Lori  T Raetzman

raetzman@life.illinois.edu

535 Burrill Hall
Office: (217) 244-6233
Lab: (217) 333-7913
Fax: (217) 333-1133

Mail to: Department of Molecular and Integrative Physiology
524 Burrill Hall, MC-114
407 S. Goodwin Ave
Urbana, IL 61801
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Lori T Raetzman

Associate Professor of Molecular and Integrative Physiology
Associate Professor of Neuroscience

Research Topics

Development, Endocrinology, Neurobiology

Education

B.A. 1994 Ripon College, Ripon, WI
PhD. 2000 Case Western Reserve University, Cleveland, OH
Postdoc. 2000-2005 University of Michigan, Ann Arbor, MI

Teaching Interests

Notch signaling pathway in hypothalamic-pituitary gland development and disease

The pituitary is the master gland coordinating growth, fertility, metabolism and the body's response to stress. To exert these effects, the anterior pituitary has distinct cell types that produce thyroid-stimulating hormone (TSH), adrenocorticotropic hormone (ACTH), luteinizing hormone (LH), follicle-stimulating hormone (FSH), growth hormone (GH), and prolactin (PRL). If the development or function of these cells in the pituitary gland is disrupted, two main diseases result. Hypopituitarism, defined as loss of at least one pituitary hormone, occurs in 1:4000 births. Only a small number of cases are caused by known genetic mutations. The other main category of pituitary disease, tumor formation, is very common, with an incidental prevalence of 30% at autopsy. The genetic causes of pituitary tumors are largely unknown and could result from the loss or gain of function of a normal developmental process.

Research in my laboratory is focused on understanding the role of cell-cell signaling during pituitary development. We hypothesize that the Notch signaling pathway may play an important role in the proliferation and lineage specific differentiation of progenitor cells in the embryonic pituitary. The Notch signaling pathway is an evolutionarily conserved mechanism that orchestrates cell fate choices in a broad spectrum of developmental systems. The core pathway includes two transmembrane ligands, (Delta and Jagged), a transmembrane receptor (Notch), a coactivator (CSL/Rbpsuh) and a downstream transcription factor (Hes). Many components of the Notch pathway are present in the developing pituitary, but their function in this system is unknown.

We are interested in uncovering the role of Notch signaling in the normal development of the pituitary and in pituitary disease. We are exploring if Notch signaling is necessary and sufficient for obtaining the full complement of cells in the pituitary by employing transgenic and knockout mice. These studies also take advantage of molecular genetic techniques and whole animal physiology.

Representative Publications

Nantie LB, Himes AD, Getz DR, Raetzman LT. (2014) Notch signaling in postnatal pituitary expansion: proliferation, progenitors, and cell specification. Mol. Endocrinol. 28(5):731-44.[Abstract]

Aujla PK, Naratadam GT, Xu L, Raetzman LT. (2013). Notch/Rbpjκ signaling regulates progenitor maintenance and differentiation of hypothalamic arcuate neurons. Development 140(17):3511-21. [Abstract]

Moran TB, Brannick KE, Raetzman LT. (2012). Aryl-hydrocarbon receptor activity modulates prolactin expression in the pituitary. Toxicol. Appl. Pharmacol. 265(1):139-45. [Abstract]

Brannick KE, Craig ZR, Himes AD, Peretz JR, Wang W, Flaws JA, Raetzman LT. (2012). Prenatal exposure to low doses of bisphenol A increases pituitary proliferation and gonadotroph number in female mice offspring at birth. Biol. Reprod. 87(4):82. [Abstract]

Monahan P., Himes A.D., Parfieniuk A, Raetzman L.T. (2012). p21, an important mediator of quiescence during pituitary tumor formation, is dispensable for normal pituitary development during embryogenesis. Mech. Dev. 128(11-12):640-52. [Abstract]

Goldberg L.B., Aujla P.K., and Raetzman L.T. (2011). Persistent Expression of Activated Notch Inhibits corticotrope and melanotrope differentiation and results in dysfunction of the HPA axis. Dev. Biol. 358:23-32. [Abstract]

Aujla P.K., Bora A., Monahan P., Sweedler J.V., and Raetzman L.T. (2011). The Notch effector gene Hes1 regulates migration of hypothalamic neurons, neuropeptide content and axon targeting to the pituitary. Dev. Biol. 353:61-71. [Abstract]

Himes A.D., Fiddler R., and Raetzman L.T. (2011). N-cadherin loss in POMC expressing cells leads to pituitary disorganization. Mol. Endocrinol. 25:482-91. [Abstract]

Moran T.B., Goldberg L.B., Serviss, S., and Raetzman L.T. (2011). Numb deletion in POMC expressing cells impairs pituitary intermediate lobe cell adhesion, progenitor cell localization, and neuro-intermediate lobe boundary formation. Mol. Endocrinol. 25, 117-27. [Abstract]

Monahan P., Rybak S., and Raetzman L.T. (2009). The notch target gene HES1 regulates cell cycle inhibitor expression in the developing pituitary. Endocrinology, 150:4386-94. [Abstract]

Himes A.D. and Raetzman L.T. (2009). Premature differentiation and aberrant movement of pituitary cells lacking both Hes1 and Prop1. Dev. Biol., 325:151-61. [Abstract]

Complete Publications List