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Bernal-Mizrachi and Riek publish in Nature Communications

Vitamin D, 4th Edition
Carlos Bernal-Mizrachi, MD and Amy Riek, MD

Drs. Bernal-Mizrachi, Riek and collaborators had their article published in Nature Communications on September 23.

In their research, they tested the hypothesis that impaired vitamin D signaling in macrophages causes hypertension using conditional knockout of the myeloid vitamin D receptor in mice (KODMAC). These mice develop renin-dependent hypertension due to macrophage infiltration of the vasculature and direct activation of renal juxtaglomerular (JG) cell renin production.

The authors stated, “Our findings provide evidence that dysregulated macrophage signaling in response to vitamin D deficiency is sufficient to cause hypertension by a microRNA-specific mechanism that enables communication from innate immune cells to JG cells. A detailed understanding of the mechanisms by which macrophage ER stress causes miR-106b-5p secretion will direct the development of specific therapies preventing the miRNA-mediated activation of multiple signaling pathways and transcription factors involved in renin-dependent hypertension.”

Schematic diagram of relevant cell signaling pathways. Macrophage miR-106b-5p inhibits JG cell E2f1 and Pde3b, removing inhibition of PCG1 and CREB pathways to induce renin production. Blue arrows represent stimulatory pathways and red lines represent inhibitory pathways, while X represents repressed inhibition.
Jisu Oh, BS

Collaborators include J. Oh, S. Matkovich, S. M. Bindom, J. S. Shao1, R. D. Head3, R. A. Barve, M. S. Sands, G. Carmeliet, P. Osei-Owusu, R. H. Knutsen, H. Zhang, K. J. Blumer, C. G. Nichols, R. P. Mecham, Á Baldán, B. A. Benitez, M. L. Sequeira-Lopez, R. A. Gomez

Macrophage secretion of miR-106b-5p causes renin-dependent hypertension