Dynamic in vivo changes in the activities of gelatinases, matrix metalloproteinases (MMPs), and tissue inhibitor of metalloproteinases (TIMPs) in buffalo (Bubalus bubalis ) uterine luminal fluid during estrous cycle and early pregnancy

2010 ◽  
Vol 77 (11) ◽  
pp. 944-953 ◽  
Author(s):  
Sudhir C. Roy ◽  
Jyotirmoy Ghosh
Keyword(s):  
Matrix Metalloproteinases ◽  
Estrous Cycle ◽  
Early Pregnancy ◽  
Bubalus Bubalis ◽  
Tissue Inhibitor Of Metalloproteinases ◽  
Tissue Inhibitor

scholarly journals Effect of prostaglandin analogs on matrix metalloproteinases and tissue inhibitor of metalloproteinases in eyelid muscle specimens

2018 ◽  
Vol Volume 12 ◽  
pp. 2039-2046 ◽  
Author(s):  
Sapir Karli ◽  
Juan Alfredo Ayala-Haedo ◽  
William J Feuer ◽  
Maria Fernandez ◽  
Sander Dubovy ◽  
...  
Keyword(s):  
Matrix Metalloproteinases ◽  
Tissue Inhibitor Of Metalloproteinases ◽  
Tissue Inhibitor

scholarly journals Oncostatin M-induced astrocytic tissue inhibitor of metalloproteinases-1 drives remyelination

2020 ◽  
Vol 117 (9) ◽  
pp. 5028-5038 ◽  
Author(s):  
Evelien Houben ◽  
Kris Janssens ◽  
Doryssa Hermans ◽  
Jennifer Vandooren ◽  
Chris Van den Haute ◽  
...  
Keyword(s):  
Therapeutic Potential ◽  
Treatment Options ◽  
Oncostatin M ◽  
Tissue Inhibitor Of Metalloproteinases ◽  
Tissue Inhibitor ◽  
Human Value ◽  
Demyelinating Disorders ◽  
Downstream Mediator

The brain’s endogenous capacity to restore damaged myelin deteriorates during the course of demyelinating disorders. Currently, no treatment options are available to establish remyelination. Chronic demyelination leads to damaged axons and irreversible destruction of the central nervous system (CNS). We identified two promising therapeutic candidates which enhance remyelination: oncostatin M (OSM), a member of the interleukin-6 family, and downstream mediator tissue inhibitor of metalloproteinases-1 (TIMP-1). While remyelination was completely abrogated in OSMRβ knockout (KO) mice, OSM overexpression in the chronically demyelinated CNS established remyelination. Astrocytic TIMP-1 was demonstrated to play a pivotal role in OSM-mediated remyelination. Astrocyte-derived TIMP-1 drove differentiation of oligodendrocyte precursor cells into mature oligodendrocytes in vitro. In vivo, TIMP-1 deficiency completely abolished spontaneous remyelination, phenocopying OSMRβ KO mice. Finally, TIMP-1 was expressed by human astrocytes in demyelinated multiple sclerosis lesions, confirming the human value of our findings. Taken together, OSM and its downstream mediator TIMP-1 have the therapeutic potential to boost remyelination in demyelinating disorders.

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