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Dearing, C. G.

Publications and source records attributed to Dearing, C. G..

2 recordsLinked to original sources

Sex-Specific Cardiac Remodeling in Aged Rats after Early-Life Chronic Stress: Associations with Endocrine and Metabolic Factors

BackgroundCardiovascular disease is a leading cause of death worldwide. Rates of cardiovascular disease vary both across the lifespan and between sexes. While multiple factors, including adverse life experiences, impact the development and progression of cardiovascular disease, the potential interactions of biological sex and stress history on the aged heart are unknown. To this end, we examined sex- and stress-specific impacts on left ventricular hypertrophy (VH) after aging. We hypothesized that early life chronic stress exposure impacts behavioral and physiologic responses that predict cardiac remodeling in a sex-specific manner. MethodsHistological analysis was conducted on hearts of male and female rats previously exposed to chronic variable stress during the late adolescent period (postnatal days 43-62). These animals were challenged with a forced swim test and a glucose tolerance test before aging to 15 months and again being challenged. Predictive analyses were then used to isolate factors that relate to cardiac remodeling among these groups. ResultsEarly-life chronic stress impacted cardiac remodeling in a sex-specific manner. Among rats with a history of chronic stress, females had increased inward VH. However, there were few associations within the female groups among individual behavioral and physiologic parameters and cardiac remodeling. While males as a group did not have VH after chronic stress, they exhibited multiple individual associations with cardiac susceptibility. Passive coping in young males and active coping in aged males related to VH in a stress history-dependent manner. Moreover, baseline corticosterone positively correlated with VH in unstressed males, while chronically-stressed males had positive correlations between VH and visceral adiposity. ConclusionsThese results indicate that females as a group are uniquely susceptible to the effects of early-life stress on cardiac remodeling later in life. Conversely, males have more individual differences in vulnerability, where susceptibility to cardiac remodeling relates to endocrine, metabolic, and behavioral measures depending on stress history. These results ultimately support a framework for accessing cardiovascular risk based on biological sex and prior adverse experiences. HighlightsO_LIAged female rats had greater left ventricular hypertrophy (VH) than males after early-life chronic variable stress. C_LIO_LITertile divisions based on susceptibility or resilience to inward VH indicated interactions between VH, sex, and stress on multiple behavioral and physiological measures. C_LIO_LIIn males, VH correlated with endocrine and metabolic parameters in a stress history-dependent manner. C_LIO_LIPrior adverse experience and biological sex interact across the lifespan to impact cardiovascular risk. C_LI Plain English SummaryCardiovascular disease is the leading cause of death worldwide. Multiple factors influence the incidence and severity of cardiovascular disease including adverse life experiences, biological sex, and age. Alterations of heart structure predict negative cardiovascular health by impacting blood circulation; however, the potential interactions of stress history and biological sex on the aged heart are unknown. In this study, we examined how chronic stress exposure impacts heart structure in male and female rats after aging. Adolescent male and female rats were chronically stressed and then acutely challenged to examine behavioral, endocrine, and metabolic parameters both immediately following chronic stress and after aging. Heart morphology was quantified to examine how behavioral and physiological responses related to cardiac remodeling. Our results indicate that, as a group, female rats previously exposed to chronic stress were uniquely susceptible to inward remodeling of the heart. Subjects were further divided into sub-groups based on the level of inward remodeling of the ventricle. While male rats did not exhibit group effects on heart structure, individual variability in male heart morphology related to endocrine and metabolic parameters in a stress history-dependent manner. Here, there were interactions with multiple systems including coping behavior, stress hormones, and body composition. Moreover, males without a prior history of chronic stress had correlations between stress hormones and the degree of heart remodeling. However, males that were exposed to chronic stress had correlations between heart structure and abdominal fat. Overall, our results indicate that biological sex and stress history interact to predict cardiovascular susceptibility.

physiology↗

Effects of physiological deficits in pineal melatonin on Triple Negative Breast Cancer.

BackgroundTriple negative breast cancer (TNBC) is aggressive and treatment resistant. Evidence suggests that deficits in melatonin signaling increase TNBC risk: conditions that suppress melatonin increased incidence, low melatonin receptor expression correlates with worse prognosis, and high-dose melatonin can inhibit TNBC. Together this suggests that normalizing pineal melatonin could reduce TNBC incidence and/or mortality. The goal of this study was to determine whether small physiological deficits in melatonin alone, can increase risk for TNBC, and how normal melatonin would be protective. MethodsThe effect of melatonin treatment on 4t1 cells in vitro was measured using the MTT cell viability assay, and gene expression of breast cancer and melatonin signaling markers. The effect of pineal gland status on 4t1 cell allografts was tested in C3Sn mice (Mus Musculus) with either an intact pineal (control) or surgical removal of the pineal causing a ~50% deficit in plasma melatonin. Orthotopic tumors were assessed by histopathology and metastasis by strain specific qPCR against 4t1 cell and host gDNA. ResultsMelatonin treatment induced significant changes in gene expression, with a significant reduction in derived PAM50 Risk of Recurrence score (ROR in Not treated = 65.5 {+/-} 10.6 Mean SEM; Treated with 25pg/ml of melatonin 20.8 {+/-} 8.3; P = 0.008), suggesting melatonin treatment would improve prognosis. A ~50% reduction in plasma melatonin increased orthotopic tumors, but this was non-significant, and had no effect on metastasis from tail vein allograft. ConclusionsPhysiological deficits in melatonin do alter the oncogenic status of 4t1 tumor cells but this has only a limited effect on growth and metastasis in vivo. Lack of significance in orthotopic tumor formation may be due to small sample size, and it is possible that any protective effect of melatonin occurs earlier in tumor development than we have tested.

cancer biology↗