Mark B. Meyer

Mark Meyer headshot

Assistant Professor of Nutritional Sciences
UW Carbone Cancer Center Member (Cancer Genetics & Epigenetic Mechanisms)

BS 2002, Butler University (Chemistry)
PhD 2007, University of Wisconsin-Madison (Biochemistry)

 

 

Mentor Programs
Endocrinology and Reproductive Physiology (ERP)
Cellular and Molecular Biology (CMB)
Metabolism and Nutrition Training Program (MANTP)
Biotechnology Training Program (BTP)

Contact:
markmeyer@wisc.edu
(608) 890-0857

Lab Website:
http://markmeyerlab.nutrisci.wisc.edu

Research Interests:
Vitamin D metabolism, inflammatory disease, gene expression regulation, bioinformatics, genome-editing

Research Summary:

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:

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. [PubMed]

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. [PubMed] GEO Data Accession Link: GSE206777

Pike JW, Meyer MBNew 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. [PubMed]

Pike JW, Meyer MBThe 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 [PubMed]

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 [PubMed]

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)2Dand LPS in vivo. Endocrinology, 2019 Dec 1;160(12):2877-2891. doi: 10.1210/en.2019-00622 [PubMed]

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. [PubMed] GEO Data Accession Links: Mouse GSE133025 and Human GSE129585

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 [PubMed] GEO Data Accession Links: Mouse GSE133025 and Human GSE129585

Onal M, Carlson AH, Thostenson JD, Meyer MB, Lee SM, Pike JW. A Novel Distal Enhancer Mediates Inflammation-, PTH-, and Early Onset Murine Kidney Disease-Induced Expression of the Mouse Fgf23 Gene. JBMR Plus. 2018 Jan;2(1):32-47. doi: 10.1002/jbm4.10023 [PubMed]

Meyer MB, Benkusky NA, Kaufmann M, Lee SM, Onal M, Jones G, Pike JW. A kidney-specific genetic control module in mice governs endrocrine regulation of the cytochrome P450 gene Cyp27b1 essential for vitamin D3 activation. 2017 June 14. pii: jbc.M117.806901. doi: 10.1074/jbc.M117.806901. [PubMed] GEO Data Accession Link: GSE133025

 

Full Bibliography: https://www.ncbi.nlm.nih.gov/myncbi/1j3a45ctcuMQ5/bibliography/public/