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2020 Southern Regional Meeting Abstracts J Investig Med: first published as 10.1136/jim-2020-SRM on 28 January 2020. Downloaded from Cardiovascular club I mice is regulated through the TGF-b1-mediated SMAD- dependent pathway. 11:00 AM Thursday, February 13, 2020 2 INSULIN-LIKE GROWTH FACTOR-1 UPREGULATES JUNCTION PROTEINS, WHILE IT DOWNREGULATES 1 CARDIAC FIBROSIS AND HEART FAILURE IN MICE ADHESION PROTEINS IN VASCULAR ENDOTHELIAL CARRYING GENETIC ABLATION OF NATRIURETIC CELLS: POTENTIAL MECHANISMS FOR ANTI- PEPTIDE RECEPTOR-A: ROLE OF TGF-BETA1 ATHEROGENIC EFFECTS PATHWAY 1Y Higashi*, 1S Danchuk, 2Z Li, 1T Yoshida, 1S Sukhanov, 1P Delafontaine. 1Tulane H Chen, R Samivel, U Subramanian, KN Pandey*. Tulane University Health Sciences Center, University School of Medicine, New Orleans, LA; 2University of Missouri School of Medicine, New Orleans, LA Columbia, MO 10.1136/jim-2020-SRM.1 10.1136/jim-2020-SRM.2 Purpose of study Mice carrying targeted-ablation of the natriu- Purpose of study Insulin-like Growth Factor-1 (IGF-1) is an retic peptide receptor-A (NPRA) gene (Npr1) exhibit cardiac anti-atherogenic growth factor, having anti-inflammatory hypertrophy with increased collagen deposition and fibrosis. effects on macrophages and pro-survival and profibrotic The goal of this study was to determine the underlying mech- effects on vascular smooth muscle cells. However, its effects anisms that regulate the development of cardiac fibrosis and on vascular endothelial cells are not fully described. We heart failure in Npr1 gene-knockout mice. assessed IGF-1 effects on expression levels of intercellular Methods used The Npr1 null mutant (Npr1-/-, 0-copy), hetero- junction proteins and cell adhesion proteins in aortic endo- zygous (Npr1±, 1-copy), and wild-type (Npr1+/+, 2-copy) thelial cells. mice were orally administered with transforming growth fac- Methods used Human aortic endothelial cells (hAoECs) are tor-b1 (TGF-b1) receptor antagonist, GW788388 (2 mg/kg/ exposed to 0–100 ng/mL IGF-1, anti-IGF-1 receptor day) by gavage for 28 days. Together, systolic blood pressure (IGF1R) neutralizing antibody, or Picropodophyllin (PPP; (SBP), heart weight-to-body weight (HW/BW) ratio, left ven- IGF1R inhibitor), and protein expression levels were deter- tricular end-diastolic dimension (LVEDD), left ventricular mined by Western blot. Small molecule permeability was end-systolic dimension (LVEDS), and percent fractional short- assessed on monolayer of hAoECs by transwell permeability ening (FS) were analyzed. The heart was isolated and used assay. for the analysis of fibrotic markers using quantitative reverse Summary of results IGF-1 elevated expression levels of junction transcription-polymerase chain reaction (qRT-PCR) and West- proteins, namely CD31, VE-cadherin, Occludin, Claudin-5, ern blot. and Jam-A, while IGF1R inhibition by neutralizing antibody Summary of results The HW/BW ratio, LVEDD, and LVEDS or PPP decreased their expression levels. Intriguingly, IGF-1 were significantly increased in Npr1-/- and Npr1± mice than decreased expression levels of adhesion proteins, ICAM-1 and wild-type Npr1+/+ mice. At the same time the fractional VCAM-1. We next tested barrier function of monolayer of http://jim.bmj.com/ shortening was greatly reduced in Npr1-/- and Npr1± mice hAoECs. Transwell permeability assay showed that IGF1R compared with Npr1+/+ mice. The Npr1-/- null mutant (0- inhibition by PPP elevated permeation of dextran-FITC by 4.8 copy) mice showed 6-fold induction of cardiac fibrosis as ±0.4-fold (P<0.01), consistent with the downregulation of compared with wild-type (2-copy) control mice. Moreover, junction proteins. Meanwhile, IGF-1 decreased adhesion of the expression of fibrotic markers such as connective tissue THP-1 monocytes on monolayer of hAoECs by 34±5% growth factor (CTGF), a-smooth muscle actin (a-SMA), (P<0.05), while IGF1R-inhibition by PPP increased monocyte TGF-b1, TGF-bRI, TGF-bRII, and SMAD proteins were sig- adhesion by 3.1±0.2-fold (P<0.01). In aortas of endothelial on October 4, 2021 by guest. Protected copyright. nificantly increased in Npr1-/- and Npr1± mice hearts com- IGF1R-deficiency mice (Cdh5-Cre/Igf1rfl/fl mice) we found pared with age-matched wild-type control animals. The Npr1 Occludin, Claudin-5 and Jam-C are downregulated, which is gene-knockout (0-copy) mice also suffered with congestive consistent with the observation in hAoECs. Finally, the Cdh5- heart failure at early adult age as compared with Npr1 wild- Cre/Igf1rfl/fl mice on Apoe-deficient background produced more type (2-copy) mice. The treatment with TGF-b1 receptor atherosclerosis than control mice by 33±8% (P<0.05) on a antagonist, GW788388, significantly prevented the cardiac high-fat diet, suggesting anti-atherogenic effects of IGF-1 in fibrosis and potentially down-regulated the expression of the endothelium. fibrotic markers and SMAD proteins in Npr1-/- and Npr1± Conclusions Our results suggest that IGF-1 supports endothe- mice. lial barrier function by positively regulating junction proteins, Conclusions The results of the present study