PubMed · 3685193
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S J Stegman. 1987. Injectable collagen.. https://doi.org/10.1097/00006534-198712000-00034
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The importance of vicinal and long-range interresidue effects in determining the stability of the collagen triple helix has been investigated by quantum mechanical (QM) and molecular mechanical (MM) computations on suitable model polypeptides, taking into account solvent effects by the polarizable continuum model (PCM). At the QM level, the PII conformation corresponds to an energy minimum for pentapeptide analogues incorporating the sequence Gly-Pro-Pro-Gly, irrespective of the down or up puckering of the pyrrolidine ring. However, our computations indicate that the alternation of down and up prolines characterizing collagen and collagen-like peptides is not due to an intrinsic preference of the Pro-Pro-Gly sequence. This result is confirmed by MM computations of longer polypeptides. Next, MM computations on model triple helices show that a better packing is obtained for specific values of backbone dihedrals, which, in turn, favor the alternation of down and up prolines along each chain.
Our objective was to strengthen and stabilize collagen films without the introduction of cytotoxic chemical crosslinkers. We hypothesized that collagen could be rapidly crosslinked with glucose with ultraviolet (UV) irradiation as a catalyst. In theory, UV-generated free radicals can expedite collagen crosslinking with glucose via the formation of reactive, linear glucose molecules. The mechanical properties of glucose-incorporated, UV-exposed collagen films and appropriate controls were determined under various conditions: (1) hydration in phosphate-buffered saline, (2) heat-denaturation, (3) incubation in a collagenase solution, and (4) incubation in a trypsin solution. Without exposure to UV, the incorporation of glucose into the films had no effect. Without glucose, exposure to UV increased the strength but caused significant denaturation. The combination of glucose and UV, however, synergistically improved the mechanical properties and enzyme resistance of collagen films, indicative of increased crosslinking without significant denaturation effects. The addition of thiourea, a potent free-radical scavenger, or aminoguanidine, an inhibitor of glucose-derived crosslinking, to the collagen films markedly hindered these synergistic effects. These data strongly suggest that free-radical-dependent, glucose-derived crosslinks provide the enhanced strength and enzyme resistance observed in glucose-incorporated, UV-exposed collagen films. Further studies are required to explore biomaterial applications of this novel collagen crosslinking method.
Vascular Ehlers Danlos syndrome (EDS) is a rare autosomal dominant inherited disorder of connective tissue resulting from mutation of the COL3A1 gene encoding type III collagen. Affected individuals are prone to serious vascular, intestinal, and obstetrical complications. Complications are rare during infancy but occur in up to 25% of affected persons before the age of 20 and 80% before the age of 40. Median survival is 48 years. Arterial rupture accounts for most deaths. Intestinal perforation, usually involving the colon, are less fatal. Pregnancy is a high risk for women with EDS. As for many rare orphan diseases, delayed and/or improper diagnosis can lead to inadequate or inappropriate treatment and management. Diagnosis is based on clinical findings including specific facial features, thin translucent skin, propensity to bleeding, and rupture of vessels and/or viscera. Diagnosis can be confirmed either by biochemical assays showing qualitative or quantitative abnormalities in type III collagen secretion or by molecular biology studies demonstrating mutation of the COL3A1 gene. Varied molecular mechanisms have been observed with different mutations in each family. No correlation has been established between genotype and phenotype. Diagnosis should be suspected in any young person presenting with arterial or visceral rupture, carotid dissection, or colonic perforation. There are currently no specific treatments for EDS.