Bookmark and Share

Loren P Thompson
 

Loren P Thompson Ph.D.

Academic Title: Associate Professor
Primary Appointment: Obstetrics, Gynecology and Reproductive Sciences
Secondary Appointments: Physiology
lthompson1@umm.edu
Location: 655 West Baltimore St. BRB 11-040
Phone: (410) 706-4422
Fax: (410) 706-5747

Personal History:

I received my Ph.D. in cardiovascular physiology from Michigan State University in East Lansing, MI in 1984.  I spent 2 years at the University of Michigan in Ann Arbor, MI and 5 years at the University of Vermont in Burlington, VT as a post-doctoral fellow studying vascular mechanisms in hypertensive diseased models.  I spent 5 years at the University of Iowa in Iowa City, IA as a Research Scientist.  I joined the faculty at the University of Maryland, Baltimore in 1996 in the Dept. of Obstetrics, Gynecology and Reproductive Sciences where I currently reside.  I also have a secondary appointment in the Dept. of Physiology in the same institution.  I am a member of the Center for Studies in Reproduction at UM,B, The American Physiological Society, The Perinatal Research Society and The Society for Gynecological Investigation.

Research Interests:

Prolonged exposure to reduced oxygen levels (hypoxic stress) is the leading cause of fetal morbidity and mortality.  Under normal conditions, the fetus develops in a relatively reduced oxygen environment.  Yet, it has undergone cardiovascular adaptations that favor delivery of its oxygen and nutrient needs.  Under conditions of intrauterine hypoxia (where oxygen levels are further reduced from normal), the fetus is vulnerable to hypoxic stress.  The fetus’s ability to adapt to this stress depends on the length and severity of the exposure, although may result in intrauterine growth restriction, fetal brain damage and altered cardiac function.  Epidemiological studies and animal models have now identified a strong association between reduced fetal growth and an increased risk of disease in the adult, suggesting the importance of fetal health on adult well-being.
 
A reduction in oxygen levels has been shown to stimulate the expression of oxygen-sensitive genes (such as HIF-1, iNOS, and VEGF) as adaptive mechanisms for cell survival.  We have identified that prolonged exposure to hypoxia increases gene expression of some of these factors, contributing to both adaptive and maladaptive responses in the fetal cardiovascular system. Thus, our research interest focuses on the effect of hypoxic stress on the expression of oxygen-sensitive genes and how altered gene expression influences cardiac function and blood vessel reactivity in both the fetus and the affected offspring. Further, we are also interested in other intrauterine stressors, such as exposure to prenatal nicotine, on fetal cardiovascular function and its lasting impact on the offspring.

Prolonged exposure to reduced oxygen levels (hypoxic stress) is the leading cause of fetal morbidity and mortality.  Under normal conditions, the fetus develops in a relatively reduced oxygen environment.  Yet, it has undergone cardiovascular adaptations that favor delivery of its oxygen and nutrient needs.  Under conditions of intrauterine hypoxia (where oxygen levels are further reduced from normal), the fetus is vulnerable to hypoxic stress.  The fetus’s ability to adapt to this stress depends on the length and severity of the exposure, although may result in intrauterine growth restriction, fetal brain damage and altered cardiac function.  Epidemiological studies and animal models have now identified a strong association between reduced fetal growth and an increased risk of disease in the adult, suggesting the importance of fetal health on adult well-being.

A reduction in oxygen levels has been shown to stimulate the expression of oxygen-sensitive genes (such as HIF-1, iNOS, and VEGF) as adaptive mechanisms for cell survival.  We have identified that prolonged exposure to hypoxia increases gene expression of some of these factors, contributing to both adaptive and maladaptive responses in the fetal cardiovascular system.  Thus, our research interest focuses on the effect of hypoxic stress on the expression of oxygen-sensitive genes and how altered gene expression influences cardiac function and blood vessel reactivity in both the fetus and the affected offspring.  Further, we are also interested in other intrauterine stressors, such as exposure to prenatal nicotine, on fetal cardiovascular function and its lasting impact on the offspring.



Lab Techniques and Equipment:

We have developed an animal model of chronic fetal hypoxia using the pregnant guinea pig. We use a combination of techniques to investigate the effect of hypoxia on gene expression in the fetal heart and blood vessels. We utilize the wire myograph and isolated, perfused heart preparations to quantify effects on vascular and cardiac function, respectively. mRNA expression is quantified using rt-PCR, protein expression by Western blot analysis and protein localization by immunocytochemistry. We utilize a variety of commercially available kits to assess enzymatic activity and protein levels in tissues and isolated cells.


Laboratory Personnel:

  • Gerard A. Pinkas Senior Research Assistant
  • Hongshan Liu, M.D., postdoctoral fellow
  • LaShauna Evans, predoctoral graduate student

Publications:

Selected Publications

Thompson LP
. Effects of chronic hypoxia on fetal coronary responses. High Altitude Medicine & Biology. 4 (No. 2): 215-224, 2003.

Thompson LP, Aguan K, Zhou H. Chronic hypoxia inhibits contraction of fetal arteries by increasing nitric oxide and prostaglandin synthesis. J. Soc. Gynecol. Invest. 11:511-20, 2004.

Thompson, LP and Dong Y. Chronic hypoxia decreases endothelial nitric oxide synthase protein expression in fetal guinea pig hearts. J. Soc. Gynecol. Invest. 12(6): 388-395, 2005.

Dong Y and Thompson LP. Differential expression of eNOS in coronary and cardiac tissue of hypoxic fetal guinea pig hearts. J. Soc. Gynecol. Invest. 13: 483-90, 2006.

Oh C, Dong Y, Liu H, and Thompson LP. Intrauterine hypoxia upregulates pro-inflammatory cytokines and matrix metalloproteinases in fetal guinea pig hearts. Am. J. Obstet. Gynecol. 2008 Jul;199(1):78.e1-6. (Epub 2008 Feb 15.)

Bonnette MD, Pavlova VR, Rodier DN, Thompson LP, Boone EL, Brown KL, Meyer KM, Trevino MB, Champagne JR, Cruz TD. dcDegenerate oligonucleotide primed-PCR for multilocus, genome-wide analysis from limited quantities of DNA. Diagn Mol Pathol. 2009 Sep;18(3):165-75.

Katari MS, Nowicki SD, Aceituno FF, Nero D, Kelfer J, Thompson LP, Cabello JM, Davidson RS, Goldberg AP, Shasha DE, Coruzzi GM, Gutiérrez RA. VirtualPlant: a software platform to support systems biology research. Plant Physiol. 2010 Feb;152(2):500-15. Epub 2009 Dec 9.