Transcription profiling of mouse aorta smooth muscle cells reveals they differentiate into lymphoid tissue organizers upon combined TNFR1/LTBR NF-kB signaling

ABSTRACT: Mouse aorta smooth muscle cells (SMCs) express TNF receptor superfamily member 1A (TNFR1) and lymphotoxin ß receptor (LTßR). Circumstantial evidence has linked the SMC LTßR to tertiary lymphoid organogenesis in diseased aortae of hyperlipidemic mice. Here, we explored potential roles of TNFR1 and LTßR activation in cultured SMCs. TNFR1 signaling by TNF activated the classical RelA NF-κB pathway, whereas LTßR signaling by agonistic anti LTßR antibody activated both the classical RelA and alternative RelB NF-κB pathways. Addition of both agonists synergized to enhance p100 inhibitor processing to the p52 subunit of NF-κB and promoted its nuclear translocation suggesting RelA-RelB cross-talk in transcription regulation. Correspondingly, microarrays showed that simultaneous TNFR1 and

ORGANISM(S): Mus musculus

SUBMITTER: Andreas Johann Richard Habenicht 

PROVIDER: E-GEOD-15062 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress