Article citationsMore>>

Gathiaka, S., Nanayakkara, G., Boncher, T., Acevedo, O., Wyble, J., Patel, S., Patel, A., Shane, M.E., Bonkowski, B., Wieczorek, J., Rong, Y., Huggins, K., Smith, F. and Amin, R.H. (2013) Design, Development and Evaluation of Novel Dual PPARdelta/PPARgamma Agonists. Bioorganic & Medicinal Chemistry Letters, 23, 873-879.

has been cited by the following article:

• TITLE: LXR, PPARγ, and PPARδ Agonists Are Not Sufficient to Demonstrate Therapeutic Potential against Mouse Model of Systemic Lupus Erythematosus

  AUTHORS: Noriko Toyota Tatebe, Katsue Sunahori Watanabe, Sonia Zeggar, Sumie Hiramatsu, Minglu Yan, Takayuki Katsuyama, Eri Katsuyama, Haruki Watanabe, Ken-ei Sada, Jun Wada

  KEYWORDS: Nuclear Receptors, Liver X Receptor (LXR), Peroxisome Proliferator-Activated Receptor (PPAR), Systemic Lupus Erythematosus (SLE)

  JOURNAL NAME: Open Journal of Rheumatology and Autoimmune Diseases, Vol.7 No.2, May 31, 2017

  ABSTRACT: Aim: We aimed to investigate whether the agonists for liver X receptor (LXR) ameliorate lupus-like phenotypes in mice mediated by the clearance of apoptotic cells, and compare with peroxisome proliferator-activated receptor (PPAR) γ plus PPARδ agonists, which also facilitate the clearance of apoptotic cells and exert anti-inflammatory effects in systemic lupus erythematosus (SLE). Methods: We investigated the efficacy of LXR agonist (GW3965) or dual treatment of PPARγ (pioglitazone) and PPARδ (GW0742) agonists in SLE animal models, female MRL/MpJ-Fas/J mice and BALB/cAJcl mice treated with pristane. The data were analyzed with one-way analysis of variance and Tukey’s honestly significant difference tests. Results: The treatment with LXR or PPARγ/δ agonists did not significantly alter the swelling of lymph nodes, ds-DNA production, albuminuria, histological score of glomerular lesions, and mRNA expression of target genes including Abca1, C1qa, Icam1, Mertk and Tnf. Conclusion: LXR or PPARγ/δ agonists targeting the impaired clearance for apoptosis cells may not be efficient in the remission induction therapy in SLE.