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Loss of progesterone receptor membrane component 1 promotes hepatic steatosis via the induced de novo lipogenesis

Lee, Sang R., Kwon, Sun Woo, Kaya, Pelin, Lee, Young Ho, Lee, Jong Geol, Kim, Globinna, Lee, Geun-Shik, Baek, In-Jeoung, Hong, Eui-Ju·2018·Scientific Reports

Abstract

Non-alcoholic fatty liver disease (NAFLD) results from triglyceride accumulation within the liver and some of them advances to non-alcoholic steatohepatitis (NASH). It is important to note that in NAFLD development, hepatic de novo lipogenesis (DNL) derives from excess carbohydrates and fats under a condition of excess energy through β-oxidation. As a main regulator for DNL, sterol regulatory element-binding protein 1 (Srebp-1) forms complex with progesterone receptor membrane component 1 (Pgrmc1). To investigate whether Pgrmc1 may have a notable effect on DNL via SREBP-1 activation, we generated Pgrmc1 knockout (KO) mice and fed a high fat diet for one month. High-fat-fed Pgrmc1 KO mice showed a substantial increase in levels of hepatic TG accumulation, and they were predisposed to NAFLD when compared to WT mice. Loss of Pgrmc1 increased mature SREBP-1 protein level, suggesting that induction of hepatic steatosis in Pgrmc1 KO mice might be triggered by de novo lipogenesis. Moreover, Pgrmc1 KO mice were also more vulnerable to early stage of NASH, showing high levels of alanine aminotransferase, obesity-linked pro-inflammatory cytokines, and fibrosis markers. This is interesting because Pgrmc1 involves with the first step in regulating the hepatic de novo lipogenesis under an excess energy condition.

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  • TMEM97 levels can be regulated by changes in cholesterol levels; when cholesterol levels are reduced, TMEM97 expression can be induced by sterol regulatory element-binding protein-2.

    “Although TMEM97, unlike emopamil binding protein, is not thought to have isomerase activity, TMEM97 levels can be regulated by changes in cholesterol levels. More specifically, when cholesterol levels are reduced, TMEM97 expression can be induced by sterol regulatory element-binding protein-2 [75,76,77,78].”

