Heather Doherty

Assistant Professor of Molecular Genetics; Graduate Program Coordinator, Biological Sciences

BS, Purdue University; PhD, University of North Carolina
Email: hedoherty@plymouth.edu

Contact information 

Office: Boyd Science Center, Room 108
Lab: Boyd Science Center, Room 115
Phone: 603-535-3181

 About Professor Doherty

Dr. Doherty recently joined the faculty of PSU from Harvard Medical School.  Although originally from Northern Connecticut, she is still readjusting to New England weather after nearly a decade in North Carolina.  She has experience in curriculum design, best teaching methods in the sciences, and laboratory research in cardiovascular disease and obesity.  Her teaching focuses on genetics, human disease, and molecular biology.  In her laboratory, an ongoing research program is working to discover genetic targets for treating scarring of the heart caused by cardiovascular disease (See below for more details).  Dr. Doherty is also Co-Director of the Biotechnology Program and accompanying Biotechnology major.  She is looking forward to skiing in the White Mountains as well as meeting and interacting with PSU students in the classroom and laboratory.

Selected publications

Doherty HE, Hagaman J, Kim HS, Hiller S, and Maeda N.  Increased Ctgf gene expression exacerbates Angiotensin II-induced cardiac hypertrophy.  In preparation.

Doherty HE, Kim HS, Hiller S, Sulik KK, Maeda N.  Altering the Ctgf-3’UTR to make a mouse with low and high basal gene expression. PLoS ONE. 2010 Sept; 22. 5(9): e12909.

Altenburg M, Homeister J, Doherty H, Maeda N.  Genetics of atherosclerosis in murine models.  Curr Drug Targets. 2007 Nov;8(11):1161-71.

Bell TA, de la Casa-Esperon E, Doherty HE, Ideraabdullah F, Kim K, Wang Y, Lange L, Wilhemsen K, Lange E, Sapienza C, Pardo-Manuel de Villena F.  The paternal gene of the DDK syndrome maps to the Schlafen gene cluster on mouse chromosome 11.  Genetics. 2006 Jan;172(1):411-23. Epub 2005 Sep 19.

Kim K, Thomas S, Howard IB, Bell TA, Doherty HE, Ideraabdullah F, Detwiler DA, Pardo-Manuel de Villena F. Meiotic drive at the Om locus in wild derived mouse inbred strains. Biol J Linnean Soc.  Volume 84, Issue 3, Page 487-492, March 2005.

 Awards or recognition

  • Plymouth State University RAC Grant 2013
  • Honorable mention NSF pre-doctoral fellowship 2004
  • International Mouse Genome Society member 2003-2010
  • Phi Beta Kappa 2002-present
  • Beta Beta Beta Biology Honorary 2001-present
  • Alpha Chi Sigma Chemistry fraternity 1999-present

Courses Taught

Genetics for Nurses (BI 2360)
Molecular Biology (BI 4185)
Senior Research (BI 4200)

Obesity: Biology & Sociology (WECO & INCO) (BI 3025)
Genetics (BI 3060)
Introduction to Research (BI 4190)


Cardiovascular disease is the most common cause of death in the United States accounting for about 1 in every 5 death.  Myocardial infarction caused by ongoing cardiovascular disease is survived by about 60% of patients, but most patients who survive suffer from scarring of the heart.  The scar, also referred to as fibrosis, is a knot of fibrous tissue that can disrupt the electrical signaling of the heart and can reduce the elasticity of the tissue.  Cardiac dysfunction triggered by fibrosis can progress to heart failure and is a major cause of sudden death due to cardiovascular disease.  Despite the health consequences of cardiac scarring, there are no FDA-approved treatments for the prevention or reduction of cardiac fibrosis.  In an effort to better understand cardiac fibrosis, the lab is interested in finding genetic targets for anti-fibrotic therapies.  A candidate gene approach is being pursued by investigating the role of the gene connective tissue growth factor (CTGF) in fibrosis.  CTGF has been widely implicated in fibrosis in skin, kidney, liver, lung, and heart.  Elucidation of how CTGF expression causes or modulates fibrosis could explain the consistent presence of CTGF if fibrous tissue.  In addition, the lab is pursuing projects to generally define the network of genes that play a role in fibrosis in pursuit of a more complete and holistic view of how fibrosis is caused and regulated.  Projects cover topics such as: 1) Diversity of alleles present in the human CTGF gene, 2) Characterizing the fibroblast gene expression profile in tissue culture, and 3) Understanding the role of the CTGF gene in cardiac scarring.