PMID- 33903711
OWN - NLM
STAT- MEDLINE
DCOM- 20211018
LR  - 20211018
IS  - 2045-2322 (Electronic)
IS  - 2045-2322 (Linking)
VI  - 11
IP  - 1
DP  - 2021 Apr 26
TI  - Prostaglandin F2alpha agonists induced enhancement in collagen1 expression is 
      involved in the pathogenesis of the deepening of upper eyelid sulcus.
PG  - 9002
LID - 10.1038/s41598-021-88562-4 [doi]
LID - 9002
AB  - Previous our study reported that three-dimension (3D) cultures of human orbital 
      fibroblasts (HOFs) replicated the etiology of deepening of the upper eyelid 
      sulcus (DUES) caused by prostaglandin F2alpha analogues (PGF2alpha-ags). To examine this 
      further, the effects of PGF2alpha-ags on HOFs were characterized by (1) lipid 
      staining (2D; two-dimension, 3D), (2) comparison of the 3D organoid sizes of 
      preadipocytes (DIF-) or adipocytes (DIF+) that had been treated with various 
      concentrations of several PGF2alpha-ags, (3) physical stiffness (3D), and (4) the 
      mRNA expression of adipogenic related genes, extracellular matrix (ECM), tissue 
      inhibitors of metalloproteinases (TIMPs) and matrix metalloproteinases (MMPs) 
      (3D). PGF2alpha-ags caused a dramatic down-sizing of the 3D DIF+ organoids and this 
      reduction was concentration dependent. The effects caused by PGF2alpha-ags were also 
      observed in 3D preadipocytes. Micro-squeezer analysis clearly indicated that 
      PGF2alpha-ags induced an increase in their physical solidity. The size of each 
      organoid under several conditions was inversely correlated with the mRNA 
      expression profile of collagen1 (COL1), TIMP2, and MMP2 and 9. These findings 
      indicate that PGF2alpha-ags affect the expression of COL1, TIMP2, and MMP2 and 9 
      which, in turn, modulate the 3D ECM network within the organoids, thus resulting 
      in their downsizing.
FAU - Itoh, Kaku
AU  - Itoh K
AD  - Departments of Ophthalmology, Sapporo Medical University School of Medicine, 
      Sapporo, Japan.
FAU - Ida, Yosuke
AU  - Ida Y
AD  - Departments of Ophthalmology, Sapporo Medical University School of Medicine, 
      Sapporo, Japan.
FAU - Ohguro, Hiroshi
AU  - Ohguro H
AD  - Departments of Ophthalmology, Sapporo Medical University School of Medicine, 
      Sapporo, Japan.
FAU - Hikage, Fumihito
AU  - Hikage F
AD  - Departments of Ophthalmology, Sapporo Medical University School of Medicine, 
      Sapporo, Japan. hikage@sapmed.ac.jp.
LA  - eng
PT  - Journal Article
DEP - 20210426
PL  - England
TA  - Sci Rep
JT  - Scientific reports
JID - 101563288
RN  - 0 (Collagen Type I)
RN  - B7IN85G1HY (Dinoprost)
SB  - IM
MH  - Adipogenesis/drug effects
MH  - Cell Culture Techniques
MH  - Cell Differentiation/drug effects/genetics
MH  - Collagen Type I/*genetics/metabolism
MH  - Dinoprost/*agonists/pharmacology
MH  - *Disease Susceptibility
MH  - Extracellular Matrix/metabolism
MH  - Eyelid Diseases/diagnosis/*etiology/metabolism
MH  - Fibroblasts/drug effects/metabolism
MH  - Fluorescent Antibody Technique
MH  - *Gene Expression
MH  - Humans
MH  - Organoids
PMC - PMC8076191
COIS- The authors declare no competing interests.
EDAT- 2021/04/28 06:00
MHDA- 2021/10/21 06:00
PMCR- 2021/04/26
CRDT- 2021/04/27 06:45
PHST- 2020/11/02 00:00 [received]
PHST- 2021/04/14 00:00 [accepted]
PHST- 2021/04/27 06:45 [entrez]
PHST- 2021/04/28 06:00 [pubmed]
PHST- 2021/10/21 06:00 [medline]
PHST- 2021/04/26 00:00 [pmc-release]
AID - 10.1038/s41598-021-88562-4 [pii]
AID - 88562 [pii]
AID - 10.1038/s41598-021-88562-4 [doi]
PST - epublish
SO  - Sci Rep. 2021 Apr 26;11(1):9002. doi: 10.1038/s41598-021-88562-4.