Methods: BeWo were treated with A.a. LPS, and mRNA levels were detected using an Affymetrix GeneChip (Human Genome U133 plus 2.0 array, ca. 47,000 genes). GeneChip data showed that the heat shock protein family expression increased in trophoblast cells after A.a. LPS challenge. Altered mRNA levels in GeneChip results were confirmed by RT-PCR and real-time PCR.
Results: GeneChip analysis revealed increased mRNA levels of HSPA1A (Heat shock 70kDa protein 1A), HSPA1B (Heat shock 70kDa protein 1B), HSPA6 (Heat shock 70kDa protein 6), HSPA8 (Heat shock 70kDa protein 8), HSPD1 (heat shock 60kDa protein 1), HSPCA (Heat shock 90kDa protein 1, alpha) HSPE1 (Heat shock 10kDa protein 1), DNAJA1 (DnaJ [Hsp40] homolog, subfamily A, member 1), DNAJB1 (DnaJ [Hsp40] homolog, subfamily B, member 1) and HSPH1 (Heat shock 105kDa/110kDa protein 1). Real-time PCR analyses successfully confirmed these mRNA level changes from the GeneChip data.
Conclusion: HSP70 has been reported to be associated with placental vascular diseases, such as preeclampsia and intrauterine growth restriction (IUGR). Higher expression of HSP60, HSP70 and HSP90 were also detected in various pathological findings of placentas, which were related with IUGR. In line with previous studies, our results showed increased mRNA expression of a total of 10 memebers of heat shock protein family. These results suggest that A.a LPS may induce adverse pregnant outcome through increased expression of heat shock proteins. This might be one of the molecular mechanisms of periodontitis associated low birth weight.