovirus was used to infect the keloid fibroblasts. The Smad7 mRNA transcription of the infected cells was detected by RT-PCR. The recombinant Adeno-Smad7 was correctly constructed and confirmed by both restriction analysis and PCR analysis. RT-PCR showed the over expression of adenovirus mediated Smad7 mRNA in keloid cells. These results demonstrated that the recombinant Smad7 adenoviral vector can be expressed in cultured cells in vitro, and it may provide a new therapeutic strategy for keloid gene therapy.
Subject(s)
Humans , Adenoviridae , Genetics , Metabolism , Cells, Cultured , Fibroblasts , Metabolism , Pathology , Genetic Vectors , Genetics , Metabolism , Keloid , Metabolism , Pathology , RNA, Messenger , Genetics , Recombinant Fusion Proteins , Genetics , Smad7 Protein , Genetics , TransfectionABSTRACT
<p><b>OBJECTIVE</b>To study transforming growth factor-beta1 (TGF-beta1) autoproduction in keloid fibroblasts and the regulation effect of blocking TGF-beta intracellular signaling on rhTGF-beta1 autoproduction.</p><p><b>METHODS</b>Keloid fibroblasts cultured in vitro were treated with either rhTGF-beta1 (5 ng/ml) or recombinant adenovirus containing a truncated type II TGF-beta receptor gene (50 pfu/cell). Their effects of regulating gene expression of TGF-beta1 and its receptor I and II were observed with Northern blot.</p><p><b>RESULTS</b>rhTGF-beta1 up-regulated the gene expression of TGF-beta1 and receptor I, but not receptor II. Over-expression of the truncated receptor II down-regulated the gene expression of TGF-beta1 and its receptor I, but not receptor II.</p><p><b>CONCLUSIONS</b>TGF-beta1 autoproduction was observed in keloid fibroblasts. Over-expression of the truncated TGFbeta receptor II decreased TGF-beta1 autoproduction via blocking TGF-beta receptor signaling.</p>