Parathyroid hormone increases the expression level of matrix metalloproteinase-13 in vivo

2001 ◽  
Vol 19 (4) ◽  
pp. 207-212 ◽  
Author(s):  
Motoyuki Uchida ◽  
Hideyuki Yamato ◽  
Yumiko Nagai ◽  
Hiroshi Yamagiwa ◽  
Tadashi Hayami ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Matrix Metalloproteinase ◽  
Expression Level ◽  
Matrix Metalloproteinase 13

scholarly journals In Vivo Interstitial Migration of Primitive Macrophages Mediated by JNK-Matrix Metalloproteinase 13 Signaling in Response to Acute Injury

2008 ◽  
Vol 181 (3) ◽  
pp. 2155-2164 ◽  
Author(s):  
Yong Zhang ◽  
Xue-Tao Bai ◽  
Kang-Yong Zhu ◽  
Yi Jin ◽  
Min Deng ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Acute Injury ◽  
Matrix Metalloproteinase 13

Silencing matrix metalloproteinase-13 (Mmp-13) reduces inflammatory bone resorption associated with LPS-induced periodontal disease in vivo

2020 ◽  
Author(s):  
Morgana R. Guimaraes-Stabili ◽  
Marcell Costa de Medeiros ◽  
Danuza Rossi ◽  
Angelo Constantino Camilli ◽  
Cleslei Fernando Zanelli ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Matrix Metalloproteinase ◽  
Periodontal Disease ◽  
Matrix Metalloproteinase 13

miR‐873‐3p targets HDAC4 to stimulate matrix metalloproteinase‐13 expression upon parathyroid hormone exposure in rat osteoblasts

2020 ◽  
Vol 235 (11) ◽  
pp. 7996-8009 ◽  
Author(s):  
Desai Malavika ◽  
Srinivasan Shreya ◽  
Vembar Raj Priya ◽  
Muthukumar Rohini ◽  
Zhiming He ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Matrix Metalloproteinase ◽  
Matrix Metalloproteinase 13 ◽  
Hormone Exposure ◽  
Rat Osteoblasts

scholarly journals Radiolabeled Selective Matrix Metalloproteinase 13 (MMP-13) Inhibitors: (Radio)Syntheses and in Vitro and First in Vivo Evaluation

2016 ◽  
Vol 60 (1) ◽  
pp. 307-321 ◽  
Author(s):  
Verena Hugenberg ◽  
Stefan Wagner ◽  
Klaus Kopka ◽  
Michael Schäfers ◽  
Robert C. Schuit ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
In Vivo Evaluation ◽  
Matrix Metalloproteinase 13

scholarly journals Parathyroid hormone‐induced down‐regulation of miR‐532‐5p for matrix metalloproteinase‐13 expression in rat osteoblasts

2018 ◽  
Vol 119 (7) ◽  
pp. 6181-6193 ◽  
Author(s):  
Vishal Mohanakrishnan ◽  
Arumugam Balasubramanian ◽  
Gokulnath Mahalingam ◽  
Nicola Chennell Partridge ◽  
Ilangovan Ramachandran ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Matrix Metalloproteinase ◽  
Down Regulation ◽  
Matrix Metalloproteinase 13 ◽  
Rat Osteoblasts

Abstract 311: Inhibition Of Matrix Metalloproteinase-13 Dependent Protease-activated Receptor-1 Activation Attenuates Fibrotic Signaling

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Allison E Dixon ◽  
Fabrice Jaffre ◽  
Nigel Mackman ◽  
Burns C Blaxall
Keyword(s):  
Matrix Metalloproteinase ◽  
Cardiac Remodeling ◽  
Cardiac Fibroblasts ◽  
The United States ◽  
Matrix Metalloproteinase 13 ◽  
Ecm Proteins ◽  
Excess Production ◽  
Potential Therapeutic Role ◽  
Protease Activated Receptor 1

Heart failure (HF) is the leading cause of morbidity and mortality in the United States and is characterized by progressive myocardial fibrosis, pathologic remodeling and deteriorating cardiac function. Cardiac fibroblasts (CF) are largely responsible for the secretion of ECM proteins as well as cytokines and growth factors in the heart. Upon injury or pathologic stimulation, CF transition to a myofibroblast phenotype, leading to excess production of ECM proteins and pro-inflammatory cytokines. Previous studies in our lab have indicated a role for protease-activated receptor-1 (PAR-1), the most highly expressed GPCR on CF, in pathologic cardiac remodeling. In particular, we reported the novel cleavage of PAR-1 via matrix metalloproteinase-13 (MMP-13) and cardioprotective effects of MMP-13 inhibition in an acute model of HF. Therefore, we hypothesize that MMP-13 plays an important role in cardiac remodeling through activation of PAR-1, particularly in the pathologic transition of CF to myofibroblasts. To investigate this hypothesis, RNA was collected from hearts of mice infused with isoproterenol (ISO) for 7 days and concurrently treated with a specific MMP-13 inhibitor, WAY170523, or vehicle. To evaluate the effect of WAY170523, we used qRT-PCR to measure changes in the expression of fibrotic markers, COL1a1, COL3a1, and TGF-β. Inhibition of MMP-13 with WAY170523 attenuated expression of these genes compared to vehicle treated animals. We previously reported that stimulation of CF and cardiomyocytes with MMP-13 induces phosphorylation of ERK1/2, a member of the MAPK family known to play a role in cardiac hypertrophy, and treatment with a direct PAR-1 antagonist decreased the activation of ERK1/2. We have found that ERK1/2 phosphorylation is directly attenuated following inhibition of MMP-13 with WAY170523. Overall, these data suggest a role for MMP-13 dependent PAR-1 activation in pathologic myofibroblast transition and a potential therapeutic role for MMP-13 inhibition, possibly through its inhibition of ERK1/2 phosphorylation. Treatment with WAY170523 also attenuates markers of fibrosis in vivo, indicating a potential salutary role for MMP-13 inhibition in the treatment of HF.

Overexpression of Runx2 directed by the matrix metalloproteinase-13 promoter containing the AP-1 and Runx/RD/Cbfa sites alters bone remodeling in vivo

2006 ◽  
Vol 99 (2) ◽  
pp. 545-557 ◽  
Author(s):  
Nagarajan Selvamurugan ◽  
Stephen C. Jefcoat ◽  
Sukyee Kwok ◽  
Rodney Kowalewski ◽  
Joseph A. Tamasi ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Bone Remodeling ◽  
Matrix Metalloproteinase 13 ◽  
The Matrix

scholarly journals Matrix Metalloproteinase 13 Activity is Required for Normal and Hypoxia-Induced Precocious Hatching in Zebrafish Embryos

2020 ◽  
Vol 8 (1) ◽  
pp. 3
Author(s):  
Christopher D. Small ◽  
Megan el-Khoury ◽  
Ghislain Deslongchamps ◽  
Tillmann J. Benfey ◽  
Bryan D. Crawford
Keyword(s):  
Matrix Metalloproteinase ◽  
Environmental Conditions ◽  
Molecular Mechanisms ◽  
Zebrafish Embryos ◽  
Clear Understanding ◽  
Hatching Enzyme ◽  
Pharmacological Inhibition ◽  
Matrix Metalloproteinase 13 ◽  
Hatching Gland

Hypoxia induces precocious hatching in zebrafish, but we do not have a clear understanding of the molecular mechanisms regulating the activation of the hatching enzyme or how these mechanisms trigger precocious hatching under unfavorable environmental conditions. Using immunohistochemistry, pharmacological inhibition of matrix metalloproteinase 13 (Mmp13), and in vivo zymography, we show that Mmp13a is present in the hatching gland just as embryos become hatching competent and that Mmp13a activity is required for both normal hatching and hypoxia-induced precocious hatching. We conclude that Mmp13a likely functions in activating the hatching enzyme zymogen and that Mmp13a activity is necessary but not sufficient for hatching in zebrafish. This study highlights the broad nature of MMP function in development and provides a non-mammalian example of extra-embryonic processes mediated by MMP activity.

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