Loss of MMP 13 attenuates murine hepatic injury and fibrosis during cholestasis

Uchinami, Hiroshi; Seki, Ekihiro; Brenner, David A.; DʼArmiento, Jeanine

doi:10.1002/hep.21268

Cited by 175 publications

(158 citation statements)

References 54 publications

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“…The importance of Mmp13 metalloproteinase to innate immune cell recruitment has been documented recently. For example, hepatic neutrophil recruitment is reduced in Mmp-13-deficient mice (53), and the Gr-1 ϩ CD11b ϩ myeloid cells express high levels of Mmp13 and Mmp14 to enhance migration and tumor metastasis (54), suggesting an important function for Mmp13 in ECM remodeling and cellular movement.…”

Section: Discussionmentioning

confidence: 99%

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

Zhang

Bai

Zhu

et al. 2008

The Journal of Immunology

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Section: Discussionmentioning

confidence: 99%

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

Zhang

Bai

Zhu

et al. 2008

The Journal of Immunology

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“…Conversely, Tgfb1 RGE/RGE ;Tgfb3 -/ -mice are all born with brain hemorrhage, the only phenotype in mice lacking avb8 that is not seen in mice lacking just TGF-b1 or TGF-b3 (Mu et al 2008). Thus, avb6 and Lyons et al (1990) and Flaumenhaft et al (1992); osteoclast data from Oursler (1994); MMP-13 data from Uchinami et al (2006) and Nannuru et al (2010); TSP1 data from Crawford et al (1998); Itgav 2/2 data from Bader et al (1998); avb6 data from Munger et al (1999); avb8, MT1-MMP data from Mu et al (2002); avb3, avb5 data from Wipff et al (2007); ROS data from Jobling et al (2006); shear force data from Ahamed et al (2008).…”

Section: Redundancy Among Tgf-b Isoforms and Integrin Activatorsmentioning

confidence: 98%

Cross Talk among TGF- Signaling Pathways, Integrins, and the Extracellular Matrix

Munger¹,

Sheppard²

2011

Cold Spring Harbor Perspectives in Biology

309

275

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The growth factor TGF-b is secreted in a latent complex consisting of three proteins: TGF-b, an inhibitor (latency-associated protein, LAP, which is derived from the TGF-b propeptide) and an ECM-binding protein (one of the latent TGF-b binding proteins, or LTBPs). LTBPs interact with fibrillins and other ECM components and thus function to localize latent TGF-b in the ECM. LAP contains an integrin-binding site (RGD), and several RGD-binding integrins are able to activate latent TGF-b through binding this site. Mutant mice defective in integrin-mediated activators, and humans and mice with fibrillin gene mutations, show the critical role of ECM and integrins in regulating TGF-b signaling.

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“…In the liver, hepatic stellate cells and Kupffer cells are thought to be the main source of MMPs (Arthur, 2000). Hepatocytes produce MMP-13 upon injury and loss of MMP-13 has lead to attenuation of fibrosis in a mouse model of liver disease (Uchinami et al, 2006).…”

Section: Neoplastic Diseasesmentioning

confidence: 99%

Human matrix metalloproteinases: An ubiquitarian class of enzymes involved in several pathological processes

Sbardella

Fasciglione

Gioia

et al. 2012

Molecular Aspects of Medicine

205

212

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a b s t r a c tHuman matrix metalloproteinases (MMPs) belong to the M10 family of the MA clan of endopeptidases. They are ubiquitarian enzymes, structurally characterized by an active site where a Zn 2+ atom, coordinated by three histidines, plays the catalytic role, assisted by a glutamic acid as a general base. Various MMPs display different domain composition, which is very important for macromolecular substrates recognition. Substrate specificity is very different among MMPs, being often associated to their cellular compartmentalization and/or cellular type where they are expressed. An extensive review of the different MMPs structural and functional features is integrated with their pathological role in several types of diseases, spanning from cancer to cardiovascular diseases and to neurodegeneration. It emerges a very complex and crucial role played by these enzymes in many physiological and pathological processes.

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Loss of MMP 13 attenuates murine hepatic injury and fibrosis during cholestasis

Cited by 175 publications

References 54 publications

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

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

Cross Talk among TGF- Signaling Pathways, Integrins, and the Extracellular Matrix

Human matrix metalloproteinases: An ubiquitarian class of enzymes involved in several pathological processes

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