Differential Regulation of Matrix Metalloproteinase-2 and -9 Expression and Activity in Adult Rat Cardiac Fibroblasts in Response to Interleukin-1β

Xie, Zhonglin; Singh, Mahipal; Singh, Krishna

doi:10.1074/jbc.m405844200

Cited by 139 publications

(140 citation statements)

References 46 publications

Supporting

Mentioning

121

Contrasting

Unclassified

Order By: Relevance

“…Interestingly, MMP-9 was activated by IL-1␤, whereas MMP-2 was activated by both IL-1␤ and TNF-␣. This differential regulation of MMP-9 and MMP-2 activation is consistent with a previous report (36). Because IL-1␤ and TNF-␣ are chronically elevated in myocardium remote from the area of infarct (24) and play crucial roles in the development of LV enlargement, it is noteworthy that IMD decreased the activity of MMPs both in vivo and in vitro under stimulation by these cytokines.…”

Section: Diastolic Dysfunction and Nf-b Inhibitionsupporting

confidence: 92%

“…In fact, MMP-9 has a NF-B-binding site in its promoter region (34). Although there is no consensus with regard to the NF-B binding site in the MMP-2 promoter, it is possible that NF-B modulates MMP-2 activation directly via interaction with other transcriptional factors (36) or indirectly by inducing increased expression of membrane-type 1 MMP (9,22,36). Thus, inhibition of NF-B by IMD may modulate the activity of MMPs directly and/or indirectly, resulting in improvement of unfavorable LV remodeling, particularly LV enlargement.…”

Section: Diastolic Dysfunction and Nf-b Inhibitionmentioning

confidence: 99%

See 1 more Smart Citation

Inhibition of NF-κB improves left ventricular remodeling and cardiac dysfunction after myocardial infarction

Onai¹,

Suzuki²,

Maejima³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

109

View full text Add to dashboard Cite

August 18, 2006; doi:10.1152/ajpheart.00549.2006.-Several studies have demonstrated that NF-B is substantially involved in the progression of cardiac remodeling; however, it remains uncertain whether the continuous inhibition of NF-B is effective for the prevention of myocardial remodeling. Myocardial infarction (MI) was produced by ligation of the left anterior coronary artery of rats. IMD-0354 (10 mg/kg per day), a novel phosphorylation inhibitor of I B that acts via inhibition of IKK-␤, was injected intraperitoneally starting 24 h after induction of MI for 28 days. After 28 days, the IMD-0354-treated group showed significantly improved survival rate compared with that of the vehicle-treated group (P Ͻ 0.05). Although infarct size was similar in both groups, improved left ventricular (LV) remodeling and diastolic dysfunction, as indicated by smaller LV cavity (LV enddiastolic area: vehicle, 74.13 Ϯ 3.57 mm 2 ; IMD-0354, 55.00 Ϯ 3.73 mm 2 ; P Ͻ 0.05), smaller peak velocity of early-to-late filling wave (E/A) ratio (vehicle, 3.87 Ϯ 0.26; IMD-0354, 2.61 Ϯ 0.24; P Ͻ 0.05), and lower plasma brain natriuretic peptide level (vehicle, 167.63 Ϯ 14.87 pg/ml; IMD-0354, 110.75 Ϯ 6.41 pg/ml; P Ͻ 0.05), were observed in the IMD-0354-treated group. Moreover, fibrosis, accumulation of macrophages, and expression of several factors (transforming growth factor-␤1, monocyte chemoattractant protein-1, matrix metalloproteinase-9 and -2) in the noninfarcted myocardium was remarkably inhibited by IMD-0354. In conclusion, inhibition of NF-B activation may reduce the proinflammatory reactions and modulate the extracellular matrix and provide an effective approach to prevent adverse cardiac remodeling after MI. experimental heart failure; nuclear factor-b; matrix metalloproteinase; echocardiography MYOCARDIAL INFARCTION (MI) frequently leads to left ventricular (LV) dilatation and associated interstitial fibrosis in the noninfarcted myocardium. This adverse LV remodeling causes depressed cardiac performance and is an independent determinant of morbidity and mortality after MI (20). One of the recent conceptual advances in our understanding of the pathogenesis of LV remodeling is that this process is driven by the overexpression of various factors, including proinflammatory cytokines, angiotensin II, and norepinephrine, which have direct pathophysiological effects on cardiac myocytes, noncardiac myocytes, and the extracellular matrix (20). Although the expression of proinflammatory cytokines may be involved in wound healing after MI, it is believed that the overexpression of cytokines damages cardiac tissue and evokes excess deposition of fibrotic components, even in the noninfarcted myocardium.Several recent studies reported that nuclear factor-B (NF-B) is involved in the pathogenesis of heart failure (7, 35). Activation of NF-B induces activation of genetic programs that lead to transactivation of cytokines, chemokines, and matrix metalloproteinases (MMPs), promoting inflammatory and fibrotic responses that participate in the progre...

