PMID- 34098046
OWN - NLM
STAT- MEDLINE
DCOM- 20211207
LR  - 20211214
IS  - 1873-1708 (Electronic)
IS  - 0890-6238 (Linking)
VI  - 103
DP  - 2021 Aug
TI  - The effect of adipose-derived mesenchymal stem cell treatment on mTOR and p-mTOR 
      expression in ovarian damage due to cyclophosphomide.
PG  - 71-78
LID - S0890-6238(21)00087-3 [pii]
LID - 10.1016/j.reprotox.2021.06.003 [doi]
AB  - Our aim is to investigate the effect of the Mesenchymal stem cell (MSC) 
      administration on the release of Mammalian Target of Rapamycin (mTOR) and 
      Phosphorylated- mTOR(p-mTOR) in Cyclophosphomide (CTX) induced ovarian damage. 
      Rats divided into three groups. The first group was categorized as the control(C 
      group;n = 6), the second group as CTX-administered group (CTX group;n = 6), and 
      the third group as CTX and MSC-administered group (CTX + SC group;n = 6). CTX was 
      injected intraperitoneally at 50 mg/kg on the first day and at 8 mg/kg during the 
      following 13 days. In Group 3, adipose-derived MSCs (5 x 10(4)) were injected 
      locally into the ovary. Both ovaries were removed at the end of the 8th week. The 
      follicle count was made. The expression of mTOR and p-mTOR was analyzed 
      immunohistochemically. The follicles in the ovary of Group C were observed in 
      normal structures. Degeneration was evident in the CTX group. In the CTX + SC 
      group, the degenerative appearance monitored in the CTX group vanished in most 
      areas, and fibrosis was greatly reduced. The number of follicles in the CTX group 
      was lower than that of both C and CTX + SC groups (p < 005). In the C group, mTOR 
      showed strong positive staining while mTOR and p-mTOR expression was negative in 
      all follicles in the CTX group. Both mTOR and p-mTOR revealed moderate positive 
      expression in the CTX + SC group. MSC therapy rescued the damage ovarian function 
      created by CTX, reducing follicle loss. MSCs were shown to inhibit the loss of 
      mTOR and p-mTOR signaling, which is key to meiosis in oocytes.
CI  - Copyright (c) 2021 Elsevier Inc. All rights reserved.
FAU - Cil, Nazli
AU  - Cil N
AD  - Department of Histology and Embryology, Faculty of Medicine, Pamukkale 
      University, Denizli, Turkey. Electronic address: ncil@pau.edu.tr.
FAU - Mete, Gulcin Abban
AU  - Mete GA
AD  - Department of Histology and Embryology, Faculty of Medicine, Pamukkale 
      University, Denizli, Turkey. Electronic address: gabban@pau.edu.tr.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20210610
PL  - United States
TA  - Reprod Toxicol
JT  - Reproductive toxicology (Elmsford, N.Y.)
JID - 8803591
RN  - 0 (Mutagens)
RN  - 8N3DW7272P (Cyclophosphamide)
RN  - EC 2.7.1.1 (mTOR protein, rat)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Animals
MH  - Cyclophosphamide/*toxicity
MH  - Female
MH  - *Mesenchymal Stem Cells
MH  - Mutagens/*toxicity
MH  - Ovarian Follicle/drug effects
MH  - Ovary
MH  - Primary Ovarian Insufficiency
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Signal Transduction
MH  - TOR Serine-Threonine Kinases/*metabolism
OTO - NOTNLM
OT  - Cyclophosphomide
OT  - Mesenchymal stem cell
OT  - Ovary
OT  - mTOR
OT  - p-mTOR
EDAT- 2021/06/08 06:00
MHDA- 2021/12/15 06:00
CRDT- 2021/06/07 20:14
PHST- 2021/04/06 00:00 [received]
PHST- 2021/05/29 00:00 [revised]
PHST- 2021/06/01 00:00 [accepted]
PHST- 2021/06/08 06:00 [pubmed]
PHST- 2021/12/15 06:00 [medline]
PHST- 2021/06/07 20:14 [entrez]
AID - S0890-6238(21)00087-3 [pii]
AID - 10.1016/j.reprotox.2021.06.003 [doi]
PST - ppublish
SO  - Reprod Toxicol. 2021 Aug;103:71-78. doi: 10.1016/j.reprotox.2021.06.003. Epub 
      2021 Jun 10.