Hyperosmolar stress induces global mRNA responses in placental trophoblast stem cells that emulate early post-implantation differentiation.

摘要: Hyperosmolar stress acts in two ways on the implanting embryo and its major constituent, placental trophoblast stem cells (TSC). Stress causes homeostasis that slows development with lesser cell accumulation, increased cycle arrest, apoptosis. may also cause differentiation at implantation. To test for homeostatic differentiation-inducing consequences of stress, TSC were exposed to hyperosmolar 24 h tested using whole mouse genome arrays Real-time quantitative (Q)PCR. At 0.5 h, all 31 highly changing mRNA (>1.5-fold compared unstressed TSC) decreased, but by 158/288 genes upregulated. Many upregulated near baseline levels TSC, suggesting new transcription. Thus few change during early response, have adapted start transcription large gene sets. Types included regulating growth DNA damage induced (GADD45beta/gamma), activator protein (AP)-1 (junB/junC/ATF3/4), heat shock proteins (HSP22/68), cyclin-dependent kinase inhibitor [CDKI; p15, p21]. But, factors mediate giant (TGC) (Stra13, HES1, GATA-binding2), hormones [proliferin, lactogen (PL)1, prolactin-like (PLP)M], extracellular matrix (CCN1/2). Transcription later lineages, spongiotrophoblast (MASH2, TPBPalpha) syncytiotrophoblast (GCM1, TEF5) (PLPA, PLII) not stress. temporal spatial normal after Although was induced, markers stemness such as (ID)2 remained 100% retained might dedifferentiation subside.