@msu.edu.my
Senior Lecturer / Physiology /International Medical School
Manangement and Science University
Abu-Hayyeh S, Papacleovoulou G, Lövgren-Sandblom A, Tahir M, Oduwole O, Jamaludin NA, Ravat S, Nikolova V, Chambers J, Selden C, Rees M, Marschall HU, Parker MG, Williamson C. Intrahepatic cholestasis of pregnancy levels of sulfated progesterone metabolites inhibit farnesoid X receptor resulting in a cholestatic phenotype. Hepatology. 2013 Feb;57(2):716-26. doi: 10.1002/. Epub 2013 Jan 8
Cited by: 104
Jamaludin NA, Basatvat S, Aboussahoud W, Elliott S, Hunt S, Peacock B, Ebbens S, Fazeli F. Characterisation of extracellular vesicles produced by the Porcine oviductal epithelial cells using size exclusion chromatography. Society for Reproduction and fertility Annual Conference 2016, Winchester, UK, 11-13 July 2016.
Jamaludin NA, Meikle A, Hunt S, Wachernig H, Thurston LM, Andronowska A,Ebbens S, Fazeli A. Characterisation of extracellular vesicles secreted byoviductal and endometrial epithelial cells. UKEV 2016 congress, Oxford Brookes University, UK.
UNIVERSITY OF SHEFFIELD [June 2013 until May 2018]
PhD
IMPERIAL COLLEGE LONDON [October 2008 until October 2009]
MSc in Reproductive and Developmental Biology
Role of extracellular vesicles in reproductive medicine.
Scopus Publications
Scholar Citations
Scholar h-index
Scholar i10-index
Nurul Akmal Jamaludin, Lisa Marie Thurston, Krzysztof Jan Witek, Albany Meikle, Shaghayegh Basatvat, Sarah Elliott, Stuart Hunt, Aneta Andronowska, and Alireza Fazeli
Elsevier BV
Shadi Abu‐Hayyeh, Georgia Papacleovoulou, Anita Lövgren‐Sandblom, Mehreen Tahir, Olayiwola Oduwole, Nurul Akmal Jamaludin, Sabiha Ravat, Vanya Nikolova, Jenny Chambers, Clare Selden,et al.
Wiley
Intrahepatic cholestasis of pregnancy (ICP) is the most prevalent pregnancy‐specific liver disease and is associated with an increased risk of adverse fetal outcomes, including preterm labor and intrauterine death. The endocrine signals that cause cholestasis are not known but 3α‐sulfated progesterone metabolites have been shown to be elevated in ICP, leading us to study the impact of sulfated progesterone metabolites on farnesoid X receptor (FXR)‐mediated bile acid homeostasis pathways. Here we report that the 3β‐sulfated progesterone metabolite epiallopregnanolone sulfate is supraphysiologically raised in the serum of ICP patients. Mice challenged with cholic acid developed hypercholanemia and a hepatic gene expression profile indicative of FXR activation. However, coadministration of epiallopregnanolone sulfate with cholic acid exacerbated the hypercholanemia and resulted in aberrant gene expression profiles for hepatic bile acid‐responsive genes consistent with cholestasis. We demonstrate that levels of epiallopregnanolone sulfate found in ICP can function as a partial agonist for FXR, resulting in the aberrant expression of bile acid homeostasis genes in hepatoma cell lines and primary human hepatocytes. Furthermore, epiallopregnanolone sulfate inhibition of FXR results in reduced FXR‐mediated bile acid efflux and secreted FGF19. Using cofactor recruitment assays, we show that epiallopregnanolone sulfate competitively inhibits bile acid‐mediated recruitment of cofactor motifs to the FXR‐ligand binding domain. Conclusion: Our results reveal a novel molecular interaction between ICP‐associated levels of the 3β‐sulfated progesterone metabolite epiallopregnanolone sulfate and FXR that couples the endocrine component of pregnancy in ICP to abnormal bile acid homeostasis. (HEPATOLOGY 2013;)