Skip to main content
. 2023 Jun 5;11(6):1638. doi: 10.3390/biomedicines11061638

Figure 6.

Figure 6

Crosstalk between protein phosphatase 2A (PP2A) and myosin light chain (MLC) phosphatase (MLCP) in pulmonary EC barrier regulation. (A) PKA-mediated activation of PP2A strengthens the EC barrier via dephosphorylation (deactivation) of specific MLCP inhibitor, CPI17, and dephosphorylation of Myosin phosphatase targeting subunit 1 (MYPT1) leading to MLCP activation (de-inhibition of PP1c catalytic activity towards MLC), which may be accompanied by direct PP2A-mediated endothelial nitric oxide synthase (eNOS) dephosphorylation. (B) Pro-inflammatory agonists such as VEGF may hyperactivate eNOS leading to excessive NO production. In parallel, pro-inflammatory agonists may inhibit MLCP via direct phosphorylation of MYPT1 resulting in the inhibition of PP1c catalytic activity toward MLC or activation (phosphorylation) of CPI17 leading to EC hyperpermeability. Additional abbreviations: EGCG—epigallocatechin gallate; VEGFR2—VEGF receptor 2; PG—plakoglobin (γ-catenin). This figure was created with BioRender.com.