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Transcription Profiles of the Ductus Arteriosus in Brown-Norway Rats Advance Publication by-J-STAGE Circulation Journal Official Journal of the Japanese Circulation Society http://www.j-circ.or.jp Transcription Profiles of the Ductus Arteriosus in Brown-Norway Rats With Irregular Elastic Fiber Formation Yi-Ting Hsieh, BSc; Norika Mengchia Liu, BSc; Eriko Ohmori, BSc; Tomohiro Yokota, PhD; Ichige Kajimura, MD; Toru Akaike, MD, PhD; Toshio Ohshima, MD, PhD; Nobuhito Goda, MD, PhD; Susumu Minamisawa, MD, PhD Background: Patent ductus arteriosus (PDA) is one of the most common congenital cardiovascular defects in children. The Brown-Norway (BN) inbred rat presents a higher frequency of PDA. A previous study reported that 2 different quantitative trait loci on chromosomes 8 and 9 were significantly linked to PDA in this strain. Nevertheless, the genetic or molecular mechanisms underlying PDA phenotypes in BN rats have not been fully investigated yet. Methods and Results: It was found that the elastic fibers were abundant in the subendothelial area but scarce in the media even in the closed ductus arteriosus (DA) of full-term BN neonates. DNA microarray analysis identified 52 upregulated genes (fold difference >2.5) and 23 downregulated genes (fold difference <0.4) when compared with those of F344 control neonates. Among these genes, 8 (Tbx20, Scn3b, Stac, Sphkap, Trpm8, Rup2, Slc37a2, and RGD1561216) are located in chromosomes 8 and 9. Interestingly, it was also suggested that the significant decrease in the expression levels of the PGE2-specfic receptor, EP4, plays a critical role in elastogenesis in the DA. Conclusions: BN rats exhibited dysregulation of elastogenesis in the DA. DNA microarray analysis identified the candidate genes including EP4 involved in the DNA phenotype. Further investigation of these newly identified genes will hopefully clarify the molecular mechanisms underlying the irregular formation of elastic fibers in PDA. Key Words: Congenital heart disease; DNA microarray; Elastic fiber; Patent ductus arteriosus; Vascular remodeling he ductus arteriosus (DA) between the pulmonary ar- as patent ductus arteriosus (PDA) and is frequently observed tery (PA) and the descending aorta is essential for in preterm infants.4,5 In the case of premature infants, devel- T maintaining fetal circulation. The DA begins to close opmental prematurity of the DA is an important determinant shortly after birth via a combination of 2 events: functional and of PDA. In contrast, PDA that occurs in term infants is usu- anatomical closure. Functional closure happens within the first ally associated with a structural abnormality. The prevalence few hours after birth. Subsequent to functional closure is ana- of PDA in term infants is approximately 2–8 per 10,000 live tomical closure, which refers to the structural remodeling and births, and it represents 5–7% of all cases of congenital heart fibrosis of the DA leading to permanent closure. Progressive diseases in term infants.5 In some of these cases, a genetic intimal thickening that appears prominently at late gestation background underlies an impaired structural remodeling of the represents the structural remodeling of the DA. This physio- DA; the intimal cushion formation is abnormal or absent, and logical intimal thickening is characterized by: (a) the detach- the endothelium remains attached to the IEL or to an addi- ment of the endothelium from the internal elastic lamina (IEL); tional subendothelial elastic lamina; additionally, invagination (b) the fragmentation of the IEL and loss of elastic fibers in the of the endothelium or migration of SMCs from the media are medial layer; (c) the deposition of an extracellular matrix not observed.6,7 (ECM) in the subendothelial area; and (d) the migration of To understand the molecular mechanisms underlying PDA smooth muscle cells (SMCs) into the subendothelial space.1–3 associated with impaired structural remodeling, researchers This series of events contributes to the reorganization and have made use of animal models as a powerful experimental permanent closure of the DA. A failure of DA closure is known tool. The Brown-Norway (BN) inbred rat strain is characterized Received August 19, 2013; revised manuscript received January 25, 2014; accepted January 27, 2014; released online March 19, 2014 Time for primary review: 21 days Department of Life Science and Medical Bioscience, Waseda University, Tokyo (Y.