Serum levels of MMP-9 and TIMP-1 in primary hypertension and effect of antihypertensive treatment

Önal, İbrahi̇m Koral; Altun, Bülent; Önal, Eda Demir; Kırkpantur, Alper; Öz, Şerife Gül; Turgan, Çetin

doi:10.1016/j.ejim.2008.10.003

Cited by 70 publications

(74 citation statements)

References 21 publications

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“…Another study by Onal et al confirms the finding that MMP-9 levels are higher in individuals with hypertension and that antihypertensive treatment lowers MMP-9 to control group levels (Onal et al, 2009). Furthermore, MMP-9 is induced by EMMPRIN in the atherosclerotic carotid lesion of advanced atherosclerotic plaque, leading to abnormal ECM remodeling and atheroma instability (Yoon et al, 2005).…”

Section: Mmp-9 and Diseasesupporting

confidence: 69%

“…Hcy associated vascular inflammation and remodeling is largely due to increased ROS (Hayden & Tyagi, 2004;Signorello et al, 2007) and MMP-9 production (Moshal et al, 2006;Tyagi et al, 2009) as well as an inhibition of peroxisome proliferator-activated receptor-γ (PPAR-γ), a proantioxidant (Mujumdar et al, 2002). MMP-9 is activated by Hcy through an extracellular signal-regulated kinase (ERK) pathway in vascular endothelial cells (Moshal et al, 2006;Tyagi et al, 2009) and is thought to be a primary factor in vascular remodeling and arterial stiffness (Onal et al, 2009;Wiernicki et al, 2011;Yasmin et al, 2005). However, studies have shown that extracellular matrix metalloproteinase inducer (EMMPRIN) activation not only correlates with MMP activity, but may be largely responsible for increased synthesis of MMP-9 (Ge et al, 2007;Major et al, 2002;Reddy et al, 2010;Yoon et al, 2005;Zhu et al, 2005).…”

Section: Hcy Treatment Induces Cd40 In Murine Macrophagesmentioning

confidence: 99%

“…Excessive inflammation and oxidative stress can lead to abnormal activation of MMP-9, causing excessive degradation of the ECM, abnormal vascular remodeling and endothelial dysfunction, which are associated with hypertension and arterial stiffness (Onal et al, 2009;Wallace et al, 2005).…”

Section: Mmp-9 and Diseasementioning

confidence: 99%

“…Its ability to degrade the extracellular matrix has been implicated in cardiovascular remodeling (Spinale et al, 2000;Tyagi et al, 2010). It is strongly associated with heart failure, hypertension and arterial stiffness and positively correlates with Hcy levels (Onal et al, 2009;Spinale et al, 2000;Wiernicki et al, 2011;Yasmin et al, 2005). Macrophages are required for the growth and repair of damaged muscle tissue, but chronic inflammation can cause macrophages to become hyperactive and destructive, leading to fibrosis of tissue.…”

Section: Introductionmentioning

confidence: 99%

“…MMP-9 is an endoproteinase that is known to degrade components of the extracellular matrix, such as elastin and collagen type IV. Excessive MMP-9 activity has been associated with endothelial dysfunction and vascular remodeling, leading to diseases such as atherosclerosis (Onal et al, 2009;Wiernicki et al, 2011;Yasmin et al, 2005). More recently it has been discovered that MMP-9 production and activity are increased through an EMMPRIN mediated pathway involving NF-κB (Ge et al, 2007;Major et al, 2002;Reddy et al, 2010;Yoon et al, 2005;Zhu et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

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Exercise mitigates the effects of hyperhomocysteinemia on adverse skeletal muscle remodeling.

