Angiotensin-Receptor Blockade Reduces Border Zone Myocardial Monocyte Chemoattractant Protein-1 Expression and Macrophage Infiltration in Post-Infarction Ventricular Remodeling

Kohno, Takashi; Anzai, Toshihisa; Naito, Kunihiko; Sugano, Yasuo; Maekawa, Yuichiro; Takahashi, Toshiyuki; Yoshikawa, Tsutomu; Ogawa, Satoshi

doi:10.1253/circj.cj-08-0115

Cited by 51 publications

(41 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…23 Recent studies have shown that the marginal myocardial area might be a novel therapeutic target in the treatment of post-MI LV remodeling. 25,26 Extension of the macrophage-mediated inflammation in the infarcted region might cause the inflammatory response in the marginal region, although the mechanism underlying the inflammatory response in the latter has not been fully elucidated. In addition, geometric changes in hearts with LV aneurysm after MI are known to increase wall stress in the marginal region, 20 and pressure-overload-induced cardiac fibrosis is mediated through MCP-1 induction and macrophage accumulation.…”

Section: Discussionmentioning

confidence: 99%

Tolvaptan Improves Left Ventricular Dysfunction after Myocardial Infarction in Rats

Yamazaki

Izumi

Nakamura

et al. 2012

Circ: Heart Failure

View full text Add to dashboard Cite

Arginine vasopressin (AVP) is a 9-amino acid peptide secreted from the posterior pituitary, in response to high plasma osmolality and hypotension. AVP is known to play an important role in water metabolism by inducing water reabsorption at the renal collecting duct via the V 2 receptor (V 2 R). AVP is also involved in the maintenance of blood pressure © 2012 American Heart Association, Inc. Background-Arginine vasopressin, which promotes the reabsorption of renal water is increased in chronic heart failure.Here, we compared the effects of tolvaptan, a newly developed nonpeptide V 2 receptor antagonist, with those of furosemide, a loop diuretic, and a combination of these 2 agents in rats with left ventricular dysfunction after myocardial infarction (MI). Methods and Results-After 10 weeks of MI induction, the rats were separated them into the following 6 groups adjusted to the infarct size: a vehicle group, a group treated with 15 mg·kg tolvaptan. Each treatment agent was administered for 4 weeks, and all groups had similar blood pressure levels and infarct size. The tolvaptan-treated groups were found to have lower levels of left ventricular end-diastolic and systolic cardiac volumes than the vehicle group did. Furthermore, the improvement in the ejection fraction in the tolvaptan-treated groups was significantly greater than those in the vehicle group. ED-1 immunostaining and Sirius red staining revealed that tolvaptan significantly repressed MI-induced macrophage infiltration and interstitial fibrosis in the left ventricle, respectively. Tolvaptan attenuated the MI-induced mRNA expressions of atrial and brain natriuretic peptides, monocyte chemotactic protein-1, transforming growth factor-β1, arginine vasopressin V 1a receptor, and endothelin-1 in the marginal infarct region. Conclusions-Tolvaptan may improve cardiac dysfunction after MI, which is partially mediated by the suppression of V 1a receptor, neurohumoral activation and inflammation. (Circ Heart Fail. 2012;5:794-802.)

show abstract

Section: Discussionmentioning

confidence: 99%

Tolvaptan Improves Left Ventricular Dysfunction after Myocardial Infarction in Rats

Yamazaki

Izumi

Nakamura

et al. 2012

Circ: Heart Failure

View full text Add to dashboard Cite

show abstract

“…The AT1 activation has a key role in these actions. The therapeutic use of ARB has extensively beneficial effects in attenuating the development of atherosclerosis and hypertension [29,[31][32][33]. Moreover, VSMCs play a fundamental role in maintaining vascular structure and function.…”

Section: Il-17mentioning

confidence: 99%

Angiotensin II Induces TSLP via an AT1 Receptor/NF-KappaB Pathway, Promoting Th17 Differentiation

Zhao

Wang

et al. 2012

Cell Physiol Biochem

View full text Add to dashboard Cite

Background: Adaptive immunity plays a critical role in atherosclerosis and hypertension. T helper 17 (Th17) cells, as a new T-cell lineage, are involved in cardiovascular diseases. Dendritic cells (DCs) are the professional antigen-presenting cells with the pivotal role in orchestrating adaptive immunity. Thymic stromal lymphopoietin (TSLP) can activate DCs and trigger adaptive immune responses. What the role of TSLP in atherosclerosis and hypertension has not been investigated. Methods and Results: We measured the expression of TSLP in primary rat vascular smooth muscle cells (VSMCs) exposed to angiotensin II (Ang II) and evaluated the capacity of TSLP induced by Ang II to induce the differentiation of Th17 Cells. We then sought to identify the involved upstream regulatory mechanisms. We found that VSMCs express TSLP in response to Ang II in an AT1 receptor/NF-KappaB manner. TSLP can induce the differentiation of Th17 Cells by triggering DCs. Conclusion: Through DC activation, Ang II-induced TSLP enhances Th17-driven immune response in atherosclerosis and hypertension.