-T.H., N.M.L., E.O., T.Y., T.O., N.G., S.M.); Depart- ment of Cell Physiology, Jikei University, Tokyo (I.K., T.A., S.M.), Japan Mailing address: Susumu Minamisawa, MD, PhD, Department of Cell Physiology, Jikei University School of Medicine, 3-25-8 Nishishimbashi, Minato-ku, Tokyo 105-8461, Japan. E-mail: [email protected] ISSN-1346-9843 doi: 10.1253/circj.CJ-13-1029 All rights are reserved to the Japanese Circulation Society. For permissions, please e-mail: [email protected] Advance Publication by-J-STAGE HSIEH YT et al. Figure 1. Dysregulated elastic fiber for- mation in the ductus arteriosus (DA) of Brown-Norway (BN) rats. To determine the boundary line of intimal cushion for- mation (ICF, 2-way arrow) and internal elastic lamina (IEL, arrowhead), tissue sections of the DA 1 h after birth were stained with Elastica van Gieson. (a and b) In the comparable longitudinal sec- tions of the DA, the lumen of the DA is almost closed with ICF and the frag- mented IEL in a F344 neonate (a), whereas the DA was widely open with minimal ICF and thick IEL in a BN neo- nate (b). (c and d) In the comparable oblique sections of the DA, the lumen of the DA is closing in both F344 (c) and BN neonates (d). The F344 DA exhibits the fragmented IEL and apparent ICF (c), whereas the DA of the BN neonate has thick IEL and less ICF (d). (e and f) In the comparable cross-sections of the DA, the lumen of the DA is closed in both F344 (e) and BN (f) neonates. The F344 DA exhibits the fragmented IEL (e), whereas the DA of BN neonate has thick IEL and the scarcer elastic lamellae in the media (f). Scale bar: 200 μm. as a novel animal model of PDA.8,9 Bokenkamp et al. demon- strated that the elastin lamellae were virtually absent in the Methods media but had accumulated in the intima of the DA in the BN Animals rat, resulting in the formation of a subendothelial elastic lamina Timed-pregnant BN and Fisher 344 (F344) rats were pur- and an inhibition of intimal SMC migration.8 These histologi- chased from Japan SLC, Inc. (Shizuoka, Japan). F344 rats are cal features were also found in human and canine PDA.6,7 The commonly used as the control strain when compared with BN BN rat also develops several elastin-related arterial impair- rats. After pregnant rats were anesthetized with tribromoetha- ments such as ruptures of the IEL in the abdominal aorta, and nol (Avertin®) on the 21st day of gestation (full-term), neonates aortic elastin deficit in adults.10 Therefore, these findings sug- were delivered by cesarean section and confirmed to be breath- gest that the inbred BN rat strain exhibits systemic elastin-re- ing. The average number of offspring from pregnant BN rats lated impairments that might cause PDA. The genetic or mo- was 3~4 per mother, which was lower than the approximately lecular mechanisms underlying elastin impairment and PDA 10 neonates obtained from a F344 pregnant rat. All animals phenotypes in this rat strain have not yet been fully investi- were cared for in compliance with the American Physiological gated, although a study of a genome-wide scan with linkage Society. The experiments were approved by the Ethical Com- analysis in BN rats reported that 2 different quantitative trait mittee on Animal Experiments of Waseda University. loci (QTL) on chromosomes 8 and 9 were significantly linked to PDA in this strain.10 Furthermore, our recent findings dem- Histological Analyses onstrated that prostaglanding E2 (PGE2) and its receptor type After delivery, the neonates were placed into a 37°C incubator 4 (EP4, or Ptger4) play a critical role in impaired elastogenesis for 1 h. After 1 h the neonates were decapitated and incised of the DA via degradation of lysyl oxidase (Lox), a key en- through the sternum. The thoracic cavity containing the aorta, zyme that catalyzes elastin cross-links in DA SMCs, and that PA and DA was dehydrated and embedded in paraffin (BN: EP4 knockout mice displayed the arterialized PDA,11 making n=6; F344: n=6). The paraffin-embedded blocks were cut into EP4 as a possible candidate for the PDA phenotype of BN rats. 6-μm-thick sections and placed on glass slides. To determine In the present study, we investigated the transcription profiles the boundary line of intimal cushion formation, tissue sections of the BN rat DA at birth to understand the genetic and/or were stained with Elastica van Gieson, as recommended by the molecular mechanisms underlying the structural abnormali- manufacturer (Muto Pure Chemicals). To determine the extent ties, especially the irregular elastic fiber formation. of EP4 expression in DA tissues, the tissue sections were in- cubated with anti-EP4 antibody (1:200 dilution; #LS-A3890, Advance Publication by-J-STAGE Transcription Profiles of the DA in BN Rats Table 1. Upregulated Genes in the Ductus Arteriosus (DA) of Brown-Norway (BN) Rats Gene BN/F344 DA/Aorta Chromosome Probe Set ID mRNA-Description Symbol DA Aorta F344 Location Aorta-Dominant Group 10725778 Nuclear protein, transcriptional regulator, 1 Nupr1 7.39 1.86 0.15 1q36 10829046 Glucagon-like peptide 1 receptor Glp1r 4.87 1.11 0.34 20p12 10909328 Sodium channel, voltage-gated, type III, beta Scn3b 4.73 1.01 0.3
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