Nrp2 deficiency leads to trabecular bone loss and is accompanied by enhanced osteoclast and reduced osteoblast numbers.

Neuropilin 1 (Nrp1) and Nrp2 are transmembrane receptors that can bind class 3 semaphorins (Sema3A-G) in addition to VEGF family members to play important roles in axonal guidance, vascularization and angiogenesis, as well as immune responses. Moreover, recent evidence implicates Sema3A/Nrp-mediated signaling in bone regulation. However, to date the expression of Nrp2 in bone has not been investigated and a possible role for Nrp2 in the maintenance of bone homeostasis in vivo remains unexplored.

The odd-skipped related genes Osr1 and Osr2 are induced by 1,25-dihydroxyvitamin D3.

The odd-skipped related genes Osr1 and Osr2 encode closely related zinc finger containing transcription factors that are expressed in developing limb. However, their role in osteoblast proliferation and differentiation remains controversial and little is known about their regulation. In this study we showed that both Osr1 and Osr2 were expressed in several murine and human osteoblast cell lines as well as in primary osteoblast cultures.

The vitamin D analog TX527 ameliorates disease symptoms in a chemically induced model of inflammatory bowel disease.

The vitamin D system plays a critical role in inflammatory bowel disease as evidenced by the finding that both vitamin D deficient mice and vitamin D receptor knockout mice are extremely sensitive to dextran sodium sulfate (DSS)-induced colitis. Moreover, the active form of vitamin D, 1α,25-dihydroxyvitamin D3 [1,25(OH)2D3] is an important immunomodulator that ameliorates the pathogenesis of inflammatory bowel disease. However, therapeutic application of 1,25(OH)2D3 is hampered by its calcemic activity.

Microarray analysis of MCF-7 breast cancer cells treated with 1,25-dihydroxyvitamin D3 or a 17-methyl-D-ring analog.

Background: 1alpha,25-Dihydroxyvitamin D3 [1,25-(OH)2D3] is the biological active form of vitamin D. Its antiproliferative capacities make it a potential drug to treat diseases such as cancer. The clinical use of 1,25-(OH)2D3 as an antiproliferative agent is hampered by its calcemic effects.

1alpha,25-Dihydroxyvitamin D3-induced down-regulation of the checkpoint proteins, Chk1 and Claspin, is mediated by the pocket proteins p107 and p130.

A previous cDNA microarray analysis in murine MC3T3-E1 osteoblasts revealed a cluster of genes involved in cell cycle progression that was significantly down-regulated after a single treatment with 1alpha,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] [L. Verlinden, G. Eelen, I.

Characterization of the condensin component Cnap1 and protein kinase Melk as novel E2F target genes down-regulated by 1,25-dihydroxyvitamin D3.

1,25-Dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) has potent antiproliferative effects characterized by a hampered G(1)/S transition. cDNA microarrays were used to monitor expression of 21,492 genes in MC3T3-E1 mouse osteoblasts at 1, 6, 12, 24, and 36 h after treatment with 1,25(OH)(2)D(3). Statistical analysis revealed a cluster of genes that were strongly down-regulated by 1,25(OH)(2)D(3) and which not only function in cell cycle regulation and DNA replication but also mediate checkpoint control, DNA repair, chromosome modifications, and mitosis.