Mark B. Meyer

Position title: Assistant Professor

Email: markmeyer@wisc.edu

Phone: 608-890-0857

Address:
Nutritional Sciences
Vitamin D metabolism, inflammatory disease, genetic basis of disease, gene expression regulation, bioinformatics, genome-editing

Address
NS 356
Education
Ph.D., University of Wisconsin, Madison
Department
Nutrional Sciences
Research Interests
Vitamin D metabolism, inflammatory disease, genetic basis of disease, gene expression regulation, bioinformatics, genome-editing
Research Fields
Disease Biology, Gene Expression, Genomics and Proteomics, Humans, Mouse and Other Mammals

Research Description
The Meyer lab studies the dynamic chromatin environment responsible for serum calcium and phosphate maintenance and the impacts of vitamin D metabolism in skeletal, renal, and intestinal biology. A triumvirate of endocrine hormones – parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), and calcitriol (1,25(OH)2D3) – maintain this delicate balance by influencing enzymes, transporters, and transcription factors to drive genomic change. When dysfunctional, these mechanisms allow chronic inflammation and disease progression to worsen in chronic kidney disease-metabolic bone disorder (CKD-MBD), atherosclerosis, inflammatory bowel disease (IBD), and many others. Low vitamin D status has a correlation with an increase in cancer risk in cancers such as colorectal, breast, and prostate. Higher vitamin D status has been linked to longer survival rates in cancer patients. Additionally, vitamin D deficiency is associated with low birth weight, small size for gestational age, and the increased susceptibility to obesity, insulin resistance, and diabetes later in life. Recently, maternal vitamin D deficiency in mice was found to imprint an epigenetic program in immune cells leading to insulin resistance and diabetes in offspring later in life. Dietary and nutritional supplementation of vitamin D rapidly corrects the body’s mineral deficiencies, however its ability to ameliorate inflammatory disease progression or improve cancer outcomes remains controversial. We study the intricate genomic and molecular mechanisms that regulate the biological changes controlling the intersection of metabolism, inflammation, and disease progression using unique animal models, genomic editing techniques, and -omics bioinformatic approaches to generate unbiased interrogation of chromatin changes.


Representative Publications:
Search PubMed for more publications by Mark B. Meyer

Meyer MB, Lee SM, Cichanski SR, Cobice DF, Pike JW. Spatial detection and consequences of nonrenal calcitriol production as assessed by targeted mass spectrometry imaging. JCI Insight. 2024 Jun 25:e181763. doi: 10.1172/jci.insight.181763. Epub ahead of print. PMID: 38916957.

Yoon SH, Meyer MB, Arevalo Rivas C, Tekguc M, Zhang C, Wang JS, Castro Andrade CD, Strauss KE, Sato T, Benkusky N, Lee SM, Berdeaux R, Foretz M, Sundberg TB, Xavier RJ, Adelmann CH, Brooks DJ, Anselmo A, Sadreyev RI, Rosales IA, Fisher DE, Gupta N, Morizane R, Greka A, Pike JW, Mannstadt M, Wein MN. A parathyroid hormone/salt-inducible kinase signaling axis controls renal vitamin D activation and organismal calcium homeostasis. J Clin Invest. 2023 Mar 2:e163627. doi: 10.1172/JCI163627. Epub ahead of print. PMID: 36862513.

Meyer MB, Benkusky NA, Lee SM, Yoon SH, Mannstadt M, Wein MN, Pike JW. Rapid genomic changes by mineralotropic hormones and kinase SIK inhibition drive coordinated renal Cyp27b1 and Cyp24a1 expression via CREB modules. J Biol Chem. 2022 Sep 29:102559. doi: 10.1016/j.jbc.2022.102559. Epub ahead of print. PMID: 36183832.

Pike JW, Meyer MB. New Approaches to Assess Mechanisms of Action of Selective Vitamin D Analogues. Int J Mol Sci. 2021 Nov 16;22(22):12352. doi: 10.3390/ijms222212352. PMID: 34830234; PMCID: PMC8619157.

Pike JW, Meyer MB. The unsettled science of non renal calcitriol production and its clinical relevance. J Clin Invest. 2020 Sep 1;130(9):4519-4521. doi: 10.1172/JCI141334

Meyer MB, Pike JW. Mechanistic homeostasis of vitamin D metabolism in the kidney through reciprocal modulation of Cyp27b1 and Cyp24a1 expression. J Steroid Biochem Mol Biol. 2020 Feb;196:105500. doi: 10.1016/j.jsbmb.2019.105500

Lee SM, Carlson AH, Onal M, Benkusky NA, Meyer MB, Pike JW. A control region near the fibroblast growth factor 23 gene mediates response to phosphate, 1,25(OH)2D3 and LPS in vivo. Endocrinology, 2019 Dec 1;160(12):2877-2891. doi: 10.1210/en.2019-00622

Meyer MB, Lee SM, Carlson AH, Benkusky NA, Kaufmann M, Jones G, Pike JW. A chromatin-based mechanism controls differential regulation of the cytochrome P450 gene Cyp24a1 in renal and non-renal tissues. J Biol Chem. 2019 Sep 27;294(39):14467-14481. doi: 10.1074/jbc.RA119.010173.

Meyer MB, Benkusky NA, Kaufmann M, Lee SM, Redfield RR, Jones G, Pike JW. Targeted genomic deletions identify diverse enhancer functions and generate a kidney-specific, endocrine-deficient Cyp27b1 pseudo-null mouse. J Biol Chem. 2019 Jun 14;294(24):9518-9535. doi: 10.1074/jbc.RA119.008760