PMID- 36484370
OWN - NLM
STAT- MEDLINE
DCOM- 20221215
LR  - 20221222
IS  - 1791-244X (Electronic)
IS  - 1107-3756 (Print)
IS  - 1107-3756 (Linking)
VI  - 51
IP  - 1
DP  - 2023 Jan
TI  - Cyclophilin B, a molecule chaperone, promotes adipogenesis in 3T3‑L1 
      preadipocytes via AKT/mTOR pathway.
LID - 6 [pii]
LID - 10.3892/ijmm.2022.5209 [doi]
AB  - Cyclophilin is known to act as a molecular chaperone in the endoplasmic 
      reticulum. Recent studies have reported that the expression of cyclophilin B 
      (CypB) is increased in ob/ob mice and its inhibitor suppresses adipocyte 
      differentiation. However, the mechanism of action of CypB in adipocytes remains 
      to be elucidated. The present study investigated the role of CypB in 3T3‑L1 
      adipocyte differentiation. It showed that the expression level of CypB was 
      increased during 3T3‑L1 adipocyte differentiation by reverse 
      transcription‑quantitative PCR and western blotting analysis. CypB knockdown 
      using short interfering RNA delayed cell cycle progression from the G(1)/S to 
      G(2)/M phase through the mammalian target of rapamycin (mTOR) signaling pathway 
      and inhibited the expression levels of adipogenic transcription factors including 
      peroxisome proliferator‑activated receptor gamma (PPARgamma) and CCAAT‑enhancer binding 
      protein (C/EBP)alpha. Additionally, the accumulation of lipid droplets was inhibited 
      by CypB knockdown. Conversely, overexpression of CypB promoted cell cycle 
      progression from the G(1)/S to G(2)/M phase by the mTOR signaling pathway and 
      enhanced the expression levels of adipogenic transcription factors including 
      PPARgamma and C/EBPalpha. Finally, the present study showed that CypB downregulated the 
      expression of CHOP, a well‑known negative regulator of adipogenesis. Taken 
      together, the data suggested that CypB might serve important physiological 
      regulatory roles in 3T3‑L1 adipocyte differentiation.
FAU - Yoon, Ji-Su
AU  - Yoon JS
AD  - Department of Biomedical Science, Graduate School, School of Medicine, Kyung Hee 
      University, Seoul 02447, Republic of Korea.
FAU - Kim, Sung Soo
AU  - Kim SS
AD  - Department of Biomedical Science, Graduate School, School of Medicine, Kyung Hee 
      University, Seoul 02447, Republic of Korea.
FAU - Ha, Joohun
AU  - Ha J
AD  - Department of Biomedical Science, Graduate School, School of Medicine, Kyung Hee 
      University, Seoul 02447, Republic of Korea.
FAU - Kang, Insug
AU  - Kang I
AD  - Department of Biomedical Science, Graduate School, School of Medicine, Kyung Hee 
      University, Seoul 02447, Republic of Korea.
FAU - Choe, Wonchae
AU  - Choe W
AD  - Department of Biomedical Science, Graduate School, School of Medicine, Kyung Hee 
      University, Seoul 02447, Republic of Korea.
LA  - eng
PT  - Journal Article
DEP - 20221209
PL  - Greece
TA  - Int J Mol Med
JT  - International journal of molecular medicine
JID - 9810955
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - 0 (Molecular Chaperones)
RN  - 0 (Transcription Factors)
SB  - IM
MH  - Animals
MH  - Mice
MH  - 3T3-L1 Cells
MH  - *TOR Serine-Threonine Kinases
MH  - *Molecular Chaperones
MH  - Transcription Factors
MH  - Mammals
PMC - PMC9747202
OTO - NOTNLM
OT  - 3T3‑L1 adipocyte
OT  - AKT/mTOR signaling pathway
OT  - adipogenesis
OT  - cyclophilin B
OT  - mitotic clonal expansion
OT  - obesity
COIS- The authors declare that they have no competing interests.
EDAT- 2022/12/10 06:00
MHDA- 2022/12/15 06:00
PMCR- 2022/12/02
CRDT- 2022/12/09 06:32
PHST- 2022/08/30 00:00 [received]
PHST- 2022/11/16 00:00 [accepted]
PHST- 2022/12/09 06:32 [entrez]
PHST- 2022/12/10 06:00 [pubmed]
PHST- 2022/12/15 06:00 [medline]
PHST- 2022/12/02 00:00 [pmc-release]
AID - 6 [pii]
AID - ijmm-51-1-05209 [pii]
AID - 10.3892/ijmm.2022.5209 [doi]
PST - ppublish
SO  - Int J Mol Med. 2023 Jan;51(1):6. doi: 10.3892/ijmm.2022.5209. Epub 2022 Dec 9.