Display options
Cite
Carroll WX, Kalupahana NS, Booker SL, et al. Angiotensinogen gene silencing reduces markers of lipid accumulation and inflammation in cultured adipocytes. Front Endocrinol (Lausanne). 2013;4:10doi: 10.3389/fendo.2013.00010.
Carroll, W. X., Kalupahana, N. S., Booker, S. L., Siriwardhana, N., Lemieux, M., Saxton, A. M., & Moustaid-Moussa, N. (2013). Angiotensinogen gene silencing reduces markers of lipid accumulation and inflammation in cultured adipocytes. Frontiers in endocrinology, 410. https://doi.org/10.3389/fendo.2013.00010
Carroll, Wenting X, et al. "Angiotensinogen gene silencing reduces markers of lipid accumulation and inflammation in cultured adipocytes." Frontiers in endocrinology vol. 4 (2013): 10. doi: https://doi.org/10.3389/fendo.2013.00010
Carroll WX, Kalupahana NS, Booker SL, Siriwardhana N, Lemieux M, Saxton AM, Moustaid-Moussa N. Angiotensinogen gene silencing reduces markers of lipid accumulation and inflammation in cultured adipocytes. Front Endocrinol (Lausanne). 2013 Mar 11;4:10. doi: 10.3389/fendo.2013.00010. eCollection 2013. PMID: 23483012; PMCID: PMC3593681.
Copy Download .nbib Format: NLM
Share it on

Front Endocrinol (Lausanne). 2013 Mar 11;4:10. doi: 10.3389/fendo.2013.00010. eCollection 2013.

Angiotensinogen gene silencing reduces markers of lipid accumulation and inflammation in cultured adipocytes.

Frontiers in endocrinology

Wenting X Carroll, Nishan S Kalupahana, Suzanne L Booker, Nalin Siriwardhana, Monique Lemieux, Arnold M Saxton, Naima Moustaid-Moussa

Affiliations

  1. Department of Animal Science, University of Tennessee Knoxville, TN, USA ; Obesity Research Center, University of Tennessee Knoxville, TN, USA.

PMID: 23483012 PMCID: PMC3593681 DOI: 10.3389/fendo.2013.00010

Abstract

Inflammatory adipokines secreted from adipose tissue are major contributors to obesity-associated inflammation and other metabolic dysfunctions. We and others have recently documented the contribution of adipose tissue renin-angiotensin system to the pathogenesis of obesity, inflammation, and insulin resistance. We hypothesized that adipocyte-derived angiotensinogen (Agt) plays a critical role in adipogenesis and/or lipogenesis as well as inflammation. This was tested using 3T3-L1 adipocytes, stably transfected with Agt-shRNA or scrambled Sc-shRNA as a control. Transfected preadipocytes were differentiated and used to investigate the role of adipose Agt through microarray and PCR analyses and adipokine profiling. As expected, Agt gene silencing significantly reduced the expression of Agt and its hormone product angiotensin II (Ang II), as well as lipid accumulation in 3T3-L1 adipocytes. Microarray studies identified several genes involved in lipid metabolism and inflammatory pathways which were down-regulated by Agt gene inactivation, such as glycerol-3-phosphate dehydrogenase 1 (Gpd1), serum amyloid A 3 (Saa3), nucleotide-binding oligomerization domain containing 1 (Nod1), and signal transducer and activator of transcription 1 (Stat1). Mouse adipogenesis PCR arrays revealed lower expression levels of adipogenic/lipogenic genes such as peroxisome proliferator activated receptor gamma (PPARγ), sterol regulatory element binding transcription factor 1 (Srebf1), adipogenin (Adig), and fatty acid binding protein 4 (Fabp4). Further, silencing of Agt gene significantly lowered expression of pro-inflammatory adipokines including interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and monocyte chemotactic protein-1 (MCP-1). In conclusion, this study directly demonstrates critical effects of Agt in adipocyte metabolism and inflammation and further support a potential role for adipose Agt in the pathogenesis of obesity-associated metabolic alterations.

