Abortion-Prone Mating Influences Alteration of Systemic a2 Vacuolar ATPase Expression in Spleen and Blood Immune Cells
Article first published online: 6 JAN 2012
© 2012 John Wiley & Sons A/S
American Journal of Reproductive Immunology
Volume 67, Issue 5, pages 421–433, May 2012
How to Cite
Jaiswal MK, Mallers TM, Kwong C, Chaouat G, Gilman-Sachs A, Beaman KD. Abortion-prone mating influences alteration of systemic a2 vacuolar ATPase expression in spleen and blood immune cells. Am J Reprod Immunol 2012; 67: 421–433
- Issue published online: 11 APR 2012
- Article first published online: 6 JAN 2012
- Manuscript Accepted: 8 DEC 2011
- Manuscript Received: 28 SEP 2011
- Abortion-prone mating;
a2 isoform of vacuolar ATPase (Atp6v0a2) is important for maintaining the delicate immunological balance required for successful pregnancy. The objective of this investigation is to study the dynamic changes in spleen and blood that appear during spontaneous abortion in mice.
Method of study
Atp6v0a2 was measured in multiple immune cell populations from spleen and blood recovered from non–abortion-prone and abortion-prone mating combinations.
Atp6v0a2 expression was significantly lower (P ≤ 0.01) in the spleen recovered from abortion-prone ♀CBA × ♂DBA mating on days 12 and 16 of pregnancy when compared to non–abortion-prone ♀BALB/c × ♂BALB/c and ♀CBA × ♂BALB/c matings. Flow cytometric studies showed that significantly decreased expression of Atp6v0a2 in splenic CD4+, CD8+, CD19+, and CD14+ cells directly correlated with the high percentages of fetal resorption observed in abortion-prone mating on days 12 and 16 of pregnancy. In blood, CD4+, CD8+, and CD19+ cells had a significantly reduced expression of Atp6v0a2 in abortion-prone mating compared to the non–abortion-prone mating combinations only on day 12.
This deceased expression of Atp6v0a2 in the various immune cell populations of the spleen and blood suggests that the maternal environment is not supportive to fetus and leads to poor pregnancy outcome in the abortion-prone mating model.