PMID- 35949513
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220813
IS  - 2573-9832 (Electronic)
IS  - 2573-9832 (Linking)
VI  - 4
IP  - 8
DP  - 2022 Aug
TI  - New insights into the role of matrix metalloproteinase 3 (MMP3) in bone.
PG  - 524-538
LID - 10.1096/fba.2021-00092 [doi]
AB  - The Matrix Metalloproteinases are important regulators of bone metabolism and can 
      influence bone mass and bone remodeling. We investigate the role of Matrix 
      Metalloproteinase 3 (MMP3) on bone in mice, by using Mmp3 knockout (Mmp3 KO) in 
      the context of estrogen deficiency, and in human, by analyzing the association of 
      promoter polymorphism with bone mineral density in postmenopausal women and with 
      MMP3 expression. We presented evidence in this paper that Mmp3 KO significantly 
      increases trabecular bone mass and trabecular number and does not affect cortical 
      bone thickness. We also found that Mmp3 KO protects from the deleterious effects 
      of ovariectomy on bone mineral density in mice by preventing deterioration of 
      bone microarchitecture. The effect of Mmp3 KO does not involve bone formation 
      parameters but instead acts by inhibition of bone resorption, leading to a 
      reduced bone loss associated to ovariectomy. By studying a human cohort, we found 
      that a polymorphism located in the promoter of the human MMP3 gene is associated 
      with bone mineral density in postmenopausal women and found that MMP3 rs632478 
      promoter variants are associated with change in promoter activity in transfection 
      experiments. In conclusion MMP3, although weakly expressed in bone cells, could 
      be one of the important regulators of sex hormone action in bone and whose 
      activity could be targeted for therapeutic applications such as in Osteoporosis.
CI  - (c) 2022 The Authors. FASEB BioAdvances published by Wiley Periodicals LLC on 
      behalf of The Federation of American Societies for Experimental Biology.
FAU - Jehan, Frederic
AU  - Jehan F
AD  - Inserm U1132 BIOSCAR Paris Universite Paris France.
AD  - Nantes Universite Oniris, Univ Angers, CHU Nantes, Inserm, Regenerative Medicine 
      and Skeleton RMeS, UMR 1229 F-44000 Nantes France.
FAU - Zarka, Mylene
AU  - Zarka M
AD  - Inserm U1132 BIOSCAR Paris Universite Paris France.
FAU - de la Houssaye, Guillaume
AU  - de la Houssaye G
AD  - Inserm U1132 BIOSCAR Paris Universite Paris France.
FAU - Veziers, Joelle
AU  - Veziers J
AD  - Nantes Universite Oniris, Univ Angers, CHU Nantes, Inserm, Regenerative Medicine 
      and Skeleton RMeS, UMR 1229 F-44000 Nantes France.
FAU - Ostertag, Agnes
AU  - Ostertag A
AD  - Inserm U1132 BIOSCAR Paris Universite Paris France.
FAU - Cohen-Solal, Martine
AU  - Cohen-Solal M
AD  - Inserm U1132 BIOSCAR Paris Universite Paris France.
FAU - Geoffroy, Valerie
AU  - Geoffroy V
AUID- ORCID: 0000-0003-3920-7482
AD  - Inserm U1132 BIOSCAR Paris Universite Paris France.
AD  - Nantes Universite Oniris, Univ Angers, CHU Nantes, Inserm, Regenerative Medicine 
      and Skeleton RMeS, UMR 1229 F-44000 Nantes France.
LA  - eng
PT  - Journal Article
DEP - 20220615
PL  - United States
TA  - FASEB Bioadv
JT  - FASEB bioAdvances
JID - 101733210
PMC - PMC9353456
OTO - NOTNLM
OT  - SNP
OT  - bone mineral density
OT  - bone resorption
OT  - estrogen deficiency
OT  - matrix metalloproteinase 3
OT  - osteoporosis
COIS- The authors declare that they have no conflict of interest.
EDAT- 2022/08/12 06:00
MHDA- 2022/08/12 06:01
PMCR- 2022/06/15
CRDT- 2022/08/11 02:18
PHST- 2021/08/04 00:00 [received]
PHST- 2022/03/31 00:00 [revised]
PHST- 2022/04/06 00:00 [accepted]
PHST- 2022/08/11 02:18 [entrez]
PHST- 2022/08/12 06:00 [pubmed]
PHST- 2022/08/12 06:01 [medline]
PHST- 2022/06/15 00:00 [pmc-release]
AID - FBA21318 [pii]
AID - 10.1096/fba.2021-00092 [doi]
PST - epublish
SO  - FASEB Bioadv. 2022 Jun 15;4(8):524-538. doi: 10.1096/fba.2021-00092. eCollection 
      2022 Aug.