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. 2021 Jan 23;10(2):224. doi: 10.3390/cells10020224

Figure 4.

Figure 4

Hdac1 and Hdac2 deletion disrupts jejunal epithelial differentiation and MHC class II gene expression. Total RNA was purified from enriched control and Hdac1−/−; Hdac2−/− jejunal IEC. Expression levels of secretory cell differentiation marker Reg3g, Reg3b, Cryptdin and ChgA (A), enterocyte cell marker Alpi, Slc15a1, Sis and Fabp2 (B), goblet cell marker Tff3, Muc2 and Zg16 (C), differentiation, proliferation and stem cell marker Atoh1, Jag2, Lgr5, Ccnd1 (D), as well as MHC II genes Ciita, Cd74, H2aa, H2ab1, H2eb1, H2dma1, H2dmb1 and H2d (E) were measured by qPCR. Relative RNA amounts were determined by comparing to Pbgd amplification (n = 4–5). Results represent the mean ± SEM (* p ≤ 0.05; ** p ≤ 0.01; *** p ≤ 0.005; **** p ≤ 0.001). Protein extracts enriched from control and Hdac1−/−; Hdac2−/− jejunal IEC were separated on 8% or 10% SDS-PAGE gels and transferred to PVDF membranes for Western blot analysis of phospho-STAT3, total STAT3 and phospho-p38 (F), or claudin 3, cleaved Notch and phospho-S6 (G). GAPDH was used as loading control for each membrane.