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  1. Chalasani, N. et al. The diagnosis and management of non-alcoholic fatty liver disease: practice guideline by the American Gastroenterological Association, American Association for the Study of Liver Diseases, and American College of Gastroenterology. Gastroenterology 142, 1592–1609, https://doi.org/10.1053/j.gastro.2012.04.001 (2012). · DOI
  2. Tarantino, G., Savastano, S. & Colao, A. Hepatic steatosis, low-grade chronic inflammation and hormone/growth factor/adipokine imbalance. World J Gastroenterol 16, 4773–4783 (2010). · DOI
  3. Starley, B. Q., Calcagno, C. J. & Harrison, S. A. Nonalcoholic fatty liver disease and hepatocellular carcinoma: a weighty connection. Hepatology 51, 1820–1832, https://doi.org/10.1002/hep.23594 (2010). · DOI
  4. Tarantino, G. & Finelli, C. What about non-alcoholic fatty liver disease as a new criterion to define metabolic syndrome? World J Gastroenterol 19, 3375–3384, https://doi.org/10.3748/wjg.v19.i22.3375 (2013). · DOI
  5. Buzzetti, E., Pinzani, M. & Tsochatzis, E. A. The multiple-hit pathogenesis of non-alcoholic fatty liver disease (NAFLD). Metabolism 65, 1038–1048, https://doi.org/10.1016/j.metabol.2015.12.012 (2016). · DOI · Paper page
  6. Onnerhag, K., Nilsson, P. M. & Lindgren, S. Increased risk of cirrhosis and hepatocellular cancer during long-term follow-up of patients with biopsy-proven NAFLD. Scand J Gastroenterol 49, 1111–1118, https://doi.org/10.3109/00365521.2014.934911 (2014). · DOI
  7. Shimano, H. et al. Isoform 1c of sterol regulatory element binding protein is less active than isoform 1a in livers of transgenic mice and in cultured cells. J Clin Invest 99, 846–854, https://doi.org/10.1172/JCI119248 (1997). · DOI · Paper page
  8. Horton, J. D., Goldstein, J. L. & Brown, M. S. SREBPs: activators of the complete program of cholesterol and fatty acid synthesis in the liver. J Clin Invest 109, 1125–1131, https://doi.org/10.1172/JCI15593 (2002). · DOI · Paper page
  9. Hagen, R. M., Rodriguez-Cuenca, S. & Vidal-Puig, A. An allostatic control of membrane lipid composition by SREBP1. FEBS Lett 584, 2689–2698, https://doi.org/10.1016/j.febslet.2010.04.004 (2010). · DOI
  10. Kast-Woelbern, H. R. et al. Rosiglitazone induction of Insig-1 in white adipose tissue reveals a novel interplay of peroxisome proliferator-activated receptor gamma and sterol regulatory element-binding protein in the regulation of adipogenesis. J Biol Chem 279, 23908–23915, https://doi.org/10.1074/jbc.M403145200 (2004). · DOI
  11. Shulman, A. I. & Mangelsdorf, D. J. Retinoid x receptor heterodimers in the metabolic syndrome. N Engl J Med 353, 604–615, https://doi.org/10.1056/NEJMra043590 (2005). · DOI
  12. Tobin, K. A. et al. Cross-talk between fatty acid and cholesterol metabolism mediated by liver X receptor-alpha. Mol Endocrinol 14, 741–752, https://doi.org/10.1210/mend.14.5.0459 (2000). · DOI
  13. Yoshikawa, T. et al. Cross-talk between peroxisome proliferator-activated receptor (PPAR) alpha and liver X receptor (LXR) in nutritional regulation of fatty acid metabolism. I. PPARs suppress sterol regulatory element binding protein-1c promoter through inhibition of LXR signaling. Mol Endocrinol 17, 1240–1254, https://doi.org/10.1210/me.2002-0190 (2003). · DOI
  14. Matsuda, M. et al. SREBP cleavage-activating protein (SCAP) is required for increased lipid synthesis in liver induced by cholesterol deprivation and insulin elevation. Genes Dev 15, 1206–1216, https://doi.org/10.1101/gad.891301 (2001). · DOI · Paper page
  15. Liu, F. H. et al. The gene-gene interaction of INSIG-SCAP-SREBP pathway on the risk of obesity in Chinese children. Biomed Res Int 2014, 538564, https://doi.org/10.1155/2014/538564 (2014). · DOI
