Fig. 1

Dysregulation of EndMT and major cell adhesion markers in cerebral AVM nidus. A Scatter plots with bars represent the mRNA fold changes of SNAI1, SNAI2, Calponin 1 (CNN1), transgelin (TAGLN) and cell adhesion-associated integrin α9 (ITGA9), integrin β1 subunits (ITGB1), VE-cadherin (CDH5), and N-cadherin (CDH2) in 18 human cAVM nidi and 15 control brain tissues. GAPDH was used as the endogenous control for mRNA fold analysis. Scatter dots represent expression in individual specimens and bars represent mean value. B Cerebral AVM nidus consisted of enlarged vessels with medial thickening and intimal hyperplasia. Immunohistochemical staining shows the reduced expression of activated integrin α9/β1 and overexpression of SNAI1/2, Transgelin, Calponin1, and N-cadherin in cAVM vessels compared with control brain vessels. All these EndMT-associated markers were expressed in the intima or neointima of huge AVM nidal vessels (scale bar 100 µm, magnification ×20). C Bar graph showing histoscore analysis of SNAI1/2, Transgelin, Calponin1, N-cadherin, and integrin α9/β1 in three random microscopic fields of immunostained sections. Values are mean ± SD. *p < 0.05 versus control tissue, **p < 0.01, ***p < 0.001, ****p < 0.0001. ns nonsignificant difference