show abstract

“…28 decreased, 13 suggesting involvement of sympathetic activation in the induction of inflammation. It has been also demonstrated that when an angiotensin II receptor antagonist was administered in a rat MI model, both expression of MCP-1 and macrophage infiltration in the border zone were reduced, 14 indicating the involvement of activation of the renin-angiotensin (RA) system in the promotion of inflammatory response. In chronic kidney disease patients with estimated glomerular filtration rate <60 ml · min -1 · 1.73 m -2 on admission 15 and those with the complication of so-called acute kidney injury (AKI) whose serum creatinine level increases to >0.3 mg/dl within 48 h of admission, 16 it is reported that peak CRP level increased concurrently with plasma interleukin (IL)-6 and serum malondialdehyde-modified low density lipoprotein (oxidized LDL) levels.…”

Section: Modification Of Crp Elevation By Patient Demographic Factorsmentioning

confidence: 99%

Post-Infarction Inflammation and Left Ventricular Remodeling

Anzai

2013

Circ J

Self Cite

123

107

View full text Add to dashboard Cite

Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp non-specific response to tissue damage. 1 However, an investigation into the relation between the peak body temperature during the first week and in-hospital complications since the event of MI showed that the incidence of complications of pump failure (grade of class 2 or greater according to Killip's classification or subset II or greater according to Forrester's classification) and ventricular aneurysm, as well as the incidence of cardiovascular events such as cardiac death, pump failure, fatal ventricular arrhythmias and cardiac rupture, increased in proportion to the body temperature increase. 2 Although the peak creatine kinase (CK) level, an indicator of infarct size, was similar, LV end-diastolic and LV end-systolic volumes measured by left ventriculography before discharge had increased and the LV ejection fraction decreased in proportion to the peak body temperature, demonstrating an association between body temperature increase after MI and LV remodeling. 2 Post-MI Inflammation and Infarct ExpansionDuring the acute phase of MI, resident macrophages in the myocardial tissue are activated following neutrophil infiltration into the infarcted region. CD11b/18 on the surface of neutroeft ventricular (LV) remodeling after myocardial infarction (MI) is the process of infarct expansion followed by non-infarct hypertrophy and progressive LV dilation, and is associated with adverse clinical outcomes. Defective infarct healing, as well as infarct size and wall stress, is a major determinant of infarct expansion. A well-orchestrated inflammatory response after MI leads to an appropriate infarct healing process and formation of a scar with tensile strength, preventing infarct expansion. Despite the importance of the inflammatory response and healing process in post-MI LV remodeling, the mechanisms that initiate and control these processes have not been fully elucidated. Numerous clinical and experimental studies have focused on the role of inflammation and its regulatory mechanism as a novel therapeutic target for post-infarction LV remodeling. Increase in Body Temperature and Post-MI ComplicationsThe 4 classical signs of inflammation are dolor, tumor, rubor and calor. It has also been recognized for a long time that body temperature increases after MI, reflecting the development of inflammation after tissue necrosis, but it was believed to be a After myocardial infarction (MI), inflammatory cells such as neutrophils, followed by monocytes and macrophages, infiltrate and phagocytose the necrotic tissues, as well as secreting a variety of inflammatory cytokines. The vulnerable myocardium, which consists of necrotic tissue and inflammatory cells, is susceptible to wall stress, resulting in infarct expansion. Subacute cardiac rupture is an extreme form of infarct expansion, whereas ventricular aneurysm is its chronic form and a trigger for subsequent left ventricular (LV) remodeling. Although post-infarction inflammation...

show abstract

Angiotensin-Receptor Blockade Reduces Border Zone Myocardial Monocyte Chemoattractant Protein-1 Expression and Macrophage Infiltration in Post-Infarction Ventricular Remodeling

Cited by 51 publications

References 43 publications

Tolvaptan Improves Left Ventricular Dysfunction after Myocardial Infarction in Rats

Tolvaptan Improves Left Ventricular Dysfunction after Myocardial Infarction in Rats

Angiotensin II Induces TSLP via an AT1 Receptor/NF-KappaB Pathway, Promoting Th17 Differentiation

Post-Infarction Inflammation and Left Ventricular Remodeling

Contact Info

Product

Resources

About