  16. Dong, X. Y. & Tang, S. Q. Insulin-induced gene: a new regulator in lipid metabolism. Peptides 31, 2145–2150, https://doi.org/10.1016/j.peptides.2010.07.020 (2010). · DOI
  17. Suchanek, M., Radzikowska, A. & Thiele, C. Photo-leucine and photo-methionine allow identification of protein-protein interactions in living cells. Nat Methods 2, 261–267, https://doi.org/10.1038/nmeth752 (2005). · DOI
  18. Krebs, C. J. et al. A membrane-associated progesterone-binding protein, 25-Dx, is regulated by progesterone in brain regions involved in female reproductive behaviors. Proc Natl Acad Sci USA 97, 12816–12821, https://doi.org/10.1073/pnas.97.23.12816 (2000). · DOI
  19. Selmin, O. et al. Isolation and characterization of a novel gene induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin in rat liver. Carcinogenesis 17, 2609–2615 (1996). · DOI
  20. Zhang, M. et al. Progesterone receptor membrane component 1 is a functional part of the glucagon-like peptide-1 (GLP-1) receptor complex in pancreatic beta cells. Mol Cell Proteomics 13, 3049–3062, https://doi.org/10.1074/mcp.M114.040196 (2014). · DOI
  21. Peluso, J. J., Romak, J. & Liu, X. Progesterone receptor membrane component-1 (PGRMC1) is the mediator of progesterone’s antiapoptotic action in spontaneously immortalized granulosa cells as revealed by PGRMC1 small interfering ribonucleic acid treatment and functional analysis of PGRMC1 mutations. Endocrinology 149, 534–543, https://doi.org/10.1210/en.2007-1050 (2008). · DOI
  22. Rohe, H. J., Ahmed, I. S., Twist, K. E. & Craven, R. J. PGRMC1 (progesterone receptor membrane component 1): a targetable protein with multiple functions in steroid signaling, P450 activation and drug binding. Pharmacol Ther 121, 14–19, https://doi.org/10.1016/j.pharmthera.2008.09.006 (2009). · DOI · Paper page
  23. Hughes, A. L. et al. Dap1/PGRMC1 binds and regulates cytochrome P450 enzymes. Cell Metab 5, 143–149, https://doi.org/10.1016/j.cmet.2006.12.009 (2007). · DOI · Paper page
  24. Satapati, S. et al. Mitochondrial metabolism mediates oxidative stress and inflammation in fatty liver. J Clin Invest 125, 4447–4462, https://doi.org/10.1172/JCI82204 (2015). · DOI
  25. Fabbrini, E., Sullivan, S. & Klein, S. Obesity and nonalcoholic fatty liver disease: biochemical, metabolic, and clinical implications. Hepatology 51, 679–689, https://doi.org/10.1002/hep.23280 (2010). · DOI · Paper page
  26. Farrell, G. C. & Larter, C. Z. Nonalcoholic fatty liver disease: from steatosis to cirrhosis. Hepatology 43, S99–S112, https://doi.org/10.1002/hep.20973 (2006). · DOI
  27. Caldwell, S. H., Crespo, D. M., Kang, H. S. & Al-Osaimi, A. M. Obesity and hepatocellular carcinoma. Gastroenterology 127, S97–103 (2004). · DOI
  28. Xu, X., So, J. S., Park, J. G. & Lee, A. H. Transcriptional control of hepatic lipid metabolism by SREBP and ChREBP. Semin Liver Dis 33, 301–311, https://doi.org/10.1055/s-0033-1358523 (2013). · DOI
  29. Rawson, R. B. The SREBP pathway–insights from Insigs and insects. Nat Rev Mol Cell Biol 4, 631–640, https://doi.org/10.1038/nrm1174 (2003). · DOI · Paper page
  30. Li, X. et al. SREBP-1c overexpression induces triglycerides accumulation through increasing lipid synthesis and decreasing lipid oxidation and VLDL assembly in bovine hepatocytes. J Steroid Biochem Mol Biol 143, 174–182, https://doi.org/10.1016/j.jsbmb.2014.02.009 (2014). · DOI
  31. Mao, J. et al. Liver-specific deletion of acetyl-CoA carboxylase 1 reduces hepatic triglyceride accumulation without affecting glucose homeostasis. Proc Natl Acad Sci USA 103, 8552–8557, https://doi.org/10.1073/pnas.0603115103 (2006). · DOI · Paper page
