https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:25448 Wed 24 Nov 2021 15:53:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22783 Wed 11 Apr 2018 11:21:14 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:23916 Wed 11 Apr 2018 10:32:03 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33387 34-weeks gestation; n=8) and gestational age matched preterm (31.6-35.1 weeks; n=8) and term normotensive controls were also compared. Agilent Human miRNA microarray v19 was used to detect up to 2006 miRNAs in four placentae from each group. Statistically different levels of expression were determined and refined using predictive modelling. Placental miRNAs predicted to target RAS mRNAs were identified in three databases. Differences detected on the array were confirmed for some miRNAs by semi-quantitative RT-PCR (qPCR, n=7-8 for all groups). Two differentially expressed miRNAs that were known to target human renal REN mRNA (miR-181a-5p and miR-663) were transfected into human HTR-8/SVneo trophoblast cells to examine their effect on placental REN expression and prorenin levels. In early gestation placentae, 186 miRNAs were differentially expressed compared with term placentae (109 increased, 77 decreased). Thirty of the differentially expressed miRNAs were predicted to target RAS components. In mid-gestation placentae, 117 miRNAs were differentially expressed compared with term placentae (69 increased, 48 decreased). Of these, 19 had RAS mRNAs as predicted targets. Eight miRNAs that were lower in early gestation and predicted to target RAS mRNAs were confirmed by qPCR. All showed an increase during gestation and could influence the transgestational profile of the human placental RAS. Additionally, on the array, three miRNAs predicted to target RAS mRNAs (miR-892c-3p, miR-378c and miR-514b-3p) were overexpressed in placentae from women with late-onset PE (P = 3.6E-10, P = 1.8E-05, P = 5.3E-06; respectively). miR-663, which suppresses renal REN mRNA expression, was overexpressed in early-onset PE placentae as determined by qRT-PCR analysis (P = 0.014). Transfection of miR-181a-5p and miR-663 into HTR-8/SVneo trophoblast cells suppressed REN mRNA expression (p = 0.05) and prorenin protein production (P = 0.001). Data can be found via GEO accession number GSE109832. Further validation that the differentially expressed miRNAs do indeed directly target RAS mRNAs and affect placental development and function is required. This study is limited by the small sample size. Therefore independent validation in a larger cohort is required.]]> Wed 02 Mar 2022 14:28:37 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50715 Wed 02 Aug 2023 16:17:49 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48579 Tue 21 Mar 2023 17:43:58 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:35957 Tue 21 Jan 2020 11:08:08 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:54158 Tue 06 Feb 2024 12:17:30 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:43821 +ß7⁺ gut-homing T cells appear to be linked to the pathophysiology of both FD and IBS. Studies in the area are complicated by poor phenotyping of patients into subgroups and the subtle nature of the immune activity involved in FD and IBS. CONCLUSIONS: Alterations in proportions of gut-homing T lymphocytes in both FD and IBS indicate that a loss of mucosal homeostasis may drive the symptoms of FD and IBS. There is indirect evidence that Th17 responses may play a role in FGIDs, however the evidence for a Th2 immune phenotype in FD and IBS is limited. Although immune involvement is evident, large, well-characterised patient cohorts are required to elucidate the immune mechanisms driving the development of FGIDs.]]> Tue 04 Oct 2022 10:29:25 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45013 Thu 27 Oct 2022 17:46:24 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34597 Thu 13 Jan 2022 10:31:31 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36099 Thu 06 Feb 2020 11:37:06 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:18919 Sat 24 Mar 2018 07:59:01 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42333 Mon 22 Aug 2022 11:06:25 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42306 n = 3/group). Those predicted to target RAS mRNAs, or that were decreased in early gestation, were confirmed by qPCR (n = 9/group). RAS protein levels were assessed by ELISAs or immuno-blotting. Microarray analysis identified four miRNAs predicted to target RAS mRNAs that were differentially expressed between 1 and 5% oxygen. Using qPCR, 15 miRNAs that target the RAS were measured in HTR-8/SVneo cells. Five miRNAs were downregulated in 1% compared with 5% oxygen. Expression of a number of RAS mRNAs (ATP6AP2, AGT, ACE and AGTR1) were increased in either, or both, 1 and 5% oxygen compared with 20% oxygen. AGT protein levels were increased in 1% oxygen compared with 5%. Further validation is needed to confirm that these miRNAs target RAS mRNAs directly and that placental development is partly regulated by oxygen-sensitive miRNAs that target RAS mRNAs. Since placental oxygen tension changes across gestation, changes in expression of these miRNAs may contribute to the transgestational changes in placental RAS expression and the resulting effects on placental development.]]> Mon 22 Aug 2022 09:00:22 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20880 Mon 11 Mar 2019 12:15:55 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41982 Fri 19 Apr 2024 11:58:15 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22586 Fri 10 Aug 2018 15:35:14 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49107 Fri 05 May 2023 11:32:08 AEST ]]>