Rapid Ventricular Induction of Brain Natriuretic Peptide Gene Expression in Experimental Acute Myocardial Infarction

Hama, Norio; Itoh, Hiroshi; Shirakami, Gotaro; Nakagawa, Osamu; Suga, Shin Ichi; Ogawa, Yoshihiro; Masuda, Izuru; Nakanishi, Kuniaki; Yoshimasa, Takaaki; Hashimoto, Yoshiaki; Yamaguchi, Masayuki; Hori, Ryusuke; Yasue, Hirofumi; Nakao, Kazuwa

doi:10.1161/01.cir.92.6.1558

Cited by 388 publications

(224 citation statements)

References 38 publications

Supporting

Mentioning

193

Contrasting

Unclassified

Order By: Relevance

“…This paradigm has been previously demonstrated for GC-A signaling via a rapid activation/release of cardiac natriuretic peptides (ANP and B-type natriuretic peptide) after acute myocardial infarction. 41,42 Regardless, the molecular mechanisms underlying the regulation of GC-G under I/R require further elucidation.…”

Section: Discussionmentioning

confidence: 99%

Disruption of Guanylyl Cyclase-G Protects against Acute Renal Injury

Lin

Cheng²,

Hou

et al. 2008

Journal of the American Society of Nephrology

View full text Add to dashboard Cite

The membrane forms of guanylyl cyclase (GC) serve as cell-surface receptors that synthesize the second messenger cGMP, which mediates diverse cellular processes. Rat kidney contains mRNA for the GC-G isoform, but the role of this receptor in health and disease has not been characterized. It was found that mouse kidney also contains GC-G mRNA, and immunohistochemistry identified GC-G protein in the epithelial cells of the proximal tubule and collecting ducts. Six hours after ischemia-reperfusion (I/R) injury, GC-G mRNA and protein expression increased three-fold and remained upregulated at 24 h. For determination of whether GC-G mediates I/R injury, a mutant mouse with a targeted disruption of the GC-G gene (Gucy2g) was created. At baseline, no histologic abnormalities were observed in GC-G Ϫ/Ϫ mice. After I/R injury, elevations in serum creatinine and urea were attenuated in GC-G Ϫ/Ϫ mice compared with wild-type controls, and this correlated with less tubular disruption, less tubular cell apoptosis, and less caspase-3 activation. Measures of inflammation (number of infiltrating neutrophils, myeloperoxidase activity, and induction of IL-6 and P-selectin) and activation of NF-B were lower in GC-G Ϫ/Ϫ mice compared with wild-type mice. Direct transfer of a GC-G expression plasmid to the kidneys of GC-G Ϫ/Ϫ mice resulted in a dramatically higher mortality after renal I/R injury, further supporting a role for GC-G in mediating injury. In summary, GC-G may act as an early signaling molecule that promotes apoptotic and inflammatory responses in I/R-induced acute renal injury.

show abstract

Section: Discussionmentioning

confidence: 99%

Disruption of Guanylyl Cyclase-G Protects against Acute Renal Injury

Lin

Cheng²,

Hou

et al. 2008

Journal of the American Society of Nephrology

View full text Add to dashboard Cite

show abstract

“…We demonstrated that the size of infarct was in fact proportional to the level of NT-proBNP in a high-risk population with a larger extent of muscle at risk for necrosis. Mechanistically, this may relate to the release of presynthesized BNP from necrosing areas, an increase in messenger RNA in peri-infarct myocytes or increased wall stress in the remaining viable peri-infarct myocardium (21). Although no conclusive evidence exists, elevated NT-proBNP may indicate that there is more viable myocardium surrounding the infarct zone, and this elevation in NT-proBNP may portend an increased risk of adverse outcome because the peri-infarct zones are more likely to produce a lethal arrhythmia than noninfarcted tissue or scar tissue.…”

Section: Size Of Infarctmentioning

confidence: 99%

N-terminal pro-brain natriuretic peptide and the timing, extent and mortality in ST elevation myocardial infarction

Théroux

Chang

Mahaffey

et al. 2006

Canadian Journal of Cardiology

View full text Add to dashboard Cite

“…Thus, it takes several hours for the plasma natriuretic peptide levels to increase significantly after the onset of acute myocardial stretch. 15 This process includes myocardial BNP messenger ribonucleic acid (mRNA) synthesis, prohormone synthesis, and prohormone release into the circulation (Figure 1). Similar to cardiac troponins, elevations in BNP and NTproBNP are associated with right ventricular dysfunction in acute PE.…”

Section: Natriuretic Peptidesmentioning

confidence: 99%