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. 2018 Mar 1;102(3):447–459. doi: 10.1016/j.ajhg.2018.02.002

Figure 4.

Figure 4

Immunohistochemistry of a PPCD4 Diseased Cornea Reveals GRHL2 Immunoreactivity and Cell State Transition in the Corneal Endothelium

(A) Full thickness corneal tissue from control (left) and affected (right) individual with a c.20+544G>T GRHL2 mutation (II:1 family C23) were stained with anti-GRHL2. Magnified images of the epithelium and endothelium are shown in insets. GRHL2 is detected in the nuclei of control and PPCD4 corneal epithelial cells but is absent in the control endothelium. In contrast, GRHL2 is also detected in the nuclei of the PPCD4 endothelial cells.

(B) H&E staining showing integrity of full-thickness corneal sections for the diseased and control samples.

(C) Magnified images of control and PPCD4 endothelial cells stained for GRHL2 and corneal epithelial and endothelial markers N-Cadherin (N-CAD), E-Cadherin (E-CAD), and Cytokeratin 7 (CK7). GRHL2 is localized in the nuclei in diseased endothelial cells. N-Cadherin was detected in control endothelial tissue and in the diseased endothelium. E-cadherin was negative in control endothelium but is expressed in the diseased endothelial tissue (arrowhead) with some areas of negative staining. CK7 was positive in the diseased endothelium and negative in the control sample. All sections were counterstained with Mayer’s hematoxylin to identify nuclei. Scale bar 50 μm.