Methods and Results As compared to LRP6(fl/fl);LDLR-/- controls, SM22-Cre;LRP6(fl/fl);LDLR-/- (LRP6-VKO) siblings exhibited increased aortic calcification on HFD without changes in fasting glucose, lipids, or body composition. Pulse wave velocity (index of arterial stiffness) was also increased. Vascular calcification paralleled enhanced aortic osteochondrogenic programs and circulating osteopontin (OPN), a matricellular regulator of arteriosclerosis. Survey of ligands and Frizzled (Fzd) receptor profiles in LRP6-VKO revealed upregulation of canonical and noncanonical Wnts alongside Fzd10.

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Fzd10 stimulated noncanonical signaling and OPN promoter activity via an USF-activated cognate inhibited by LRP6. RNAi revealed that USF1 but not USF2 supports OPN expression in LRP6-VKO VSM, and immunoprecipitation confirmed increased USF1 association with OPN chromatin. ML141, an antagonist of cdc42/Rac1 noncanonical signaling, inhibited USF1 activation, osteochondrogenic programs, alkaline phosphatase, and VSM calcification. Mass spectrometry identified LRP6 binding to protein arginine methyltransferase (PRMT) - 1, and nuclear asymmetric dimethylarginine modification was increased with LRP6-VKO. RNAi demonstrated that PRMT1 inhibits OPN and TNAP while PRMT4 supports expression. USF1 complexes containing the H3R17Me2a signature of PRMT4 are increased with LRP6-VKO.

Jmjd6, a demethylase downregulated with LRP6 deficiency, inhibits OPN and TNAP expression, USF1:H3R17Me2a complex formation and transactivation. INTRODUCTION Hyperglycemia, hyperlipidemia, and uremia accelerate vascular aging, compromising arterial function necessary for normal blood flow, metabolism and tissue homeostasis. Along with hypertension these dysmetabolic states induce arteriosclerotic stiffening, thereby reducing vascular compliance that underlies Windkessel physiology -- elasticity of conduit vessels that ensures smooth distal tissue perfusion throughout the cardiac cycle. Atherosclerotic burden, mural thickening and fibrosis, medial calcification, elastin fragmentation, non-enzymatic matrix crosslinking, and endothelial dysfunction are features of arteriosclerotic aging. Multiple labs have now identified bone morphogenetic proteins (BMPs) and Wnts – polypeptides that convey paracrine cues during skeletal morphogenesis – as pathogenic signals in arteriosclerotic calcification –. In studies of LDLR-/- mice fed high fat diabetogenic diets (HFD) typical of western societies, we identified that osteogenic Msx-Wnt signaling cascades are ectopically activated in the vasculature with concomitant induction of diabetes, obesity, and arterial calcification. Expression of the osteoblast transcription factor Msx2 in mural myofibroblasts was shown to be activated by inflammatory signals that support arterial mineralization,.