ArticleJournal of molecular and cellular cardiology2011
MMPs 2 and 9 are essential for coronary collateral growth and are prominently regulated by p38 MAPK.
Article in Journal of molecular and cellular cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 42 citations in OpenAlex.
- Interleukin-38 suppresses abdominal aortic aneurysm formation in mice by regulating macrophages in an IL1RL2-p38 pathway-dependent manner.Physiological reports · 2023Article
- p38 MAPK priming boosts VSMC proliferation and arteriogenesis by promoting PGC1α-dependent mitochondrial dynamics.Scientific reports · 2022Article
- Article
- Vessel Enlargement in Development and Pathophysiology.Frontiers in physiology · 2021Review
- Simultaneous Upregulation of Elastolytic and Elastogenic Factors Are Necessary for Regulated Collateral Diameter Expansion.Frontiers in cardiovascular medicine · 2021Article
- Structural Remodeling of the Extracellular Matrix in Arteriogenesis: A Review.Frontiers in cardiovascular medicine · 2021Review
- Loss of Protease-Activated Receptor 4 Prevents Inflammation Resolution and Predisposes the Heart to Cardiac Rupture After Myocardial Infarction.Circulation · 2020Article
- Review
- Reperfused hemorrhagic myocardial infarction in rats.PloS one · 2020Article
- Dickkopf‑3 upregulation mediates the cardioprotective effects of curcumin on chronic heart failure.Molecular medicine reports · 2018Article
- Elevated 20-HETE in metabolic syndrome regulates arterial stiffness and systolic hypertension via MMP12 activation.Journal of molecular and cellular cardiology · 2018Article
- Nobiletin inhibits breast cancer via p38 mitogen-activated protein kinase, nuclear transcription factor-κB, and nuclear factor erythroid 2-related factor 2 pathways in MCF-7 cells.Food & nutrition research · 2018Article
- Cellular and Molecular Heterogeneity Associated with Vessel Formation Processes.BioMed research international · 2018Review
- Rapamycin inhibits CaCl2-induced thoracic aortic aneurysm formation in rats through mTOR-mediated suppression of proinflammatory mediators.Molecular medicine reports · 2017Article
- Elevated 20-HETE impairs coronary collateral growth in metabolic syndrome via endothelial dysfunction.American journal of physiology. Heart and circulatory physiology · 2017Article
- Baicalin Attenuates Hypoxia-Induced Pulmonary Arterial Hypertension to Improve Hypoxic Cor Pulmonale by Reducing the Activity of the p38 MAPK Signaling Pathway and MMP-9.Evidence-based complementary and alternative medicine : eCAM · 2016Article
- miR-21-mediated decreased neutrophil apoptosis is a determinant of impaired coronary collateral growth in metabolic syndrome.American journal of physiology. Heart and circulatory physiology · 2015Article
- Management of hepatocellular carcinoma: Predictive value of immunohistochemical markers for postoperative survival.World journal of hepatology · 2015Review
- Role of MMP2 and MMP9 in TRPV4-induced lung injury.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- miR-21 normalizes vascular smooth muscle proliferation and improves coronary collateral growth in metabolic syndrome.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Transient, repetitive ischemia (RI) stimulates coronary collateral growth (CCG) in normal, healthy (SD) rats, which requires p38 MAPK activation. In contrast, RI does not induce CCG in the metabolic syndrome (JCR) rats, which is associated with lack of p38 MAPK activation. The functional consequences of p38 MAPK activation in CCG remain unknown. Theoretically, effective collateral growth would require extracellular matrix remodeling; however, direct assessment as well as identification of proteases responsible for this degradation are lacking. In this study, we investigated the role of p38 MAPK in the regulation of matrix metalloproteinases 2 and 9 (MMPs 2 and 9) and their requirement for CCG in SD vs. JCR rats. The rats underwent the RI protocol (8 LAD occlusions, 40s each, every 20min, in 8h cycles for 0, 3, 6, or 9days). MMP expression was measured in the ischemic, collateral-dependent zone (CZ) and the normal zone (NZ) by Western blot, and MMP activity by zymography. Expression and activation of MMP 2 and 9 were significantly increased (~3.5 fold) on day 3 of RI in the CZ of SD rats. In vivo p38 MAPK inhibition completely blocked RI-induced MMP 2 and 9 expression and activation. MMP activation correlated with increased degradation of components of the basement membrane and the vascular elastic laminae: elastin (~3 fold), laminin (~3 fold) and type IV collagen (~2 fold). This was blocked by MMP 2 and 9 inhibition, which also abolished RI-induced CCG. In contrast, in JCR rats, RI did not induce expression or activation of MMP 2 or 9 and there was no associated degradation of elastin, laminin or type IV collagen. In conclusion, MMP 2 and 9 activation is essential for CCG and is mediated, in part, by p38 MAPK. Furthermore, compromised CCG in the metabolic syndrome may be partially due to the lack of p38 MAPK-dependent activation of MMP 2 and 9 and resultant decreased extracellular matrix degradation.
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