Keywords: adipocytes; adipogenesis; adipokines; angiotensinogen; gene silencing; inflammation

References

  1. Cell. 2002 Apr;109 Suppl:S121-31 - PubMed
  2. Horm Metab Res. 2002 Nov-Dec;34(11-12):721-5 - PubMed
  3. Am J Physiol Regul Integr Comp Physiol. 2012 Jan 15;302(2):R244-51 - PubMed
  4. Int J Obes (Lond). 2007 Feb;31(2):382-4 - PubMed
  5. Cell Metab. 2008 Jan;7(1):86-94 - PubMed
  6. Am J Physiol Regul Integr Comp Physiol. 2004 Oct;287(4):R943-9 - PubMed
  7. J Hypertens. 2006 Sep;24(9):1809-16 - PubMed
  8. Diabetes. 2011 Sep;60(9):2206-15 - PubMed
  9. Kidney Int. 2006 Nov;70(10):1717-24 - PubMed
  10. FASEB J. 2001 Dec;15(14):2727-9 - PubMed
  11. Anal Biochem. 2010 Jun 15;401(2):196-202 - PubMed
  12. Obes Res. 2000 Jul;8(4):337-41 - PubMed
  13. Proc Natl Acad Sci U S A. 2009 Jan 27;106(4):1105-10 - PubMed
  14. Arterioscler Thromb Vasc Biol. 2004 Jul;24(7):1199-203 - PubMed
  15. J Lipid Res. 2003 May;44(5):994-1000 - PubMed
  16. Hypertension. 2001 May;37(5):1336-40 - PubMed
  17. Int J Obes (Lond). 2010 Jan;34(1):157-64 - PubMed
  18. N Engl J Med. 1989 Sep 28;321(13):868-73 - PubMed
  19. J Endocrinol. 2008 Apr;197(1):55-64 - PubMed
  20. Endocrinology. 1997 Apr;138(4):1512-9 - PubMed
  21. Obes Res. 2001 Aug;9(8):486-91 - PubMed
  22. J Clin Endocrinol Metab. 2005 May;90(5):2888-97 - PubMed
  23. Am J Physiol Endocrinol Metab. 2011 Oct;301(4):E587-98 - PubMed
  24. J Clin Endocrinol Metab. 1998 Nov;83(11):3925-9 - PubMed
  25. Hypertension. 2000 Jun;35(6):1270-7 - PubMed
  26. J Nutr Biochem. 2012 Dec;23(12):1661-7 - PubMed
  27. J Clin Endocrinol Metab. 2004 Jun;89(6):2690-6 - PubMed
  28. Obesity (Silver Spring). 2012 Jan;20(1):48-56 - PubMed
  29. Nat Rev Immunol. 2011 Feb;11(2):85-97 - PubMed
  30. Obes Rev. 2012 Feb;13(2):136-49 - PubMed
  31. Crit Rev Biochem Mol Biol. 2012 Jul-Aug;47(4):379-90 - PubMed
  32. Hypertension. 2005 Mar;45(3):356-62 - PubMed
  33. Trends Endocrinol Metab. 2011 Aug;22(8):325-32 - PubMed
  34. Curr Opin Clin Nutr Metab Care. 2002 Jul;5(4):385-9 - PubMed
  35. Am J Physiol. 1997 Jul;273(1 Pt 2):R236-42 - PubMed
  36. Diabetes. 2002 Jun;51(6):1699-707 - PubMed
  37. Endocrinology. 2001 Dec;142(12):5220-5 - PubMed
  38. PLoS Med. 2006 Jun;3(6):e287 - PubMed
  39. Endocrinology. 2009 Mar;150(3):1421-8 - PubMed
  40. Circulation. 2004 May 4;109(17):2054-7 - PubMed

Publication Types