Literature update

Adult wounds heal with scar-tissue formation, whereas fetal wounds heal without scarringand with a lesser inflammatory and cytokine response . We injected the margins of healing dermal wounds in adult rats with neutralising antibody (NA) to transforming growth factor-(3 (TGF-R) . All control wounds (irrelevant antibody, or TGF-R, or no injection) healed with scarring, whereas the NA-treated wounds healed without scar-tissue formation ; NA-treated wounds had fewer macrophages and blood vessels, lower collagen and fibronectin contents, but identical tensile strength and more dermal architecture than the other wounds . Early manipulation of the concentrations of selected cytokines may be a new approach to the control ofscarring. (Reprinted by permission of The Lancet, Ltd .) Comment Abnormal deposition of connective tissue matrix, especially the overabundant deposition of collagen, is a major cause of morbidity and mortality in cases of human disease . These range from the annoyance of keloid and hypertrophic scar, to the restrictions of tendon adhesions, and, finally, to the disability and death as a result of hepatic fibrosis . Control of matrix deposition after tissue injury has been a major quest of wound healing research. Scores of agents have been evaluated with disappointing results . These include glucocorticoids, proline analogs, and R-aminopropionitrile . This report by Shah et al. is the first to Literature update document that the inflammatory response to injury can be modified by inhibition ofa cytokine involved early in the response to injury. Their report is short, and the number of animals per group is small . However, the data suggest that a TGF-R antibody treatment produced healed wounds with normal organization of the collagenous matrix, less total collagen content, but normal tensile strength. The histologic differences at 42 days are dramatic. Clearly, this landmark publication will be but the first of a series that should lead to the application of cytokine inhibitors in the treatment ofhuman fibrotic states . Prevention ofcytokine effects may well have more clinical application than the enhancement of wound healing by cytokines . I. Kelman Cohen, MD The Wound Healing Center Medical College of Virginia Richmond, Va. EXTRACELLULAR MATRIXANTIGENS AND REGENERATION Yang EV, Shima DT, Tassava RA. Monoclonal antibody STI identifies an antigen that is abundant in the axolotl and newt limb stump but is absent from the undifferentiated regenerate . J Exp Zool 1992;264:337-50. Abstract Monoclonal antibodies (mAb) utilized in regeneration studies to date identify antigens that are up-regulated in the blastema. We obtained a monoclonal antibody, designated ST1 (Stump 1) that is reactive to an extracellular matrix (ECM) antigen exhibiting the opposite distribution ; ST1 is an abundant antigen ofthe limb stump soft tissues but is absent from within the blastema. The border between abundance and absence of mAb ST1 reactivity was sharp and extended as a concavity into the stump . This distinct dichotomy led to further studies relevant to understanding how this extracellular matrix antigen is modulated during regeneration . mAb ST1 reactivity decreased in the internal tissues at the distal end of the limb prior to blastema formation and remained absent until the onset of differentiation . The initial decrease in mAb ST1 reactivity was dependent onthe combined effects of injury and the wound epithelium but was nerve independent . At blastema stages of regeneration the distribution of tenascin, ascertained by mAb MT1 reactivity, closely matched the area without reactivity to mAb ST 1 . The spatial and temporal distribution of the ST1 antigen in unamputated limbs and during regeneration did not correspond to anyMonoclonal antibodies (mAb) utilized in regeneration studies to date identify antigens that are up-regulated in the blastema. We obtained a monoclonal antibody, designated ST1 (Stump 1) that is reactive to an extracellular matrix (ECM) antigen exhibiting the opposite distribution ; ST1 is an abundant antigen ofthe limb stump soft tissues but is absent from within the blastema. The border between abundance and absence of mAb ST1 reactivity was sharp and extended as a concavity into the stump . This distinct dichotomy led to further studies relevant to understanding how this extracellular matrix antigen is modulated during regeneration . mAb ST1 reactivity decreased in the internal tissues at the distal end of the limb prior to blastema formation and remained absent until the onset of differentiation . The initial decrease in mAb ST1 reactivity was dependent onthe combined effects of injury and the wound epithelium but was nerve independent . At blastema stages of regeneration the distribution of tenascin, ascertained by mAb MT1 reactivity, closely matched the area without reactivity to mAb ST 1 . The spatial and temporal distribution of the ST1 antigen in unamputated limbs and during regeneration did not correspond to any