Winchester¹

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Intro Hyperhomocysteinemia (HHcy) is associated with vascular and skeletal muscle dysfunction. HHcy induces MMP‐9 activity, myostatin release, systemic inflammation and may increase M1 macrophages. Previous reports suggest that exercise reduces HHcy and myostatin levels, however the effects of exercise on macrophages and myostatin during HHcy are unclear. We hypothesize that exercise decreases HHcy induced inflammation and muscular dysfunction by decreasing MMP‐9, myostatin and M1 macrophages. Methods C57 WT, FVB, MMP‐9‐/‐, CBS‐/+ (HHcy), and CBS‐/+/MMP‐9‐/‐ (Double KO) mice were administered 4 weeks of treadmill running, swimming, or no exercise for controls. Ultrasonography and laser Doppler were used to measure wall to lumen ratio, blood flow and perfusion rate of the femoral artery. Western Blotting, IHC, Histology and PCR were used to analyze mouse tissue samples. Results Blood flow rates in control CBS‐/+ mice were approximately 23.9% lower than in control C57 WT mice. This rate was increased by 1.89 fold with exercise. Wall to Lumen ratio was approximately 4.14 fold higher in the CBS‐/+ control mice compared with WT, but became similar to WT after exercise. Laser Perfusion imaging demonstrated a 12.5% lower femoral artery red blood cell flux in CBS‐/+ mice when compared with WT, but was increased by 1.35 fold after exercise. Collagen staining reveals higher collagen deposition in the gastrocnemius of CBS‐/+ mice compared with WT, but was completely reversed with exercise. Conclusions We conclude that Exercise Mitigates HHcy Induced Vascular Dysfunction and Adverse Skeletal Muscle Remodeling.

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Section: Mmp-9 and Diseasesupporting

confidence: 69%

Section: Hcy Treatment Induces Cd40 In Murine Macrophagesmentioning

confidence: 99%

Section: Mmp-9 and Diseasementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Exercise mitigates the effects of hyperhomocysteinemia on adverse skeletal muscle remodeling.

Winchester¹

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Matrix Metalloproteinase Inhibitors as Investigative Tools in the Pathogenesis and Management of Vascular Disease

Benjamin

Khalil

2012

Experientia Supplementum

133

139

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Matrix metalloproteinases (MMPs) are proteolytic enzymes that degrade various components of the extracellular matrix (ECM). MMPs could also regulate the activity of several non-ECM bioactive substrates, and consequently affect different cellular functions. Members of the MMPs family include collagenases, gelatinases, stromelysins, matrilysins, membrane-type MMPs and others. Pro-MMPs are cleaved into active MMPs, which in turn act on various substrates in the ECM and on the cell surface. MMPs play an important role in the regulation of numerous physiological processes including vascular remodeling and angiogenesis. MMPs may also be involved in vascular diseases such as hypertension, atherosclerosis, aortic aneurysm, and varicose veins. MMPs also play a role in the hemodynamic and vascular changes associated with pregnancy and preeclampsia. The role of MMPs is commonly assessed by measuring their gene expression, protein amount, and proteolyic activity using gel zymography. Because there are no specific activators of MMPs, MMP inhibitors are often used to investigate the role of MMPs in different physiologic processes and in the pathogenesis of specific diseases. MMP inhibitors include endogenous tissue inhibitors (TIMPs) and pharmacological inhibitors such as zinc chelators, doxycycline and marimastat. MMP inhibitors have been evaluated as diagnostic and therapeutic tools in cancer, autoimmune and cardiovascular disease. Although several MMP inhibitors have been synthesized and tested both experimentally and clinically, only on MMP inhibitor, i.e. doxycycline, is currently approved by the Food and Drug Administration. This is mainly due to the undesirable side effects of MMP inhibitors especially on the musculoskeletal system. While most experimental and clinical trials of MMP inhibitors have not demonstrated significant benefits, some trials still showed promising results. With the advent of new genetic and pharmacological tools, disease-specific MMP inhibitors with fewer undesirable effects are being developed and could be useful in the management of vascular disease.

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Vasoactive Peptides

Faria¹,

Moreno²

2018

Updates in Hypertension and Cardiovascular Protection

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Serum levels of MMP-9 and TIMP-1 in primary hypertension and effect of antihypertensive treatment

Cited by 70 publications

References 21 publications

Exercise mitigates the effects of hyperhomocysteinemia on adverse skeletal muscle remodeling.

Exercise mitigates the effects of hyperhomocysteinemia on adverse skeletal muscle remodeling.

Matrix Metalloproteinase Inhibitors as Investigative Tools in the Pathogenesis and Management of Vascular Disease

Vasoactive Peptides

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