Fig. 9: A model for the CD31-induced barrier response. | Nature Communications

Fig. 9: A model for the CD31-induced barrier response.

From: Preservation of microvascular barrier function requires CD31 receptor-induced metabolic reprogramming

Fig. 9

MHC triggering induces RhoA and Erk activation and EC contraction (1). Erk phosphorylation is modulated by CD31 signals, possibly via SHP-2 (2). MHC signals induce CD31 ITIM phosphorylation and SHP-2 recruitment. SHP-2 prevents the phosphorylation of b-catenin (5) and VE-cadherin (6), thus stabilizing the junctional complex. In addition, dephosphorylated b-catenin can transfer to the nucleus where it induces cMyc transcription. In parallel, SHP-2 induces AKT activation which in turn inhibits FoxO1 nuclear translocation, thus preventing inhibition of cMyc transcription. This leads to enhanced transcription of glycolysis enzymes and enhanced glycolysis required for actin remodeling and maintenance of junctional anchorage.

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