- B.A., 1977, Pomona College, Physics.
- Ph.D., 1983, Caltech, Biology.
- Postdoctoral research, University of California, San Diego.
- Previous faculty appointments: Rice University, Baylor College of Medicine, Howard Hughes Medical Institute.
Joined the department in 2010.
Tissue size regulation, tissue cell composition, and fibrosing diseases
Our laboratory is working on three areas of biomedicine, trying to move observations from basic research into the clinic. First, we are studying how the sizes of tissues and tumors are regulated, and how this can be manipulated for therapeutic purposes. As a model system, we are using the simple eukaryote Dictyostelium discoideum, which allows us to combine techniques such as biochemistry, genetics, computer modeling, and cell biology to study tissue size regulation. We have found that a secreted protein as well as the unusual molecule polyphosphate are signals in negative feedback loops that inhibit Dictyostelium cell proliferation, and we are studying the signal transduction pathway to understand similar mechanisms in humans.
Second, we are studying how some secreted proteins can make cells move away from the source of the signal. We found such a signal (called a chemorepellent) in Dictyostelium, and then found a similar signal in humans. We are working to understand the signal transduction pathway for both. The human signal repels neutrophils, and we found that this can be used therapeutically in mouse models of neutrophil-driven diseases such as rheumatoid arthritis and acute respiratory distress syndrome.
Third, we have found that a human blood protein called Serum Amyloid P (SAP) regulates a key step in the formation of scar tissue as well as the formation of the scar-like lesions in fibrosing diseases such as congestive heart failure and pulmonary fibrosis. We are studying this mechanism, and a biotech company (Promedior) we co-founded is testing SAP as a therapy for fibrosis in patients in two Phase 2 trials.
- Phillips, JE, Gomer, RH. A canine model for neuronal ceroid lipofuscinosis highlights the promise of gene therapy for lysosomal storage diseases. Ann Transl Med. 2016;4 (Suppl 1):S20. doi: 10.21037/atm.2016.10.16. PubMed PMID:27867988 .
- Abeydeera, ND, Egli, M, Cox, N, Mercier, K, Conde, JN, Pallan, PS et al.. Evoking picomolar binding in RNA by a single phosphorodithioate linkage. Nucleic Acids Res. 2016;44 (17):8052-64. doi: 10.1093/nar/gkw725. PubMed PMID:27566147 PubMed Central PMC5041495.
- Suess, PM, Gomer, RH. Extracellular Polyphosphate Inhibits Proliferation in an Autocrine Negative Feedback Loop in Dictyostelium discoideum. J. Biol. Chem. 2016;291 (38):20260-9. doi: 10.1074/jbc.M116.737825. PubMed PMID:27519410 PubMed Central PMC5025707.
- Herlihy, SE, Starke, HE, Lopez-Anton, M, Cox, N, Keyhanian, K, Fraser, DJ et al.. Peritoneal Dialysis Fluid and Some of Its Components Potentiate Fibrocyte Differentiation. Perit Dial Int. ;36 (4):367-73. doi: 10.3747/pdi.2014.00284. PubMed PMID:26493752 .
- White, MJ, Gomer, RH. Trypsin, Tryptase, and Thrombin Polarize Macrophages towards a Pro-Fibrotic M2a Phenotype. PLoS ONE. 2015;10 (9):e0138748. doi: 10.1371/journal.pone.0138748. PubMed PMID:26407067 PubMed Central PMC4583378.
- Pilling, D, Vakil, V, Cox, N, Gomer, RH. TNF-α-stimulated fibroblasts secrete lumican to promote fibrocyte differentiation. Proc. Natl. Acad. Sci. U.S.A. 2015;112 (38):11929-34. doi: 10.1073/pnas.1507387112. PubMed PMID:26351669 PubMed Central PMC4586854.
- Herlihy, SE, Brown, ML, Pilling, D, Weeks, BR, Myers, LK, Gomer, RH et al.. Role of the neutrophil chemorepellent soluble dipeptidyl peptidase IV in decreasing inflammation in a murine model of arthritis. 2015;67 (10):2634-8. doi: 10.1002/art.39250. PubMed PMID:26138693 PubMed Central PMC4751999.
- White, MJ, Roife, D, Gomer, RH. Galectin-3 Binding Protein Secreted by Breast Cancer Cells Inhibits Monocyte-Derived Fibrocyte Differentiation. J. Immunol. 2015;195 (4):1858-67. doi: 10.4049/jimmunol.1500365. PubMed PMID:26136428 PubMed Central PMC4530092.
- Cox, N, Pilling, D, Gomer, RH. DC-SIGN activation mediates the differential effects of SAP and CRP on the innate immune system and inhibits fibrosis in mice. Proc. Natl. Acad. Sci. U.S.A. 2015;112 (27):8385-90. doi: 10.1073/pnas.1500956112. PubMed PMID:26106150 PubMed Central PMC4500200.
- Pilling, D, Cox, N, Vakil, V, Verbeek, JS, Gomer, RH. The long pentraxin PTX3 promotes fibrocyte differentiation. PLoS ONE. 2015;10 (3):e0119709. doi: 10.1371/journal.pone.0119709. PubMed PMID:25774777 PubMed Central PMC4361553.