Role of MT1-MMP in Estrogen-Mediated Cellular Processes of Intimal Hyperplasia

Mountain, Deidra J.H.; Kirkpatrick, Stacy S.; Freeman, Michael B.; Stevens, Scott L.; Goldman, Mitchell H.; Grandas, Oscar H.

doi:10.1016/j.jss.2011.05.037

Cited by 18 publications

(7 citation statements)

References 29 publications

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“…Nonetheless, persistent overexpression of MMPs might lead to inefficient angiogenesis and tissue repair after stroke (Danielsen et al, 2011). Hyperactivation of MMP14 has been associated with increased leakiness and an immature blood vessel phenotype (Sounni et al, 2010), but also with formation of fibrous tissue by promoting collagen invasion in vascular SMCs (Mountain et al, 2012). Likewise, in the latest stage after ischemia, MMP14 is responsible for chemokine activation, in particular TGF-beta pathway via ALK5/Smad3 (Sounni et al, 2010), which can affect the stability of blood vessels.…”

Section: Discussionmentioning

confidence: 99%

Transcriptomics of Post-Stroke Angiogenesis in the Aged Brain

Buga

Mărgăritescu

Scholz

et al. 2014

Front. Aging Neurosci.

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Despite the obvious clinical significance of post-stroke angiogenesis in aged subjects, a detailed transcriptomic analysis of post-stroke angiogenesis has not yet been undertaken in an aged experimental model. In this study, by combining stroke transcriptomics with immunohistochemistry in aged rats and post-stroke patients, we sought to identify an age-specific gene expression pattern that may characterize the angiogenic process after stroke. We found that both young and old infarcted rats initiated vigorous angiogenesis. However, the young rats had a higher vascular density by day 14 post-stroke. “New-for-stroke” genes that were linked to the increased vasculature density in young animals included Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4, which are required for sprouting angiogenesis, reconstruction of the basal lamina (BL), and the resolution phase. The vast majority of genes involved in sprouting angiogenesis (Angpt2, Angptl4, Cib1, Col8a1, Nrp1, Pcam1, Pttg1ip, Rac2, Runx1, Tnp4, Wnt4); reconstruction of a new BL (Col4a2, Lamc1, Plod2); or tube formation and maturation (Angpt1, Gpc3, Igfbp7, Sparc, Tie2, Tnfsf10), had however, a delayed upregulation in the aged rats. The angiogenic response in aged rats was further diminished by the persistent upregulation of “inflammatory” genes (Cxcl12, Mmp8, Mmp12, Mmp14, Mpeg1, Tnfrsf1a, Tnfrsf1b) and vigorous expression of genes required for the buildup of the fibrotic scar (Cthrc1, Il6ra, Il13ar1, Il18, Mmp2, Rassf4, Tgfb1, Tgfbr2, Timp1). Beyond this barrier, angiogenesis in the aged brains was similar to that in young brains. We also found that the aged human brain is capable of mounting a vigorous angiogenic response after stroke, which most likely reflects the remaining brain plasticity of the aged brain.

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Section: Discussionmentioning

confidence: 99%

Transcriptomics of Post-Stroke Angiogenesis in the Aged Brain

Buga

Mărgăritescu

Scholz

et al. 2014

Front. Aging Neurosci.

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“…Estrogen deficiency induced by ovariectomy gives rise to a reduction of active MMP-2 in the initial phase and a concurrent elevation of MMP-2 and MT1-MMP expression in latter period [54]. VSMCs incubated with estrogen and progesterone show upregulation of MMP pathway by increasing MMP-2 activity via enhancement of MT1-MMP expression [55], and inhibition of MT1-MMP prevents estrogen-stimulated increases in MMP-2 activity [56]. …”

Section: Mmps: Regulators In Vascular Tissuementioning

confidence: 99%

Matrix Metalloproteinases: Inflammatory Regulators of Cell Behaviors in Vascular Formation and Remodeling

Chen

Jin

Yang

et al. 2013

Mediators of Inflammation

394

307

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Abnormal angiogenesis and vascular remodeling contribute to pathogenesis of a number of disorders such as tumor, arthritis, atherosclerosis, restenosis, hypertension, and neurodegeneration. During angiogenesis and vascular remodeling, behaviors of stem/progenitor cells, endothelial cells (ECs), and vascular smooth muscle cells (VSMCs) and its interaction with extracellular matrix (ECM) play a critical role in the processes. Matrix metalloproteinases (MMPs), well-known inflammatory mediators are a family of zinc-dependent proteolytic enzymes that degrade various components of ECM and non-ECM molecules mediating tissue remodeling in both physiological and pathological processes. MMPs including MMP-1, MMP-2, MMP-3, MMP-7, MMP-8, MMP-9, MMP-12, and MT1-MMP, are stimulated and activated by various stimuli in vascular tissues. Once activated, MMPs degrade ECM proteins or other related signal molecules to promote recruitment of stem/progenitor cells and facilitate migration and invasion of ECs and VSMCs. Moreover, vascular cell proliferation and apoptosis can also be regulated by MMPs via proteolytically cleaving and modulating bioactive molecules and relevant signaling pathways. Regarding the importance of vascular cells in abnormal angiogenesis and vascular remodeling, regulation of vascular cell behaviors through modulating expression and activation of MMPs shows therapeutic potential.

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“…A large body of evidence has demonstrated an early upregulation of MMP-9 and activation of MMP-2 during neointima formation after vascular injury, and they are implicated in VSMCs migration and proliferation [ 37 ]. MMP-14 was also demonstrated to participate in vascular remodeling by promoting the migration and proliferation of arterial VSMCs [ 38 , 39 ]. Deficiency of MMP-2, -9 and -14 decreased intima hyperplasia in mouse models [ 40 , 41 , 42 , 43 , 44 ].…”

Section: Involvement Of Mmps Adams and Adamtss In Non-neoplastic mentioning

confidence: 99%

Matrix Metalloproteinases in Non-Neoplastic Disorders

Tokito

Jougasaki

2016

IJMS

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The matrix metalloproteinases (MMPs) are zinc-dependent endopeptidases belonging to the metzincin superfamily. There are at least 23 members of MMPs ever reported in human, and they and their substrates are widely expressed in many tissues. Recent growing evidence has established that MMP not only can degrade a variety of components of extracellular matrix, but also can cleave and activate various non-matrix proteins, including cytokines, chemokines and growth factors, contributing to both physiological and pathological processes. In normal conditions, MMP expression and activity are tightly regulated via interactions between their activators and inhibitors. Imbalance among these factors, however, results in dysregulated MMP activity, which causes tissue destruction and functional alteration or local inflammation, leading to the development of diverse diseases, such as cardiovascular disease, arthritis, neurodegenerative disease, as well as cancer. This article focuses on the accumulated evidence supporting a wide range of roles of MMPs in various non-neoplastic diseases and provides an outlook on the therapeutic potential of inhibiting MMP action.

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Role of MT1-MMP in Estrogen-Mediated Cellular Processes of Intimal Hyperplasia

Cited by 18 publications

References 29 publications

Transcriptomics of Post-Stroke Angiogenesis in the Aged Brain

Transcriptomics of Post-Stroke Angiogenesis in the Aged Brain

Matrix Metalloproteinases: Inflammatory Regulators of Cell Behaviors in Vascular Formation and Remodeling

Matrix Metalloproteinases in Non-Neoplastic Disorders

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