Matrix metalloproteinaasi 13 osallistuu luun normaaliin remodeling systeemiin

MMP-13 osallistuu luun normaaliin uudismuodostus ja remodeling prosessiin.  

Jos MMP-13 geenissä on mutaatio, seuraa useita eri patologioita kuten syöpää ja artriittia.

LÄHDE: 

Int J Biol Macromol. 2017 Dec 19;109:338-349. doi: 10.1016/j.ijbiomac.2017.12.091. [Epub ahead of print]

Matrix metalloproteinase-13: A special focus on its regulation by signaling cascades and microRNAs in bone.

S S¹, R S¹, V U¹, B A¹, M V¹, N S².

Author information

Abstract

Bone remodeling is an orchestrated process involving osteoblasts and osteoclasts to maintain mineral homeostasis in the internal milieu, mediated chiefly by matrix metalloproteinases (MMPs). MMP13, one amongst the MMPs plays a premier role in bone remodeling,

and mutations in MMP13 have been implicated in various pathologies including cancer and arthritis.

 Transcriptional activation of MMP13 gene is tightly regulated by several signaling cascade components. Post-transcriptional regulators such as microRNAs (miRNAs) have also been shown to regulate MMP13 expression under physiological and pathological conditions.

 Hence, this review provides an outline of the structure of MMP13 gene and its regulation by signaling components, transcription factors and miRNAs in bone.

KEYWORDS:

Bone remodeling; Extracellular matrix; MMP13; Runx2; Signaling pathways; miRNAs

PMID:

29273522

DOI:

10.1016/j.ijbiomac.2017.12.091

MMP-13 vaikutus malli luuston remodeling- prosessissa

https://openi.nlm.nih.gov/detailedresult.php?img=PMC2063465_pone.0001150.g007&req=4


https://openi.nlm.nih.gov/imgs/512/320/2063465/PMC2063465_pone.0001150.g007.png?keywords=hypertrophic,fracture,callus


 

MMP-13 , luusto ja nivelrusto

https://www.ncbi.nlm.nih.gov/gene/4322

MMP13 matrix metallopeptidase 13 [ Homo sapiens (human) ]

Gene ID: 4322, updated on 31-Dec-2017

Summary

Official Symbol

MMP13provided by HGNC

Official Full Name

matrix metallopeptidase 13provided by HGNC

Primary source

HGNC:HGNC:7159

See related

Ensembl:ENSG00000137745 MIM:600108; Vega:OTTHUMG00000165850

Gene type

protein coding

RefSeq status

REVIEWED

Organism

Homo sapiens

Also known as

CLG3; MDST; MANDP1; MMP-13

Summary

This gene encodes a member of the peptidase M10 family of matrix metalloproteinases (MMPs). Proteins in this family are involved in the breakdown of extracellular matrix in normal physiological processes, such as embryonic development, reproduction, and tissue remodeling, as well as in disease processes, such as arthritis and metastasis. The encoded preproprotein is proteolytically processed to generate the mature protease. This protease cleaves type II collagen more efficiently than types I and III. It may be involved in articular cartilage turnover and cartilage pathophysiology associated with osteoarthritis. Mutations in this gene are associated with metaphyseal anadysplasia. This gene is part of a cluster of MMP genes on chromosome 11. [provided by RefSeq, Jan 2016]

Expression

Low expression observed in reference dataset See more

Orthologs

mouse all

• Mitä kirjallisuutta tästä MMP-13.asta on kertynyt?

Related articles in PubMed

1. Matrix Metalloproteinase-13 - A Potential Biomarker for Detection and Prognostic Assessment of Patients with Esophageal Squamous Cell Carcinoma. Sedighi M, et al. Asian Pac J Cancer Prev, 2016. PMID 27356690
2. Hyaluronic Acid Suppresses the Expression of Metalloproteinases in Osteoarthritic Cartilage Stimulated Simultaneously by Interleukin 1β and Mechanical Load. Pohlig F, et al. PLoS One, 2016. PMID 26934732, Free PMC Article
3. Induction of the Matrix Metalloproteinase 13 Gene in Bronchial Epithelial Cells by Interferon and Identification of its Novel Functional Polymorphism. Mashimo Y, et al. Inflammation, 2016 Jun. PMID 26635116
4. Function of sustained released resveratrol on IL-1β-induced hBMSC MMP13 secretion inhibition and chondrogenic differentiation promotion. Wu G, et al. J Biomater Appl, 2016 Feb. PMID 26526931
5. Modified platelet deposition on matrix metalloproteinase 13 digested collagen I. Howes JM, et al. J Thromb Haemost, 2015 Dec. PMID 26447617, Free PMC Article

• * Huomaa resveratrol mahdollisessa artriittiterapiassa
• https://www.ncbi.nlm.nih.gov/pubmed/26526931/

GeneRIFs: Gene References Into FunctionsWhat's a GeneRIF?

1. TGF-beta1 stimulates the phosphorylation of Runx2 at three serine amino acids, and this event is required for MMP-13 expression in osteoblastic cells.
2. IL-6-stimulated MMP-13 expression was independent of IL-1beta stimulation and was blocked by SAHA, suggesting that SAHA inhibits IL-6 signaling in Osteoarthritis (OA) chondrocytes.
3. High MMP13 expression is associated with intervertebral disc degeneration.
4. data demonstrate that MMP-13 is critical for the development of osteolytic lesions in Multiple myeloma and that targeting the MMP-13 protein - rather than its catalytic activity - constitutes a potential approach to mitigating bone disease in affected patients.
5. Endoplasmic reticulum stress participates in the progress of senescence and apoptosis of osteoarthritic chondrocytes, which manifested in increased expression of ADAMTS5, MMP13, and decreased COL2A1 expression.
6. Matrix metalloprotease (MMP) regulation was the top pathway involved in gingival aging. MMP3, MMP9, MMP12, and MMP13 were upregulated in old gingival tissues, concomitantly with interleukin-1 beta (IL1B) expression.
7. these findings support roles for both cFOS (indirect) and ATF3 (direct) in effecting MMP13 transcription in human chondrocytes.
8. Oxytocin prevents cartilage matrix destruction via regulating MMP1 and MMP13.
9. These studies have uncovered a new, ATP6V1H-mediated pathway that regulates bone formation, and defines a new mechanism of disease that leads to bone loss. We propose that MMP9/MMP13 could be therapeutic targets for patients with this rare genetic disease.
10. To conclude, Pseudomonas aeruginosa infection induced the expression of matrix metalloproteinases, and Pseudomonas aer

Bifosfonaatti-intioleranssi ja OP

Bone-forming agents in non-responders to bisphosphonates

Juliet CompstonEmail the author Juliet Compston

Published: 26 July 2017

DOI: http://dx.doi.org/10.1016/S0140-6736(17)31824-X

Osteoporosis is a chronic disease requiring long-term treatment. Oral bisphosphonates, which act by inhibiting bone resorption, are most commonly prescribed but inadequate response, development of intolerance, or fear of long-term side-effects sometimes necessitate change to an alternative therapy.¹ One option is to switch to teriparatide, a bone-forming agent, but enthusiasm for this strategy is tempered by the blunting of the bone mineral density (BMD) response to teriparatide seen in patients previously treated with antiresorptives.

4.1. 2018 Lancet sitaatti