Profile Photo of Richard Gomer
Richard Gomer

Thomas Powell ’62 Professor of Science

Fax: 979-845-2891

Curriculum Vitae
Gomer Lab Website

3474 TAMU
Interdisciplinary Life Sciences Building
Room 2121B

Interdisciplinary Life Sciences Building
Room 2116

Joined the Department in 2010

  • 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.

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.

  1. Karhadkar, TR, Chen, W, Gomer, RH. Attenuated Pulmonary Fibrosis in Sialidase-3 Knockout (Neu3-/-) Mice. Am. J. Physiol. Lung Cell Mol. Physiol. 2019; :. doi: 10.1152/ajplung.00275.2019. PubMed PMID:31617733 .
  2. Pilling, D, Cox, N, Thomson, MA, Karhadkar, TR, Gomer, RH. Serum Amyloid P and a Dendritic Cell-Specific Intercellular Adhesion Molecule-3-Grabbing Nonintegrin Ligand Inhibit High-Fat Diet-Induced Adipose Tissue and Liver Inflammation and Steatosis in Mice. Am. J. Pathol. 2019; :. doi: 10.1016/j.ajpath.2019.08.005. PubMed PMID:31539521 .
  3. Gomer, RH. The Use of Diffusion Calculations and Monte Carlo Simulations to Understand the Behavior of Cells in Dictyostelium Communities. Comput Struct Biotechnol J. 2019;17 :684-688. doi: 10.1016/j.csbj.2019.06.002. PubMed PMID:31303972 PubMed Central PMC6603294.
  4. Suess, PM, Chinea, LE, Pilling, D, Gomer, RH. Extracellular Polyphosphate Promotes Macrophage and Fibrocyte Differentiation, Inhibits Leukocyte Proliferation, and Acts as a Chemotactic Agent for Neutrophils. J. Immunol. 2019;203 (2):493-499. doi: 10.4049/jimmunol.1801559. PubMed PMID:31160533 PubMed Central PMC6615990.
  5. Behrens, NE, Lipke, PN, Pilling, D, Gomer, RH, Klotz, SA. Serum Amyloid P Component Binds Fungal Surface Amyloid and Decreases Human Macrophage Phagocytosis and Secretion of Inflammatory Cytokines. MBio. 2019;10 (2):. doi: 10.1128/mBio.00218-19. PubMed PMID:30862745 PubMed Central PMC6414697.
  6. Suess, PM, Tang, Y, Gomer, RH. The putative G protein-coupled receptor GrlD mediates extracellular polyphosphate sensing in Dictyostelium discoideum. Mol. Biol. Cell. 2019;30 (9):1118-1128. doi: 10.1091/mbc.E18-10-0686. PubMed PMID:30785840 PubMed Central PMC6724513.
  7. Pilling, D, Chinea, LE, Consalvo, KM, Gomer, RH. Different Isoforms of the Neuronal Guidance Molecule Slit2 Directly Cause Chemoattraction or Chemorepulsion of Human Neutrophils. J. Immunol. 2019;202 (1):239-248. doi: 10.4049/jimmunol.1800681. PubMed PMID:30510066 PubMed Central PMC6310129.
  8. Rijal, R, Consalvo, KM, Lindsey, CK, Gomer, RH. An endogenous chemorepellent directs cell movement by inhibiting pseudopods at one side of cells. Mol. Biol. Cell. 2019;30 (2):242-255. doi: 10.1091/mbc.E18-09-0562. PubMed PMID:30462573 PubMed Central PMC6589559.
  9. Pilling, D, Gomer, RH. The Development of Serum Amyloid P as a Possible Therapeutic. Front Immunol. 2018;9 :2328. doi: 10.3389/fimmu.2018.02328. PubMed PMID:30459752 PubMed Central PMC6232687.
  10. Tang, Y, Wu, Y, Herlihy, SE, Brito-Aleman, FJ, Ting, JH, Janetopoulos, C et al.. An Autocrine Proliferation Repressor Regulates Dictyostelium discoideum Proliferation and Chemorepulsion Using the G Protein-Coupled Receptor GrlH. MBio. 2018;9 (1):. doi: 10.1128/mBio.02443-17. PubMed PMID:29440579 PubMed Central PMC5821085.
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