Both of these osteoblastic markers were upregulated by DGEA and P15, in the presence and absence of differentiation-inducing media.
Meanwhile, seven markers were upregulated by C2D1 (E-Cadherin, soluble Endoglin [sEnd], E-Selectin, interleukin-6 [IL-6], osteopontin [OPN], TSP-2, and von Willebrand factor [vWF]).
At EOS, seven markers were upregulated including Ang-2, C-reactive protein (CRP), intercellular adhesion molecule-1 (ICAM-1), IGFBP-1, IL-6, TSP-2, and vascular cell adhesion molecule-1 (VCAM-1).
In contrast, many mesenchymal markers were upregulated in EPT1 cells, including cadherin 11 (CDH11), vimentin (VIM) and fibronectin (FN).
Differentiation of these hair cells started around the same time those markers were upregulated in the nearby vestibular sensory epithelia and, transiently, in the delaminating sensory neurons.
Comparative analysis of expression levels of MHC II, CD80 and CD86 showed that these surface markers were upregulated in pDCs from CCR9−/− animals (Figure 6B).
Moreover, mature pancreatic β-cell markers are upregulated in the PP2-β INS+ cells (Fig. 1h).
In agreement, expression of bone and osteoclast gene markers was upregulated in TCPs versus both TCPb and TCPs + LipClod, which were equivalent.
In spite of this, further development of the AVC is not achieved and instead, chamber markers are upregulated.
When exposed to UV-inactivated virus, expression of maturation markers was upregulated in mDC1 (Figure 4D) and pDCs (data not shown).
Although collection of exosomes from tissue is not possible, our previous studies of mtDNA damage in ARPE-19 cells demonstrated that exosome markers are upregulated and released when the cells are stressed [17].
