Hormonal regulation of complement components and receptors throughout the menstrual cycle.
OBJECTIVE
Complement components have been recently demonstrated to be present in the reproductive tract. Among these components, C3 synthesis by glandular epithelium of the rat uterus has been shown to be regulated by estrogen; progesterone inhibits this synthesis. However, the hormonal regulation of C3 and the presence of other complement factors in the human has not been investigated to date. In this study we examined the presence and the hormonal regulation of different complement components and receptors in the human endometrium at various phases of the menstrual cycle of normally cycling women with no pelvic pathologic abnormalities.


METHODS
Endometrial tissue was obtained from normally cycling women, and immunohistochemistry was performed by means of monoclonal antibodies against C3, factors B, decay-accelerating factor, membrane cofactor protein, and complement receptor types 1, 2, and 3. The tissue was incubated with minimal essential media without methionine containing methionine labeled with sulfur 35. Immunoprecipitations were performed on the media with goat antihuman C3 antibody, and the proteins were analyzed by sodium dodecyl sulfate polyacrylamide gel electrophoresis.


RESULTS
C3 was found to be present in the glandular epithelial cells of luteal endometrium. Biosynthesis as analyzed by immunoprecipitation with anti-C3 antibody was found to increase during the luteal phase of the cycle and to be minimal in the proliferative phase. Like C3, factor B and decay-accelerating factor were localized to the luteal glandular epithelial cells. In contrast, membrane cofactor protein was found to be present in the glandular epithelium throughout the menstrual cycle, and complement receptor type 1 was present only in the stromal compartment of luteal endometrium. Complement receptor type 3 was present only in the infiltrating leukocytes in the luteal endometrium, whereas complement receptor type 2 was undetectable.


CONCLUSIONS
These findings suggest that several components of the complement system exist in the human endometrium in a hormone-dependent manner and may play a role in normal reproductive function.
Hasty
L A
LA
Department of Obstetrics and Gynecology, University of Pennsylvania School of Medicine, Philadelphia.
Lambris
J D
JD
Lessey
B A
BA
Pruksananonda
K
K
Lyttle
C R
CR
D000328:Adult; D015703:Antigens, CD / Q000096:biosynthesis; D018958:CD55 Antigens; D003176:Complement C3 / Q000096:biosynthesis*; D011415:Complement Factor B / Q000096:biosynthesis; D003169:Complement Inactivator Proteins / Q000096:biosynthesis; D004591:Electrophoresis, Polyacrylamide Gel; D004717:Endometrium / Q000276:immunology / Q000378:metabolism*; D005260:Female; D005498:Follicular Phase / Q000378:metabolism; D012739:Gonadal Steroid Hormones / Q000502:physiology*; D006801:Humans; D007150:Immunohistochemistry; D008183:Luteal Phase / Q000378:metabolism; D016177:Macrophage-1 Antigen / Q000096:biosynthesis; D051916:Membrane Cofactor Protein; D008562:Membrane Glycoproteins / Q000096:biosynthesis; D008597:Menstrual Cycle / Q000276:immunology* / Q000378:metabolism; D011951:Receptors, Complement / Q000096:biosynthesis*; D017463:Receptors, Complement 3b / Q000096:biosynthesis; D017464:Receptors, Complement 3d / Q000096:biosynthesis
D015703:Antigens, CD; C497857:CD46 protein, human; D018958:CD55 Antigens; D003176:Complement C3; D003169:Complement Inactivator Proteins; D012739:Gonadal Steroid Hormones; D016177:Macrophage-1 Antigen; D051916:Membrane Cofactor Protein; D008562:Membrane Glycoproteins; D011951:Receptors, Complement; D017463:Receptors, Complement 3b; D017464:Receptors, Complement 3d; D011415:Complement Factor B