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Development of a Non-Chemical Stress Model for Environmental Studies: Effect of Maternal High Fat Diet on Postnatal Cardiac Stem\Progenitor Cells
Citation:
Dreher, K., K. Das, C. Lau, AND M. Kubo. Development of a Non-Chemical Stress Model for Environmental Studies: Effect of Maternal High Fat Diet on Postnatal Cardiac Stem\Progenitor Cells. Society of Toxicology, Baltimore, MD, March 10 - 14, 2019.
Impact/Purpose:
Developmental basis of health and disease: determining the impact of maternal diet on postnatal cardiac stem and progenitor cells in vivo. Loss of CSCs/CPCs may contribute to the postnatal loss of: heart homeostasis; injury repair and function; disease susceptibility; and potentially decreased longevity.
Description:
Stem cell biology research has demonstrated a critical role of cardiac stem/progenitor cells (CSCs/CPCs) in heart homeostasis, injury repair, function, and disease susceptibility at all life stages. The extent to which non-chemical stressors influence the effects which chemical and/or pollutant exposures may have on postnatal CSCs/CPCs is unknown. To address this uncertainty, research was conducted to examine the impact which maternal diet has on CSCs/CPCs levels in their offspring with intention of employing this non-chemical stressor model for subsequent environmental health effect studies. Pregnant Long Evans rats were maintained on either a normal rat chow diet (ND) or high-fat diet (HFD) for various gestation days (GD): GD1-11; GD11-22; or GD1-22. Hearts were recovered from offsprings at postnatal day (PND) 5 and 23. Quantitative RT-PCR was used to assess heart mRNA levels of genes (c-Kit; Islet-1; Sca1; Scf; Flk-1; Nkx2.5) associated with CPCs/CPCs. Gestational HFD significantly affected the mRNA levels encoding genes associated with CSCs/CPCs in the offsprings of dams on HFD in a complex manner and the effects were dependent on gestational HFD, specific to certain CSC\CPC related mRNAs, postnatal age, and gender of the offspring. When compared to offsprings born from dams on ND, offspring from dams fed HFD had a 2-fold increase in heart c-Kit mRNA levels at PND5 but a 10% - 25% decrease in heart c-Kit mRNA levels at PND23. There was no effect on Nkx2.5 mRNA levels in heart RNA from offspring recovered from dams on HFD versus neonates from dams on ND at PND5. However, there was a significant 50% decrease in heart Nkx2.5 mRNA levels in offspring from dams on HFD at PND23 when compared to offspring from dams on ND. These results demonstrate that a non-chemical stressor such as gestational HFD can alter CSCs/CPCs postnatally. Loss of CSCs/CPCs may contribute to the postnatal loss of: heart homeostasis; injury repair and function; disease susceptibility; and potentially decreased longevity. (This abstract does not represent EPA policy)