RESUMEN
Development and selection of an ideal scaffold is of importance for tissue engineering. Poly(3-hydroxybutyrate-co-3-hydroxyhexanoate) (PHBHHx) is a biocompatible bioresorbable copolymer that belongs to the polyhydroxyalkanoate family. Because of its good biocompatibility, PHBHHx has been widely used as a cell scaffold for tissue engineering. This review focuses on the utilization of PHBHHx-based scaffolds in tissue engineering. Advances in the preparation, modification, and application of PHBHHx scaffolds are discussed.
Asunto(s)
Humanos , /química , Materiales Biocompatibles/química , Caproatos/química , Ingeniería de Tejidos/métodos , Andamios del Tejido/química , /uso terapéutico , Materiales Biocompatibles/uso terapéutico , Huesos/fisiología , Caproatos/uso terapéutico , Cartílago/fisiología , Liofilización , Músculo Liso/fisiología , Regeneración , Propiedades de SuperficieRESUMEN
SRY-related high-mobility-group box 9 (Sox9) gene is a cartilage-specific transcription factor that plays essential roles in chondrocyte differentiation and cartilage formation. The aim of this study was to investigate the feasibility of genetic delivery of Sox9 to enhance chondrogenic differentiation of human umbilical cord blood-derived mesenchymal stem cells (hUC-MSCs). After they were isolated from human umbilical cord blood within 24 h after delivery of neonates, hUC-MSCs were untreated or transfected with a human Sox9-expressing plasmid or an empty vector. The cells were assessed for morphology and chondrogenic differentiation. The isolated cells with a fibroblast-like morphology in monolayer culture were positive for the MSC markers CD44, CD105, CD73, and CD90, but negative for the differentiation markers CD34, CD45, CD19, CD14, or major histocompatibility complex class II. Sox9 overexpression induced accumulation of sulfated proteoglycans, without altering the cellular morphology. Immunocytochemistry demonstrated that genetic delivery of Sox9 markedly enhanced the expression of aggrecan and type II collagen in hUC-MSCs compared with empty vector-transfected counterparts. Reverse transcription-polymerase chain reaction analysis further confirmed the elevation of aggrecan and type II collagen at the mRNA level in Sox9-transfected cells. Taken together, short-term Sox9 overexpression facilitates chondrogenesis of hUC-MSCs and may thus have potential implications in cartilage tissue engineering.
Asunto(s)
Humanos , Diferenciación Celular/genética , Condrogénesis/genética , Sangre Fetal/citología , Células Madre Mesenquimatosas/citología , Factor de Transcripción SOX9/genética , Agrecanos/biosíntesis , Western Blotting , Cartílago/metabolismo , Proliferación Celular/genética , Condrocitos/metabolismo , Colágeno Tipo II/biosíntesis , Citometría de Flujo , Proteínas Fluorescentes Verdes , Regulación de la Expresión Génica/fisiología , Células Endoteliales de la Vena Umbilical Humana/citología , Inmunohistoquímica , Inmunofenotipificación , Cultivo Primario de Células , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Ingeniería de Tejidos , TransfecciónRESUMEN
Angiopoietin (Ang)-1 and Ang-2 interact in angiogenesis to activate the Tie-2 receptor, which may be involved in new vessel maturation and regression. Mast cells (MCs) are also involved in formation of new blood vessels and angiogenesis. The present study was designed to test whether MCs can mediate angiogenesis in myocardial microvascular endothelial cells (MMVECs). Using a rat MMVEC and MC co-culture system, we observed that Ang-1 protein levels were very low even though its mRNA levels were increased by MCs. Interestingly, MCs were able to enhance migration, proliferation, and capillary-like tube formation, which were associated with suppressed Ang-2 protein expression, but not Tie-2 expression levels. These MCs induced effects that could be reversed by either tryptase inhibitor [N-tosyl-L-lysine chloromethyl ketone (TLCK)] or chymase inhibitor (N-tosyl-L-phenylalanyl chloromethyl ketone), with TLCK showing greater effects. In conclusion, our data indicated that MCs can interrupt neovessel maturation via suppression of the Ang-2/Tie-2 signaling pathway.