PMID- 29739101
OWN - NLM
STAT- MEDLINE
DCOM- 20190909
LR  - 20190909
IS  - 1433-6510 (Print)
IS  - 1433-6510 (Linking)
VI  - 64
IP  - 3
DP  - 2018 Mar 1
TI  - STAT1 and STAT6 Act as Antagonistic Regulators of PPARgamma in Diabetic Patients with 
      and without Cardiovascular Diseases.
PG  - 287-294
LID - 10.7754/Clin.Lab.2017.171013 [doi]
AB  - BACKGROUND: The processes that mediate an inflammatory environment and increase 
      atherosclerosis in diabetes are not well understood. Peroxisome 
      proliferator-activated receptors (PPARs) are a subgroup of the nuclear hormone 
      receptor superfamily of ligand-activated transcription factors which play an 
      important role in the pathogenesis of type 2 diabetes mellitus (T2DM) and 
      atherosclerosis. PPARgamma promotes changes in lipid metabolism, especially in fatty 
      acid (FA) trafficking, and the activity of PPARgamma could be modulated by diabetes 
      phenotype patients. Fatty acid translocase CD36 is one of the advanced PPARgamma 
      targets to arbitrate this action. In the current study, we investigated the 
      potential role of signal transducer and activator of transcription STAT1 and 
      STAT6 signaling linked to PPARgamma and its implication in the modulation of lipid 
      metabolism. METHODS: Real-time quantitative reverse transcription polymerase 
      chain reaction (RT-qPCR) was used to quantify target genes in Peripheral Blood 
      Mononuclear Cells (PBMCs) isolated from two diabetic groups: diabetic patients 
      with cardiovascular diseases (D.CVD) and without cardiovascular diseases (D). 
      RESULTS: We demonstrated that PPARgamma and CD36 mRNA expressions were downregulated 
      along D.CVD compared to D (p = 0.002; p = 0.04; respectively). Decreased CD36 was 
      accompanied by elevated levels of plasma triglyceride (TG) concentrations, 0.83 +/- 
      0.29 vs. 2.46 +/- 0.22), respectively. Furthermore, STAT1 was significantly more 
      expressed in D.CVD (p = 0.01). On the other hand, we demonstrated that STAT6 
      induces a significant level of PPARgamma mRNA expression in D patients (p = 0.01). 
      CONCLUSIONS: Our results suggest that the expression and activity of PPARgamma 
      mediates CD36 in PBMCs and varies with respect to STAT6 and STAT1 trafficking in 
      diabetic patients with and without cardiovascular diseases.
FAU - Bendaya, Imen
AU  - Bendaya I
FAU - Riahi, Aouatef
AU  - Riahi A
FAU - Kharat, Maher
AU  - Kharat M
FAU - Kahla, Saloua
AU  - Kahla S
FAU - Sdiri, Wissem
AU  - Sdiri W
FAU - Oueslati, Ridha
AU  - Oueslati R
LA  - eng
PT  - Journal Article
PL  - Germany
TA  - Clin Lab
JT  - Clinical laboratory
JID - 9705611
RN  - 0 (CD36 Antigens)
RN  - 0 (PPAR gamma)
RN  - 0 (STAT1 Transcription Factor)
RN  - 0 (STAT1 protein, human)
RN  - 0 (STAT6 Transcription Factor)
RN  - 0 (STAT6 protein, human)
RN  - 0 (Triglycerides)
SB  - IM
MH  - Aged
MH  - CD36 Antigens/genetics/metabolism
MH  - Cardiovascular Diseases/*genetics/metabolism
MH  - Diabetes Mellitus, Type 2/*genetics/metabolism
MH  - Female
MH  - *Gene Expression Regulation
MH  - Humans
MH  - Leukocytes, Mononuclear/metabolism
MH  - Lipid Metabolism/genetics
MH  - Male
MH  - Middle Aged
MH  - PPAR gamma/*genetics/metabolism
MH  - STAT1 Transcription Factor/*genetics/metabolism
MH  - STAT6 Transcription Factor/*genetics/metabolism
MH  - Signal Transduction/genetics
MH  - Triglycerides/blood
EDAT- 2018/05/09 06:00
MHDA- 2019/09/10 06:00
CRDT- 2018/05/09 06:00
PHST- 2018/05/09 06:00 [entrez]
PHST- 2018/05/09 06:00 [pubmed]
PHST- 2019/09/10 06:00 [medline]
AID - 10.7754/Clin.Lab.2017.171013 [doi]
PST - ppublish
SO  - Clin Lab. 2018 Mar 1;64(3):287-294. doi: 10.7754/Clin.Lab.2017.171013.