PubMed · 10499712
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P Rosen, R D Berlin, G P Poore. Appendagitis masquerading as appendicitis.. https://pubmed.ncbi.nlm.nih.gov/10499712/
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Decellularized tissues provide biological cues owing to the wealth of structural and regulatory factors that promote angiogenesis, adipogenesis, and myogenesis and facilitate neurite outgrowth. Here, we demonstrated the advantages of decellularized adipose tissue (adipoECM) over defined collagen-based biomaterials for host tissue integration. Three batches of human adipose tissue were decellularized using a rapid decellularization protocol and analyzed using mass spectrometry. To assess the biological activity of the decellularized materials, adipoECM and a reference standard of care biomaterial (Integra®DRT, also containing collagen I and glycosaminoglycans) were implanted subcutaneously, but far from the wound bed (in anatomical potential spaces) of immunocompetent BALB/c mice. The mice were euthanized in the acute (1 day) and chronic (day 60) inflammatory reaction phases, followed by biomaterial excision and Masson’s trichrome immunohistofluorescence imaging of the paraffin-embedded specimens. Each batch of processed tissue passed a quality control check, showing a low level of donor genomic DNA, lack of nuclei, lipids, endotoxins, and bacterial contamination. Mass spectrometry revealed that all batches of decellularized tissue mainly contained collagen I and, to a lesser degree, collagen III, collagen IV, collagen V, laminin, fibrillin, fibronectin, tenascin, and elastin. No acute inflammatory reaction was observed in either material one day post-transplantation. At 60 days post-implantation, different cell types were detected in adipoECM specimens, whereas Integra®DRT remained acellular. Additional immunohistochemical staining of adipoECM revealed CD31-positive cells in the blood vessels. Mesenchymal (CD90 positive) and myeloid (CD14 positive) cells were also detected. Primary cell types involved in soft tissue healing and remodeling were found in the adipoECM-treated group. The ingrowth of blood vessels and mesenchymal cells confirmed the effective integration of adipoECM with host tissues. Our results demonstrate that decellularized adipose tissue implanted away from the wound bed possesses contextual biological activities that promote efficient integration with host tissues.
Most endocrine hormones are produced in tissues and organs with permeable microvessels that may provide an excess of hormones to be transported by the blood circulation to the distal target organ. Here, we investigate whether leptin, an endocrine hormone, induces the formation of vascular fenestrations and permeability, and we characterize its angiogenic property in the presence of other angiogenic factors. We provide evidence that leptin-induced new blood vessels are fenestrated. Under physiological conditions, capillary fenestrations are found in the leptin-producing adipose tissue in lean mice. In contrast, no vascular fenestrations were detected in the adipose tissue of leptin-deficient ob/ob mice. Thus, leptin plays a critical role in the maintenance and regulation of vascular fenestrations in the adipose tissue. Leptin induces a rapid vascular permeability response when administrated intradermally. Further, leptin synergistically stimulates angiogenesis with fibroblast growth factor (FGF)-2 and vascular endothelial growth factor (VEGF), the two most potent and commonly expressed angiogenic factors. These findings demonstrate that leptin has another new function-the increase of vascular permeability.
The role of oxidative stress and antioxidant defense in 3,3',4,4',5-pentachlorobiphenyl (PCB 126)-induced toxicity and species-specific sensitivity was examined in White Leghorn chicken (Gallus domesticus) and Pekin duck (Anas platyrhynchos) embryos. Eggs were injected into the air cell with 0.4-1.6 microgram PCB 126/kg egg in corn oil prior to incubation. Lipid peroxidation measured by thiobarbituric acid reactive substances (TBARS), the GSSG:GSH ratio, and glutathione peroxidase (GPox) activities were determined in liver and adipose tissue of day 19 chicken and day 26 duck embryos. In chicken embryos, PCB 126 increased mortality and the incidence of edema and liver lesions, decreased embryo size, increased eye and head malformations, and markedly reduced fat storage. In contrast, no effects on the endpoints were observed in duck embryos even at the highest dose used in chicken embryos. PCB 126 increased hepatic 7-ethoxyresorufin-O-deethylase (EROD) activity in a dose-dependent manner in chicken but not duck embryos. PCB 126 significantly increased TBARS levels in liver and to a greater degree in adipose tissue of chicken embryos, indicating that adipose tissue is a sensitive target for this compound. Increases in lipid peroxidation by PCB 126 were associated with significant decreases in GPox activity in these tissues. These biochemical changes support oxidative stress playing a role in PCB 126-induced embryo toxicity while antioxidant defenses provided protection against oxidative damage induced by this compound. Ducks, the less-sensitive species, showed higher basal levels of hepatic GPox than chickens, suggesting that this antioxidant enzyme may contribute to the differences in sensitivity to this compound between the two species.