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Biology of Reproduction 63, 697-703 (2000)
© 2000 Society for the Study of Reproduction, Inc.


Regular Article

Collagen Studies in Late Pregnant Relaxin Null Mice1

Ling Zhaoa, Chrishan S. Samuel3,a, Geoffrey W. Tregeara, Felix Beck4,a, and E. Marelyn Wintour2,a

a Howard Florey Institute of Experimental Physiology and Medicine, The University of Melbourne, Parkville, Victoria 3010, Australia

ABSTRACT

The relaxin knockout (rlx -/-) mouse was used to assess the effect, during pregnancy, of relaxin with regard to water, collagen content, growth, and morphology of the nipple (N), vagina (V), uterus, cervix (C), pubic symphysis (PS), and mammary gland (MG). The results presented here indicate that during pregnancy, relaxin increases the growth of the N, C, V, and PS. Large increases in water content in the PS (20%) occurred in pregnant (Day 18.5) wild-type (rlx +/+) mice but not in rlx -/- animals. This indicates that in the PS, relaxin might increase the concentration of a water-retaining extracellular matrix component (hyaluronate). In the pregnant rlx +/+ mouse, collagen content decreased significantly in the N and V but not in other tissues. There were no significant changes in the rlx -/- mouse. This contrasts with findings in the rat, in which relaxin has been found to cause decreases in collagen concentrations in the V, C, and PS. Histological analysis showed that the collagen stain was more condensed in the tissues (V, C, PS, N, and MG) of rlx -/- mice than in those of rlx +/+ mice. This phenomenon indicates that the failure of collagen degradation and lack of growth in the N underlie the inability of the rlx -/- mice to feed their young, as reported previously. Vaginal and cervical luminal epithelia, which proliferated markedly in the rlx +/+ pregnant mice, remained relatively atrophic in the rlx -/- mice. As proliferation and differentiation of uterine and vaginal epithelia are thought to be induced by a paracrine stromal factor that acts upon estrogen stimulation, our results indicate that relaxin may be this paracrine factor.

FOOTNOTES

First decision: 25 October 1999.

1 Supported by a grant (983001) from the National Health and Medical Research Council to the Howard Florey Institute. L.Z. is supported by an Overseas Postgraduate Research Scholarship and University of Melbourne Postgraduate Research Scholarship.

2 Correspondence. FAX: 61 3 9348 1707; mwc{at}hfi.unimelb.edu.au

3 Current address: Department of Dermatology, Stanford University & Molecular Medicine Research Institute, Mountain View, CA 94043.

4 Current address: Department of Biochemistry, Leicester University, Leicester, United Kingdom.




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