PTEC, Proximal Tubule Epithelial Cells, were transfected with siRNA at 50 pmol/mL using SilenceMag.
This article highlights the capacity of Magnetofection technology to efficiently silence gene expression into primary epithelial cells with siRNA using SilenceMag from OZ Biosciences.article reference: Immunol Cell Biol. 2014 May-Jun;92(5):427-35.
BMP-7 represses albumin-induced chemokine synthesis in kidney tubular epithelial cells through destabilization of NF-κB-inducing kinase.
Abstract
Protein overload activates proximal tubule epithelial cells (PTECs) to release chemokines. Bone morphogenetic protein-7 (BMP-7)
reduces infiltrating cells and tissue damage in acute and chronic renal
injuries. The present study examines the inhibitory effect and related
molecular mechanism of BMP-7 on chemokine and adhesion molecule synthesis
by PTECs activated with human serum albumin (HSA). The expression
profiles of chemokines and adhesion molecules in cultured human PTECs
were screened by PCR array. Expression of CXCL1, CXCL2 and vascular cell
adhesion protein 1 (VCAM-1) by PTECs was significantly upregulated by
HSA and reduced by BMP-7.
HSA activated both the canonical and noncanonical nuclear factor
(NF)-κB pathways in PTECs, as indicated by the increased nuclear
translocation of NF-κB p50 and p52 subunits. The nuclear translocation
of NF-κB p52 was completely abrogated by BMP-7, whereas NF-κB p50 activation was only partially repressed. BMP-7
increased the expression of cellular inhibitor of apoptosis 1 (cIAP1),
tumor necrosis factor receptor-associated factor (TRAF)2 and TRAF3, but
not of NF-κB-inducing kinase (NIK) that was significantly upregulated by
HSA. Silencing NIK recapitulated the partial inhibitory effect on
HSA-induced chemokine synthesis by BMP-7. Complete abolishment of the chemokine synthesis
was only achieved by including additional blockade of the NF-κB p65
translocation on top of NIK silencing. Our data suggest that BMP-7 represses the NIK-dependent chemokine synthesis
in PTECs activated with HSA through blocking the noncanonical NF-κB
pathway and partially interfering with the canonical NF-κB pathway.
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