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C-reactive protein overexpression exacerbates pressure overload-induced cardiac remodeling through enhanced inflammatory response.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Nagai, Toshiyuki Anzai, Toshihisa Kaneko, H. Hidehiro Mano, Yoshinori Anzai, Atsushi Maekawa, Yuichiro Takahashi, Toshiyuki Meguro, Tomomi Yoshikawa, Tsutomu Fukuda, Keiichi |
| Copyright Year | 2011 |
| Abstract | Serum C-reactive protein (CRP) elevation predicts the development of heart failure in patients with hypertension. CRP activates macrophages and enhances oxidative stress. We hypothesize that CRP itself has a pathogenic role in the development of pressure overload-induced cardiac remodeling. Transgenic mice with human CRP overexpression (CRPtg) and nontransgenic littermates (CON) were subjected to transverse aortic constriction (TAC/CRPtg and TAC/CON) or sham operation (Sham/CRPtg and Sham/CON). One week after operation, in TAC/CRPtg, myocardial mRNA levels of interleukin (IL)-6, CD68, glutathione peroxidase-3 (GPx3), 47-kDa α-subunit of nicotinamide adenine dinucleotide phosphate oxidase (p47(phox)), and collagen-I, the number of infiltrating Mac-2-positive macrophages, nuclear localization of phosphorylated NF-κB/p65 (p-p65) in cardiomyocytes, nuclear NF-κB-DNA-binding activity, and reactive oxygen species (ROS) content were increased compared to those in TAC/CON. Cardiac fibrosis was more prominent in TAC/CRPtg compared to TAC/CON. Four weeks after operation, heart and lung weights, cardiomyocyte cross-sectional area, and the extent of cardiac fibrosis were greater in TAC/CON than in Sham/CON, and these differences were further augmented in TAC/CRPtg compared to TAC/CON. Left ventricular (LV) fractional shortening was less and LV end-diastolic pressure was higher in TAC/CRPtg than in TAC/CON. Myocardial mRNA levels of angiotensin type 1 receptor, atrial natriuretic factor, IL-6, GPx3, p47(phox), collagen-I, and transforming growth factor (TGF)-β1, the protein level of TGF-β1, and the numbers of Mac-2-positive macrophages and p-p65-positive cells were higher in TAC/CRPtg than in TAC/CON. In conclusion, CRP itself may have a pathogenic role in the development of pressure overload-induced cardiac remodeling, possibly through enhanced inflammation and oxidative stress. |
| Starting Page | P281 |
| Ending Page | P281 |
| Page Count | 1 |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | http://hyper.ahajournals.org/content/hypertensionaha/early/2011/01/10/HYPERTENSIONAHA.110.158915.full.pdf |
| PubMed reference number | 21220701v1 |
| Alternate Webpage(s) | https://doi.org/10.1161/HYPERTENSIONAHA.110.158915 |
| DOI | 10.1161/hypertensionaha.110.158915 |
| Journal | Hypertension |
| Volume Number | 57 |
| Issue Number | 2 |
| Language | English |
| Access Restriction | Open |
| Subject Keyword | Adenine Angiotensins Atrial Natriuretic Factor C-reactive protein Carbamoyl-Phosphate Synthase I Deficiency Disease Cardiopulmonary Diastole Diastolic blood pressure Dinucleoside Phosphates Fibrosis Glutathione Heart Atrium Heart failure Hypertensive disease Infiltration Interleukins Myocytes, Cardiac NADP Natriuretic Hormones Niacin Oxidative Stress Patients Protein Overexpression Reactive Oxygen Species Receptor, Angiotensin, Type 1 Structure of parenchyma of lung Tacrolimus Transforming Growth Factors Weight inflammatory response |
| Content Type | Text |
| Resource Type | Article |
