Fig 2: The a2-activated TLR4 signal controls CRF and TH expression (A) Protein extracts from N2a cells mock- or a2-transfected in the presence or absence of pHSVsiTLR4 or pHSVsiNC (n = 5/group) were immunoblotted with antibodies to CRF, TLR4, or ß-Actin, and the results are expressed as densitometric units normalized to ß-Actin ± SEM. The levels of CRF and TLR4 are significantly higher in the a2- than in the mock-transfected cells, and upregulation is inhibited by siTLR4 but not siNC (* p = 0.05, *** p = 0.001 by t-test). (B) Protein extracts from mock- or TLR4-transfected SK-N-SH cells (n = 5 each) were immunoblotted with antibodies to pCREB, pPKA, TH, TLR4, or GAPDH, and the results are expressed as GAPDH-normalized densitometric units ± SEM. The levels of pCREB, pPKA and TH are significantly higher in the TLR4- than in the mock-transfected cells. The pCREB and TH upregulation is inhibited by treatment with the PKA-specific inhibitor H89 (10 µM) (* p < 0.05; ** p < 0.01; *** p < 0.001 by t-test).

Fig 3: Correlations between podocyte FPE and WT1(TI) (a), vimentin(glom) (b), and CRF(glom) (c).

Fig 4: Immunofluorescence staining of kidney biopsy samples (a, b). Staining intensities of WT1, vimentin, and CRF in kidney biopsy samples (c–e). Magnification, ×40.

Fig 5: Effect of para-, meta-, and ortho-Try on WT1, vimentin, and CRF expression in HEK 293 cells. a Immunofluorescence staining of HEK 293 cells. Staining intensities of WT1, vimentin, and CRF in HEK 293 cells (b–d). Magnification, ×40.