  32. Sun, Y. et al. SREBP1 regulates tumorigenesis and prognosis of pancreatic cancer through targeting lipid metabolism. Tumour Biol 36, 4133–4141, https://doi.org/10.1007/s13277-015-3047-5 (2015). · DOI
  33. Zhang, H. et al. Differential effects of estrogen/androgen on the prevention of nonalcoholic fatty liver disease in the male rat. J Lipid Res 54, 345–357, https://doi.org/10.1194/jlr.M028969 (2013). · DOI
  34. Brookheart, R. T., Michel, C. I. & Schaffer, J. E. As a matter of fat. Cell Metab 10, 9–12, https://doi.org/10.1016/j.cmet.2009.03.011 (2009). · DOI · Paper page
  35. Li, Z. Z., Berk, M., McIntyre, T. M. & Feldstein, A. E. Hepatic lipid partitioning and liver damage in nonalcoholic fatty liver disease: role of stearoyl-CoA desaturase. J Biol Chem 284, 5637–5644, https://doi.org/10.1074/jbc.M807616200 (2009). · DOI
  36. Peter, A. et al. Individual stearoyl-coa desaturase 1 expression modulates endoplasmic reticulum stress and inflammation in human myotubes and is associated with skeletal muscle lipid storage and insulin sensitivity in vivo. Diabetes 58, 1757–1765, https://doi.org/10.2337/db09-0188 (2009). · DOI
  37. Verma, S., Jensen, D., Hart, J. & Mohanty, S. R. Predictive value of ALT levels for non-alcoholic steatohepatitis (NASH) and advanced fibrosis in non-alcoholic fatty liver disease (NAFLD). Liver Int 33, 1398–1405, https://doi.org/10.1111/liv.12226 (2013). · DOI
  38. Hotamisligil, G. S. Inflammation and metabolic disorders. Nature 444, 860–867, https://doi.org/10.1038/nature05485 (2006). · DOI · Paper page
  39. Park, E. J. et al. Dietary and genetic obesity promote liver inflammation and tumorigenesis by enhancing IL-6 and TNF expression. Cell 140, 197–208, https://doi.org/10.1016/j.cell.2009.12.052 (2010). · DOI · Paper page
  40. Tarantino, G. et al. Could inflammatory markers help diagnose nonalcoholic steatohepatitis? European journal of gastroenterology & hepatology 21, 504–511, https://doi.org/10.1097/MEG.0b013e3283229b40 (2009). · DOI
  41. Matsumoto, M. et al. An improved mouse model that rapidly develops fibrosis in non-alcoholic steatohepatitis. Int J Exp Pathol 94, 93–103, https://doi.org/10.1111/iep.12008 (2013). · DOI · Paper page
  42. Lee, N. P. et al. Proteomic expression signature distinguishes cancerous and nonmalignant tissues in hepatocellular carcinoma. J Proteome Res 8, 1293–1303, https://doi.org/10.1021/pr800637z (2009). · DOI
  43. Hampton, K. K., Stewart, R., Napier, D., Claudio, P. P. & Craven, R. J. PGRMC1 Elevation in Multiple Cancers and Essential Role in Stem Cell Survival. Adv Lung Cancer (Irvine) 4, 37–51, https://doi.org/10.4236/alc.2015.43006 (2015). · DOI
  44. Zhang, D. et al. PGRMC1 Is a Novel Potential Tumor Biomarker of Human Renal Cell Carcinoma Based on Quantitative Proteomic and Integrative Biological Assessments. PLoS One 12, e0170453, https://doi.org/10.1371/journal.pone.0170453 (2017). · DOI
  45. Sung, Y. H. et al. Knockout mice created by TALEN-mediated gene targeting. Nat Biotechnol 31, 23–24, https://doi.org/10.1038/nbt.2477 (2013). · DOI
  46. Doyle, E. L. et al. TAL Effector-Nucleotide Targeter (TALE-NT) 2.0: tools for TAL effector design and target prediction. Nucleic Acids Res 40, W117–122, https://doi.org/10.1093/nar/gks608 (2012). · DOI

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Metadata

Authors
Lee, S. R., Kwon, S. W., Kaya, P., Lee, Y. H., Lee, J. G., Kim, G., Lee, G.-S., Baek, I.-J., & Hong, E.-J.
Venue
Scientific Reports
Published
2018-10-24
Volume
8
Issue
1
ISSN
2045-2322
Cited by
37
References
4
Language
en
Funders
National Research Foundation of Korea (2014R1A1A2057405, 2015R1D1A1A01060335, 2018R1D1A1A02043102)

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