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PMID:12861045

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Citation

Samuel, CS, Tian, H, Zhao, L and Amento, EP (2003) Relaxin is a key mediator of prostate growth and male reproductive tract development. Lab. Invest. 83:1055-67

Abstract

Male mice deficient in relaxin showed retarded growth and marked deficiencies in the reproductive tract within 1 month of age. At 3 months of age, male reproductive organ weight (including the testis, epididymis, prostate, and seminal vesicle) from relaxin null (RLX-/-) mice were significantly (p < 0.05) smaller than those of wild-type (RLX+/+) male mice. Histologic examination of RLX-/- mouse tissues demonstrated decreased sperm maturation (testis), increased collagen, and decreased epithelial proliferation in the prostate compared with tissues obtained from RLX+/+ animals. The degree of sperm maturation in the testes of sexually mature RLX-/- mice (3 months) resembled that of immature (1 month) RLX+/+ mice and correlated with a decrease in fertility in RLX-/- mice. The marked differences in the extracellular matrix of the testis and prostate in RLX-/- males also correlated with an increase in the rate of cell apoptosis. Relaxin and LGR7 (relaxin receptor) mRNA expression was demonstrated in the prostate gland and testis of the normal mouse. Data from this study demonstrate that relaxin is an important factor in the development and function of the male reproductive tract in mice and has an essential role in the growth of the prostate and maintenance of male fertility. Relaxin may mediate its effects on growth and development by serving as an antiapoptotic factor.

Links

PubMed

Keywords

Animals; Apoptosis/genetics; Cell Division; Epididymis/growth & development; Epididymis/pathology; Female; Fertility/genetics; Fertility/physiology; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Organ Size; Proliferating Cell Nuclear Antigen/metabolism; Prostate/growth & development; Prostate/pathology; RNA, Messenger/metabolism; Receptors, G-Protein-Coupled; Receptors, Peptide/genetics; Receptors, Peptide/metabolism; Relaxin/deficiency; Relaxin/genetics; Relaxin/physiology; Seminal Vesicles/growth & development; Seminal Vesicles/pathology; Spermatogenesis/genetics; Testis/growth & development; Testis/pathology

Significance

Annotations

Gene product Qualifier GO Term Evidence Code with/from Aspect Extension Notes Status

MOUSE:REL1

acts_upstream_of_or_within

GO:0060736: prostate gland growth

ECO:0000315: mutant phenotype evidence used in manual assertion

MGI:MGI:2668458

P

  • occurs_in:(EMAPA:32290)

Seeded From UniProt

complete

MOUSE:REL1

acts_upstream_of_or_within

GO:0048589: developmental growth

ECO:0000315: mutant phenotype evidence used in manual assertion

MGI:MGI:2668458

P

  • occurs_in:(EMAPA:19180)|occurs_in:(EMAPA:19290)|occurs_in:(EMAPA:17972)

Seeded From UniProt

complete

MOUSE:REL1

acts_upstream_of_or_within

GO:0048589: developmental growth

ECO:0000315: mutant phenotype evidence used in manual assertion

MGI:MGI:2668458

P

occurs_in:(EMAPA:19180)|occurs_in:(EMAPA:19290)|occurs_in:(EMAPA:17972)

Seeded From UniProt

complete

MOUSE:REL1

acts_upstream_of_or_within

GO:0060736: prostate gland growth

ECO:0000315: mutant phenotype evidence used in manual assertion

MGI:MGI:2668458

P

occurs_in:(EMAPA:32290)

Seeded From UniProt

complete

MOUSE:REL1

involved_in

GO:0042981: regulation of apoptotic process

ECO:0000315: mutant phenotype evidence used in manual assertion

P

Seeded From UniProt

complete

MOUSE:REL1

involved_in

GO:0007283: spermatogenesis

ECO:0000315: mutant phenotype evidence used in manual assertion

P

Seeded From UniProt

complete

MOUSE:REL1

GO:0007283: spermatogenesis

ECO:0000315:

P

In figure 2 E,F,G &H, the authors demonstrate that there is a reduction in mature spermatozoa formation in seminiferous tubules of homozygous relaxin knockout mice.

complete
CACAO 2083

MOUSE:REL1

GO:0042981: regulation of apoptosis

ECO:0000315:

P

In table 2, the authors demonstrate that homozygous relaxin knockout mice had more Bax and caspase-9 positive cells in the testis.

complete
CACAO 2084


See also

References

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