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Letters to the Editor |
New York University Medical Center New York, NY 10016
We would like to thank Dr. Smith for his interest and comments concerning our paper entitled "Apoptosis and Fas Expression in Human Fetal Membranes," which appeared in the February 1998 issue of this journal. We agree with Dr. Smith that TUNEL staining can lead to inflated estimates of apoptosis. This is discussed in our manuscript and is the reason why TUNEL data were presented as an apoptotic index (TUNEL stained nuclei/total nuclei) and not as a percentage of apoptotic cells. We feel that it is unlikely that a 25-min incubation with proteinase K instead of a 15-min treatment was responsible for high apoptotic indices. In our laboratory the effectiveness of proteinase K treatment for in situ procedures is determined by the appearance of "pepper spots" within tissue (indicative of permeabilization) that varies not only with respect to the type of tissue but also with the lot of proteinase K. Others have found that the length of proteinase K treatment required to permeabilize tissue was proportional to the strength of tissue fixation (1). It is likely that necrosis, occurring concomitant with apoptosis in fetal membranes, may lead to overestimates of apoptotic cells by TUNEL.
As it has been established by our group and others that apoptosis does occur in fetal membranes (2, 3, 4, 5), the question remains as to the biological significance of apoptosis at this site. Several research groups (2, 4, 5, 6) are currently exploring the role of apoptosis and its potential relationship to premature rupture of the fetal membranes, a leading cause of neonatal mortality and morbidity (7). Elegant morphological studies indicated that the "rupture site" in fetal membranes was most likely characterized by a "zone of altered morphology," containing cell layers of reduced thickness and disrupted connective tissue (8). Lei et al. (5) suggested that a coordinated program of metalloproteinase activation and collagenolysis promoted amnion epithelial cell apoptosis before the onset of labor. It has also been proposed that alterations in collagen synthesis and/or assembly and loss of cell/matrix associations may play a critical role in regulating fetal membrane apoptosis and integrity in association with labor (6, 9, 10). Thus, it is likely that the percentage of apoptotic cells in fetal membranes will be determined by periparturitional events that may be localized to specific regions of fetal membranes. Therefore, extrapolation of apoptotic indices observed in other tissues to fetal membranes may be inappropriate. We look forward to future studies that will explore the "where, when, and how" aspects of fetal membrane apoptosis.
Footnotes
Address correspondence to: Seth Guller, Ph.D., Department of Obstetrics and Gynecology, New York University Medical Center, 550 First Avenue, New York, New York 10016.
Received July 13, 1998.
References
R, Lockwood CJ, LaChapelle L, et al. 1998 Apoptosis and Fas expression in human fetal membranes. J Clin
Endocrinol Metab. 83:660–666. R, Lockwood CJ, LaChapelle L, et al. 1996 Apoptosis in human fetal membranes: implications in
parturition-associated changes in fetal membrane integrity. J Soc
Gynecol Invest. 3:293A.
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