Neuroendocrine Profiling of Humans Receiving Cardiac Allografts

Ogawa, Tsuneo; Veinot, John P.; Davies, Ross A.; Haddad, Haissam; Smith, Stuart J.; Masters, Roy G.; Hendry, Paul; Starling, Randall C.; Bold, Mercedes L. Kuroski de; Ponce, Amalia; Kenneth, K.; Williams, Kathryn; Bold, Adolfo J. de

doi:10.1016/j.healun.2004.06.023

Cited by 43 publications

(45 citation statements)

References 25 publications

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“…The elevation of plasma BNP levels found in EAM rats in the absence of changes in plasma ANF levels in these investigations is similar to that reported previously by our laboratory in episodes of acute cardiac allograft rejection in humans (15,18). Separate quantifications of heart chambers were carried because our laboratory has shown previously that changes in ANF and BNP gene expression may occur in a chamberspecific manner (26).…”

Section: Discussionsupporting

confidence: 87%

“…In humans, increased circulating BNP during cardiac allograft rejection does not correlate with right atrial pressure, pulmonary artery pressure, pulmonary capillary wedge pressure, or cardiac index (18). Additionally, IL-1␤ and TNF-␣ increase the secretion and expression of BNP but not of ANF in neonatal rat cardiocyte culture (13) in the absence of any mechanical stimulus.…”

Section: Discussionmentioning

confidence: 91%

“…RNA from tissue samples (n ϭ 4, each chamber, each group) was extracted using TRIzol (GIBCO) following manufacturer's instructions. RT was performed with SuperScript II Reverse Transcriptase (Invitrogen) using oligo(dT) [12][13][14][15][16][17][18] (Invitrogen) according to the manufacturer's instruction. Real-time PCR was performed using a LightCycler FastStart DNA Master SYBR Green I (Roche) according to the manufacturer's instruction.…”

Section: Methodsmentioning

confidence: 99%

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Angiotensin II receptor antagonism reverts the selective cardiac BNP upregulation and secretion observed in myocarditis

Ogawa

Veinot²,

Bold³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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The cardiac natriuretic peptides atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP) are discoordinately regulated in myocardial inflammation associated with acute allograft rejection in humans and during in vitro exposure of cardiocyte cultures to some proinflammatory cytokines. We used experimental autoimmune myocarditis (EAM) to determine whether the discoordinate regulation of ANF and BNP was specific to the situations above or was generally associated with other types of myocardial inflammation. The dependency of this process to angiotensin signaling was also determined, given that previous work demonstrated beneficial effects of the angiotensin receptor blocker olmesartan in myocarditis. Histopathological changes, plasma and cardiac ANF, BNP, and selected cytokines gene expression as well as plasma cytokine levels using a cytokine array were determined in EAM, angiotensin receptor blocker-treated, and control rats. It was found that EAM specifically increases BNP but not ANF circulating levels, thus mimicking the findings in acute cardiac allograft rejection and the effect of some proinflammatory cytokines on cardiocyte cultures in vitro. Plasma cytokine array and real-time PCR revealed that lipopolysaccharide-induced CXC chemokine, monocyte chemotactic protein-1, and tissue inhibitor of metalloproteinase-1 were increased in plasma and in the myocardium of EAM rats. Olmesartan treatment reversed virtually all neuroendocrine and histopathological cardiac changes induced by EAM, thus providing a mechanistic insight into this phenomenon. It is concluded that the inflammatory process contributes specific cytokines, leading to the disregulation of cardiac ANF and BNP production observed during myocardial inflammation, and that this process is angiotensin receptor 1 dependent. cytokines; brain natriuretic peptide; atrial natriuretic factor THE NATRIURETIC PEPTIDES atrial natriuretic factor (ANF; and atrial natriuretic peptide) and brain natriuretic peptide (BNP) are cardiac hormones that increase in blood in pathophysiological states such as arterial hypertension and chronic congestive heart failure (17, 26). However, we previously found that during an acute cardiac allograft rejection episode in humans, plasma BNP may be elevated above prerejection levels independent of hemodynamic parameters, whereas plasma ANF levels did not change in unison with BNP. Successful treatment of the acute rejection episode reversed the increased circulating BNP, suggesting that cytokines released from activated T lymphocytes may stimulate BNP secretion from cardiocytes (15).In support of this view, we found that the conditioned medium derived from a mixed lymphocyte reaction, an in vitro model of transplantation immunity, stimulates BNP mRNA content and BNP secretion in rat neonatal cardiocyte cultures but did not produce similar changes in ANF gene expression or secretion (13). It was further determined that proinflammatory cytokines, such as IL-1␤ and TNF-␣, specifically stimulated BNP mRNA and BNP secretion in ...

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Section: Discussionsupporting

confidence: 87%

Section: Discussionmentioning

confidence: 91%

Section: Methodsmentioning

confidence: 99%

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Angiotensin II receptor antagonism reverts the selective cardiac BNP upregulation and secretion observed in myocarditis

Ogawa

Veinot²,

Bold³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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“…However, other groups did not ¢nd any signi¢cant relationship between cTnT and the rejection grade of a cardiac transplantation. 9,10 Therefore, further investigations are still necessary in order to elucidate the potential utility of cTnT as a marker of the rejection grade in speci¢c groups of transplanted patients.…”

Section: Introductionmentioning

confidence: 99%

N-Terminal pro-Brain natriuretic peptide as a potential non-invasive marker of cardiac transplantation rejection

Avello

Molina

Llorente³

et al. 2007

Ann Clin Biochem

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“…Thus, circulating BNP, but not ANF, increased during acute rejection episodes. [1][2][3][4][5] In investigating this finding we found that the pro-inflammatory cytokines interleukin-1␤ (IL-1␤) and tumor necrosis factor-␣ (TNF-␣) had a selective, highly significant upregulating effect on gene expression and promoter activity and on secretion of BNP in cultures of cardiocytes derived from neonatal rat hearts. No other pro-inflammatory cytokine tested had a similar effect.…”

mentioning

confidence: 99%

Relationship Between Natriuretic Peptides and Inflammation: Proteomic Evidence Obtained During Acute Cellular Cardiac Allograft Rejection in Humans

Meirovich

Veinot

Bold

et al. 2008

The Journal of Heart and Lung Transplantation

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Neuroendocrine Profiling of Humans Receiving Cardiac Allografts

Cited by 43 publications

References 25 publications

Angiotensin II receptor antagonism reverts the selective cardiac BNP upregulation and secretion observed in myocarditis

Angiotensin II receptor antagonism reverts the selective cardiac BNP upregulation and secretion observed in myocarditis

N-Terminal pro-Brain natriuretic peptide as a potential non-invasive marker of cardiac transplantation rejection

Relationship Between Natriuretic Peptides and Inflammation: Proteomic Evidence Obtained During Acute Cellular Cardiac Allograft Rejection in Humans

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