PMID- 31871428
OWN - NLM
STAT- MEDLINE
DCOM- 20200608
LR  - 20200608
IS  - 1466-1861 (Electronic)
IS  - 0962-9351 (Print)
IS  - 0962-9351 (Linking)
VI  - 2019
DP  - 2019
TI  - PPAR gamma/Nnat/NF-kappaB Axis Involved in Promoting Effects of Adiponectin on 
      Preadipocyte Differentiation.
PG  - 5618023
LID - 10.1155/2019/5618023 [doi]
LID - 5618023
AB  - A previous study has demonstrated that adiponectin (APN) could promote 
      preadipocyte differentiation, and the present study further explored its 
      mechanism. 3T3-L1 cells were infected with adenovirus holding human adiponectin 
      gene apM1 and mouse neuronatin (Nnat) shRNA and initiated differentiation while 
      coculturing with mature adipocytes stimulated with LPS. After 8 days, 
      preadipocyte differentiation was observed by Oil Red O staining. Real-time 
      quantitative PCR was used to evaluate mRNA expression levels of monocyte 
      chemoattractant protein-1 (MCP-1), interleukin- (IL-) 6, IL-8, and tumor necrosis 
      factor alpha (TNF-alpha). The levels of reactive oxygen species (ROS), total antioxidant 
      capacity (T-AOC), malondialdehyde (MDA), and superoxide dismutase (SOD) in 3T3-L1 
      cells were detected. Western blotting was done to quantify the protein expression 
      levels of Nnat, peroxisome proliferator-activated receptor (PPAR) gamma, p65, and 
      inhibitor of nuclear factor kappaB (IkappaB) alpha. Results demonstrated that APN 
      overexpression markedly increased preadipocyte differentiation; inhibited gene 
      expression of MCP-1, IL-6, IL-8, and TNF-alpha; reduced ROS and MDA release; 
      increased T-AOC and SOD levels; upregulated Nnat, PPAR gamma, and IkappaB alpha protein 
      expressions; and downregulated p65 protein expression under LPS stimulation. 
      However, the effects of APN were markedly attenuated when Nnat expression was 
      knocked down. Taken together, the present study provided evidences that the 
      effects of APN on promoting preadipocyte differentiation under inflammatory 
      conditions via anti-inflammation and antioxidative stress may be regulated by the 
      PPAR gamma/Nnat/NF-kappaB signaling pathway.
CI  - Copyright (c) 2019 Wenkai Yang et al.
FAU - Yang, Wenkai
AU  - Yang W
AUID- ORCID: 0000-0002-3358-2911
AD  - Department of Cardiovascular Surgery, Affiliated Central People's Hospital of 
      Zhanjiang of Guangdong Medical University, Zhanjiang 524045, China.
FAU - Yuan, Wenjin
AU  - Yuan W
AD  - Department of Cardiovascular Medicine, Ganzhou People's Hospital, Ganzhou 341000, 
      China.
FAU - Peng, Xinghua
AU  - Peng X
AD  - Department of Cardio-Thoracic Surgery, Ganzhou People's Hospital, Ganzhou 341000, 
      China.
FAU - Wang, Meiling
AU  - Wang M
AD  - Department of Cardio-Thoracic Surgery, Ganzhou People's Hospital, Ganzhou 341000, 
      China.
FAU - Xiao, Jie
AU  - Xiao J
AD  - Department of Cardio-Thoracic Surgery, Ganzhou People's Hospital, Ganzhou 341000, 
      China.
FAU - Wu, Cheng
AU  - Wu C
AD  - Department of Cardio-Thoracic Surgery, Ganzhou People's Hospital, Ganzhou 341000, 
      China.
FAU - Luo, Lie
AU  - Luo L
AD  - Department of Cardio-Thoracic Surgery, Ganzhou People's Hospital, Ganzhou 341000, 
      China.
LA  - eng
PT  - Journal Article
DEP - 20191121
PL  - United States
TA  - Mediators Inflamm
JT  - Mediators of inflammation
JID - 9209001
RN  - 0 (Adiponectin)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-6)
RN  - 0 (Interleukin-8)
RN  - 0 (Membrane Proteins)
RN  - 0 (NF-kappa B)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Nnat protein, mouse)
RN  - 0 (PPAR gamma)
SB  - IM
MH  - 3T3-L1 Cells
MH  - Adipocytes/*cytology/*metabolism
MH  - Adiponectin/genetics/*metabolism
MH  - Animals
MH  - Cell Differentiation/genetics/physiology
MH  - Chemokine CCL2/genetics/metabolism
MH  - Humans
MH  - Interleukin-6/metabolism
MH  - Interleukin-8/metabolism
MH  - Membrane Proteins/genetics/*metabolism
MH  - Mice
MH  - NF-kappa B/genetics/*metabolism
MH  - Nerve Tissue Proteins/genetics/*metabolism
MH  - PPAR gamma/genetics/*metabolism
MH  - Signal Transduction/genetics/physiology
PMC - PMC6906841
COIS- The authors declare no conflict of interest.
EDAT- 2019/12/25 06:00
MHDA- 2020/06/09 06:00
PMCR- 2019/11/21
CRDT- 2019/12/25 06:00
PHST- 2019/07/11 00:00 [received]
PHST- 2019/09/07 00:00 [revised]
PHST- 2019/10/16 00:00 [accepted]
PHST- 2019/12/25 06:00 [entrez]
PHST- 2019/12/25 06:00 [pubmed]
PHST- 2020/06/09 06:00 [medline]
PHST- 2019/11/21 00:00 [pmc-release]
AID - 10.1155/2019/5618023 [doi]
PST - epublish
SO  - Mediators Inflamm. 2019 Nov 21;2019:5618023. doi: 10.1155/2019/5618023. 
      eCollection 2019.