indicate that, the while it suppresses leukocyte adhesion by negatively regulating induction and development of cardiac fibrosis and heart fail- adhesion proteins in endothelial cells, thereby exerting anti- ure in Npr1 gene-disrupted (0-copy) and haplotype (1-copy) atherogenic effects. J Investig Med 2020;68:431–720 435 Abstracts J Investig Med: first published as 10.1136/jim-2020-SRM on 28 January 2020. Downloaded from 3 SPONTANEOUS SUPERIMPOSED PREECLAMPSIA IS Abstract 4 Table 1 Baseline characteristics and outcomes of ASSOCIATED WITH IMPAIRED GUT MICROBIOME heart failure admissions divided by geographic region REMODELING JA Ishimwe*, A Akinleye, A Johnson, MR Garrett, JM Sasser. University of Mississippi Medical Center, Jackson, MS 10.1136/jim-2020-SRM.3 Purpose of study Preeclampsia (PE), a hypertensive disorder of pregnancy, is a leading cause of maternal deaths. It affects 2– 8% of all pregnancies, and its pathophysiology is not fully understood. Recent studies in preeclamptic patients have sug- gested a role for the gut microbiome in the disease. We have characterized the Dahl salt-sensitive (Dahl S) rat as a sponta- neous rodent model of superimposed PE. Here, our purpose was to test the hypothesis that preexisting chronic hyperten- sion impairs maternal gut microbiome remodeling and contrib- utes to the development and/or progression of superimposed PE. Methods used Female Sprague Dawley (SD) and Dahl S rats were maintained in conventional caging in the same room and on the same diet (Teklad 7034, 0.3% NaCl). Half of the rats of each strain were mated to have pregnant and virgin groups (n=7–9/group). Fecal samples were collected at baseline (BL), gestation day 20 (GD20) and one-week postpartum (PP) to assess gut microbiome via 16S rRNA gene sequencing. Alpha diversity (Shannon index), beta diversity (Bray-Curtis index), and linear discriminant analysis effect size (LEfSe) were deter- mined from the sequenced data to assess microbial differences. At BL, Dahl S rats had higher alpha diversity (P<0.0001) and heart failure admissions by geographic regions in the United distinctly clustered beta diversity (p<0.001) compared to SD States. rats. Methods used The National Inpatient Sample (NIS) database Summary of results Dahl S had higher proteobacteria abun- for the year 2016 was queried. Adult patients admitted with a dance (665,980 vs 51,240, p<0.05), a marker of dysbiosis. In principal diagnosis of heart failure were identified using vali- response to pregnancy, we observed significant differences dated ICD-10 codes. Comparisons were made between four among groups in both alpha and beta diversity during late regions - Northeast, Midwest, South and West. Statistical anal- pregnancy. Also, proteobacteria abundance in the SD rats rose ysis was performed using STATA. http://jim.bmj.com/ from 0.56% (BL) to 13.46% (GD20) before subsiding to Summary of results A total of 807,764 heart failure hospitaliza- 7.36% (PP) suggesting that changes may be a normal adapta- tions were identified. Of these, 153,233 were in the North- tion to pregnancy. The Dahl S, however, showed no change east; 184,090 in the Midwest; 331,506 in the South; and in proteobacteria: 5.29% (BL) to 6.35% (GD20) and 7.8% 138,935 in the West. There was a small difference in the (PP). In addition, the SD displayed elevations in pathogenic mortality rates (highest in West at 3%, and lowest in South at bacteria genera. The Helicobacter genus was higher in SD 2.66%, p=0.03) and length of stay (longest in the Northeast, on October 4, 2021 by guest. Protected copyright. pregnant than SD virgin (580,110 vs 3,045, p<0.05) but simi- and shortest in the West, p<0.001) between regions. A signifi- lar between Dahl S groups (p=0.87). The Bacteroides and tre- cant difference was observed in the total hospital charges per ponema genera exhibited a similar pattern. hospitalization (nearly $65,000 in the West, and only $37,000 Conclusions In this study, we have presented preclinical evi- in the Midwest, p<0.001). dence for pregnancy-specific alterations in the gut microbiota, Conclusions Our study demonstrates the existence of regional and we suggest that these may be impaired in PE. differences in the costs and outcomes of healthcare delivery to heart failure patients. Further research is needed to explore the reasons for these differences. 4 REGIONAL DIFFERENCES IN EPIDEMIOLOGY AND OUTCOMES OF HEART FAILURE ADMISSIONS ACROSS 5 INHIBITION OF ANGIOTENSIN II TYPE 1 RECEPTOR IN THE UNITED STATES SKELETAL MUSCLE STEM (SATELLITE) CELLS PREVENTS ANGIOTENSIN II-INDUCED SKELETAL MUSCLE WASTING A Goel*, H Paydak, JL Mehta. University of Arkansas for Medical Sciences (UAMS), Little Rock, AR T Yoshida*, P Delafontaine. Tulane University, New Orleans, MO 10.1136/jim-2020-SRM.4 10.1136/jim-2020-SRM.5 Purpose of study Periodic surveillance of geographical varia- Purpose of study Patients with advanced congestive heart fail- tions in cardiovascular health is important to achieve the goal ure (CHF) or chronic kidney disease (CKD) often have of reducing regional disparities in healthcare delivery.
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