Membrane-type MMPs enable extracellular matrix permissiveness and mesenchymal cell proliferation during embryogenesis

Shi, Joanne; Son, Mi-Young; Yamada, Susan S.; Szabova, Ludmila; Kahan, Stacie; Chrysovergis, Kaliopi; Wolf, Lauren K.; Surmak, Andrew; Holmbeck, Kenn

doi:10.1016/j.ydbio.2007.10.017

Cited by 94 publications

(109 citation statements)

References 50 publications

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“…Turnover of ECM components is effected by some MMPs to control processes in stem cell biology, muscle biology, central nervous system homeostasis and disease, angiogenesis, tissue repair in skin and liver, inflammation, vascular disease, destructive lung disease, and some cancers. For instance, the collagenolytic enzymes MMP13, MMP14 (MT1-MMP), and MMP16 (MT3-MMP) are involved in the remodeling of the collagen matrix in bone and elsewhere (36,37). Thanks to the information derived from a number of parallel studies, it has emerged that many MMPs act beyond the ECM with roles in the modulation of effectors within signaling pathways associated with inflammation and immunity.…”

Section: Basic Science Catches Upmentioning

confidence: 99%

Riding the metalloproteinase roller coaster

Murphy

2017

Journal of Biological Chemistry

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To many of us in the field, working on matrix metalloproteinases (MMPs) has felt like riding a roller coaster, traveling through times of both excitement and despair. I was fortunate to join the ride when it was a mere carousel of three activities thought to target the proteins that comprise the extracellular matrix (ECM). New technologies brought the thrills of discovery as we uncovered specific proteinase genes and defined specialized activities in different cellular processes. The MMPs and the sister families of "a disintegrin and metalloproteinase" (ADAMs), ADAMs with thrombospondin domains (ADAM-TS), and Astacins are now recognized as key signaling "scissors" that drive rapid changes in a plethora of cellular pathways. My many excellent colleagues and collaborators and I were enthused to contribute to the early development of the field and continue to be amazed at its growth and sophistication. In contrast, the hype and failure of early inhibitor discovery have dogged our standing with the pharmaceutical industry and grant-giving bodies. However, the true believers have kept going, and knowledge of particular functions of MMPs and their contributions to disease progression has progressed. Recognition of the strategic importance of proteinase function should inspire more work harnessing new technologies such as imaging, proteomics, and gene editing to generate a more precise understanding of individual situations. New approaches to inhibitor design and assessment are possible, and the consequent ability to precisely abrogate specific MMP activity could contribute to the fight against a number of pathologies with unmet needs. What a ride it could be!

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Section: Basic Science Catches Upmentioning

confidence: 99%

Riding the metalloproteinase roller coaster

Murphy

2017

Journal of Biological Chemistry

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Section: Mmp-16mentioning

confidence: 99%

“…73 The mechanism of ECM degradation via MMP-16 is necessary for the proper functioning of mesenchymal cells expressed on skeletal tissue. 73,74 In fact, mice lacking MMP-16 demonstrate stunted growth due to the decreased viability of these mesenchymal cells. 73 MMP-16 has been examined along with MMP-14, as both enzymes have similar molecular structures and tissue expression patterns.…”

Section: Mmp-16mentioning

confidence: 99%

Matrix metalloproteinases in bone development and pathology: current knowledge and potential clinical utility

Liang¹,

Xu²,

Xue³

et al. 2016

MNM

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Matrix metalloproteinases (MMPs) are degrading enzymes that have a pivotal function in extracellular matrix remodeling. More than half of the MMP members are expressed by bone and cartilage cells under physiological or pathological conditions such as rheumatoid arthritis, osteoarthritis, and osteoporosis. Through studies on the various bone diseases and on genetically modified mouse models in which one or more of the MMPs or their associated proteins and downstream signaling molecules have been targeted, it is becoming increasingly evident that MMPs and other players in their cellular pathway play a pivotal role in bone development and remodeling. This review details the latest findings related to MMPs and bone development and pathology.

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“…Their expression increases during physiological or pathological tissue remodeling with the influence of signaling molecules able to modulate gene expression 8 . MMPs and TIMPs have been suggested to be candidate genes based on research of their spatial and temporal expression patterns during palatogenesis in animals 9 . Thus, the process of CLP morphogenesis is closely accompanied by changes in the composition of the extracellular matrix that promote cell migration and differentiation, cell-cell interactions, and tissue resorption.…”

Section: Introductionmentioning

confidence: 99%

MMPs and TIMPs expression in facial tissue of children with cleft lip and palate

Smane-Filipova¹,

Pilmane²,

Akota³

2016

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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Background and Aims. Morphogenesis of the upper lip and palate is a complex process involving highly regulated interactions between epithelial and mesenchymal cells. Genetic evidence in humans and mice indicates the involvement of matrix metalloproteinases (MMPs) and their endogenous tissue inhibitors (TIMPs) in cleft lip palate (CLP) aetiology. This study investigated whether expression of MMP-2, MMP-8, MMP-9, TIMP-2, and TIMP-4, which are essential for the upper lip and palate fusion, is dysregulated in children with CLP. Methods. Oral mucosa tissue samples were obtained from patients with complete unilateral (CU) CLP (n = 25) and complete bilateral (CB) CLP (n = 19) during corrective plastic surgery and in unaffected control subjects (n = 10). MMPs and TIMPs expression was assessed by immunohistochemistry, and the data were analyzed using the Kruskal -Wallis test with the Bonferroni correction. Results. In CLP patients, MMP-2, TIMP-2 immunoreactivity in the oral mucosa was seen to have a few to abundant structures, but the overall number of MMP-2, TIMP-2-positive structures was greater than that in controls (P < 0.01). The total number of TIMP-4, MMP-9-positive cells showed a significant decrease in the CBCLP compared with that of CUCLP (P < 0.001). MMP-8 expression trends in the CLP group were similar to those of the control group. Conclusions. The results suggest that TIMP-4 and MMP-9 are the main ECM remodeling regulatory proteins expressed in CUCLP affected tissues of the oral mucosa. The increased expression of MMP-2 and TIMP-2 in CLP tissues implicates these factors in the regulation of cell migration during ECM turnover independently of different types of clefts. Investigation of MMP and TIMP expression in tissue samples from patients with CLP appears to be a promising approach to the etiopathogenesis of CLP.

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Membrane-type MMPs enable extracellular matrix permissiveness and mesenchymal cell proliferation during embryogenesis

Cited by 94 publications

References 50 publications

Riding the metalloproteinase roller coaster

Riding the metalloproteinase roller coaster

Matrix metalloproteinases in bone development and pathology: current knowledge and potential clinical utility

MMPs and TIMPs expression in facial tissue of children with cleft lip and palate

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