show abstract

Section: Diastolic Dysfunction and Nf-b Inhibitionsupporting

confidence: 92%

Section: Diastolic Dysfunction and Nf-b Inhibitionmentioning

confidence: 99%

Inhibition of NF-κB improves left ventricular remodeling and cardiac dysfunction after myocardial infarction

Onai¹,

Suzuki²,

Maejima³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

109

View full text Add to dashboard Cite

show abstract

“…Previous studies suggested that TNFa and/or IL1b could induce MMP9 expression via the NF-kB signaling pathway in different types of cells (Esteve et al 2002, Xie et al 2004, Liang et al 2007. MMP9 is activated by reactive oxygen species and its expression is likely to be regulated by oxidative stress (Rajagopalan et al 1996, Mori et al 2004, Pustovrh et al 2005.…”

Section: Discussionmentioning

confidence: 99%

Melatonin inhibits IL1β-induced MMP9 expression and activity in human umbilical vein endothelial cells by suppressing NF-κB activation

Qin

Lu²,

Li³

et al. 2012

Journal of Endocrinology

View full text Add to dashboard Cite

Matrix metalloproteinases (MMPs) have been involved in inflammatory and degradative processes in pathologic conditions. The purpose of this study was to investigate the protective effect of melatonin in human umbilical vein endothelial cell (HUVEC) monolayer permeability and the regulation of MMP9 induced by interleukin 1b (IL1b (IL1B)) in HUVECs. Protection studies were carried out with melatonin, a well-known antioxidant and antiinflammatory molecule. MMP9 expression was increased with IL1b induction in HUVECs. Melatonin showed a barrier-protective role by downregulation of MMP9 and upregulation of tissue inhibitor of metalloproteinase-1 expression in HUVECs. Meanwhile, melatonin also decreased sodium fluorescein permeability and counteracted the downregulation of vascular endothelial cadherin and occludin expression in HUVECs. During inflammatory stimulus, nuclear factor-kB (NF-kB) plays a significant role in regulating MMP genes expression, thus the function of NF-kB in HUVECs' barrier disruption was investigated. IL1b induced nuclear translocation of NF-kB in HUVECs and regulated MMP9 expression. However, NF-kB translocation into the nucleus was inhibited significantly by melatonin. Our results show that melatonin decreases the permeability of monolayer endothelial cell induced by IL1b. At the same time, melatonin decreased the expression and activity of MMP9 by a NF-kB-dependent pathway in HUVECs induced by IL1b.

show abstract

“…Members of the MMP family include collagenases (MMP-1, -8, and -13), gelatinases (MMP-2 and -9), stromelysins (MMP-3, -7, -10, -11, and -12), and membrane-type MMPs (MT1-MMP to MT6-MMP) (9 -11). Among MMPs, gelatinases such as MMP-2 (gelatinase A) and MMP-9 (gelatinase B) can degrade collagenous ECM proteins and collagen IV, a major component of basement membranes (6,12,13).…”

mentioning

confidence: 99%

“…In contrast, MMP-2 is expressed constitutively in diverse cell types (10). Furthermore, up-regulation of MMP-9 expression contributes to the development of tumor progression, including angiogenesis (11,12) and invasion and metastasis (1,16,17). High levels of MMP-9 have been related to several inflammatory diseases, such as multiple sclerosis and rheumatoid arthritis (7,18), in addition to a variety of cancers, such as gliomas and breast and lung cancers (19 -21).…”

mentioning

confidence: 99%

Human Leucine Zipper Protein sLZIP Induces Migration and Invasion of Cervical Cancer Cells via Expression of Matrix Metalloproteinase-9

Kang¹,

Jang²,

2011

Journal of Biological Chemistry

View full text Add to dashboard Cite

Background: Proteolytic degradation of the extracellular matrix and basement membranes by matrix metalloproteinases (MMPs) is crucial in tumor invasion and metastasis. Results: sLZIP induces the expression of MMP-9, leading to enhancement of migration and invasion of cervical cancer cells. Conclusion: A novel regulatory mechanism of MMP-9 expression is characterized. Significance: sLZIP is a potential target for preventing the invasion and metastasis of cervical cancer.

show abstract

Differential Regulation of Matrix Metalloproteinase-2 and -9 Expression and Activity in Adult Rat Cardiac Fibroblasts in Response to Interleukin-1β

Cited by 139 publications

References 46 publications

Inhibition of NF-κB improves left ventricular remodeling and cardiac dysfunction after myocardial infarction

Inhibition of NF-κB improves left ventricular remodeling and cardiac dysfunction after myocardial infarction

Melatonin inhibits IL1β-induced MMP9 expression and activity in human umbilical vein endothelial cells by suppressing NF-κB activation

Human Leucine Zipper Protein sLZIP Induces Migration and Invasion of Cervical Cancer Cells via Expression of Matrix Metalloproteinase-9

Contact Info

Product

Resources

About