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Evidence of Increased Gc: Actin Complexes in Pregnant Serum: A Possible Result of Trophoblast Embolism
Author(s) -
EMERSON DAVID L.,
ARNAUD PHILIPPE,
GALBRAITH ROBERT M.
Publication year - 1983
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
eISSN - 1600-0897
pISSN - 0271-7352
DOI - 10.1111/j.1600-0897.1983.tb00276.x
Subject(s) - trophoblast , actin , pregnancy , vitamin d and neurology , biology , placenta , vitamin d binding protein , vitamin , lysis , isoelectric focusing , biochemistry , chemistry , microbiology and biotechnology , endocrinology , fetus , genetics , enzyme
ABSTRACT: The molecular configuration of group‐specific component Gc protein in sera from pregnant and nonpregnant individuals was compared by analytical isoelectric focusing and by print immunofixation in conjunction with known standards of Gc:actin and Gc:vitamin D 3 complexes. These studies revealed that while complexes of Gc with actin and with vitamin D were detectable in small amounts in nonpregnant sera, much larger quantities of both types of complexes were consistently visualized in pregnancy. In addition, when actin was added to pregnant sera containing Gc:vitamin D 3 complexes, a third anodal complex was revealed which presented the molecular configuration of actin: Gc: vitamin D 3 . These results demonstrate that Gc:actin complexes may be present under physiological circumstances in the circulation. Since large amounts of trophoblast enter the maternal circulation during both normal and abnormal human pregnancy, experiments were undertaken that showed that actin was released from isolated trophoblast membranes and also upon lysis of other viable cells under physiological conditions similar to those obtained in serum, and such actin complexed rapidly with Gc. Although the effects of this phenomenon upon the immunobiology of pregnancy are unknown, these findings are consistent with the concept that Gc protein may exert a “scavenger” function in mopping up actin released from damaged cells.