Pretreatment with B-type Natriuretic Peptide Protects the Heart From Ischemia-Reperfusion Injury by Inhibiting Myocardial Apoptosis

Wu, Bing; Jiang, Hong; Lin, Rong; Cui, Bo; Wen, Huazhi; Lu, Zhibing

doi:10.1620/tjem.219.107

Cited by 24 publications

(22 citation statements)

References 27 publications

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“…Overall, our results are consistent with previous studies showing that BNP reduces IS [ 4 – 7 ] and improves post-ischemic recovery [ 54 ]. As reported for BNP, the beneficial effect of L2 in acute cardiac ischemia can be related to inhibition of apoptotis [ 3 ], inflammation [ 55 ] and oxidative stress [ 56 ]. Furthermore, IR has been found to markedly decrease myocardial cGMP content in ischemic heart [ 42 ].…”

Section: Resultsmentioning

confidence: 99%

“…This emphasizes need of finding new pharmacological agents capable of preventing ischemia-reperfusion (IR) injury. Recent works indicate that B-type natriuretic peptide (BNP) can attenuate irreversible ischemic injury in man [ 2 ], in vivo animal models [ 3 , 4 ] and in isolated hearts [ 5 – 7 ]. BNP has hypotensive, natriuretic and diuretic properties [ 8 ] and inhibits the sympathetic nervous system and the renin-angiotensin-aldosterone axis [ 9 ] leading to a decrease in pre- and after- load, thus maintaining blood supply to myocardial cells.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Lebetin 2, a Snake Venom-Derived Natriuretic Peptide, Attenuates Acute Myocardial Ischemic Injury through the Modulation of Mitochondrial Permeability Transition Pore at the Time of Reperfusion

et al. 2016

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Cardiac ischemia is one of the leading causes of death worldwide. It is now well established that natriuretic peptides can attenuate the development of irreversible ischemic injury during myocardial infarction. Lebetin 2 (L2) is a new discovered peptide isolated from Macrovipera lebetina venom with structural similarity to B-type natriuretic peptide (BNP). Our objectives were to define the acute cardioprotective actions of L2 in isolated Langendorff-perfused rat hearts after regional or global ischemia-reperfusion (IR). We studied infarct size, left ventricular contractile recovery, survival protein kinases and mitochondrial permeability transition pore (mPTP) opening in injured myocardium. L2 dosage was determined by preliminary experiments at its ability to induce cyclic guanosine monophosphate (cGMP) release without changing hemodynamic effects in normoxic hearts. L2 was found to be as effective as BNP in reducing infarct size after the induction of either regional or global IR. Both peptides equally improved contractile recovery after regional IR, but only L2 increased coronary flow and reduced severe contractile dysfunction after global ischemia. Cardioprotection afforded by L2 was abolished after isatin or 5-hydroxydecanote pretreatment suggesting the involvement of natriuretic peptide receptors and mitochondrial KATP (mitoKATP) channels in the L2-induced effects. L2 also increased survival protein expression in the reperfused myocardium as evidenced by phosphorylation of signaling pathways PKCε/ERK/GSK3β and PI3K/Akt/eNOS. IR induced mitochondrial pore opening, but this effect was markedly prevented by L2 treatment. These data show that L2 has strong cardioprotective effect in acute ischemia through stimulation of natriuretic peptide receptors. These beneficial effects are mediated, at least in part, by mitoKATP channel opening and downstream activated survival kinases, thus delaying mPTP opening and improving IR-induced mitochondrial dysfunction.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Lebetin 2, a Snake Venom-Derived Natriuretic Peptide, Attenuates Acute Myocardial Ischemic Injury through the Modulation of Mitochondrial Permeability Transition Pore at the Time of Reperfusion

et al. 2016

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“…Even if our Sca-1 + cells were not “pure” precursor cells, BNP effect on these cells or on a part of these cells must contribute to its “protective” effect in vivo 16 26 27 28 . In this work, we showed in Supplemental Fig.…”

Section: Discussionmentioning

confidence: 99%

Natriuretic Peptide Receptor B modulates the proliferation of the cardiac cells expressing the Stem Cell Antigen-1

Rignault-Clerc

Bielmann

Liaudet

et al. 2017

Sci Rep

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Brain Natriuretic Peptide (BNP) injections in adult “healthy” or infarcted mice led to increased number of non-myocyte cells (NMCs) expressing the nuclear transcription factor Nkx2.5. The aim of this study was to identify the nature of the cells able to respond to BNP as well as the signaling pathway involved. BNP treatment of neonatal mouse NMCs stimulated Sca-1+ cell proliferation. The Sca-1+ cells were characterized as being a mixed cell population involving fibroblasts and multipotent precursor cells. Thus, BNP treatment led also to increased number of Sca-1+ cells expressing Nkx2.5, in Sca-1+ cell cultures in vitro and in vivo, in the hearts of neonatal and adult infarcted mice. Whereas BNP induced Sca-1+ cell proliferation via NPR-B receptor and protein kinase G activation, CNP stimulated Sca-1+ cell proliferation via NPR-B and a PKG-independent mechanism. We highlighted here a new role for the natriuretic peptide receptor B which was identified as a target able to modulate the proliferation of the Sca-1+ cells. The involvement of NPR-B signaling in heart regeneration has, however, to be further investigated.

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“…Wu et al sho wed that BNP-me di a ted at te nu a ti on of apop to sis was as so ci a ted with in cre a sed ex pres si on of an an ti-apop to tic pro te in Bcl-2 and re du ced expres si on of a pro-apop to tic pro te in Bax. 29 BNP can be con si de red as an an ti-re mo de ling pep ti de and serum BNP le vels sho uld be di rectly pro por ti o nal with the re mo de ling pro cess and LVES VI.…”

Section: Discussionmentioning

confidence: 99%

Amino Terminal Pro-B-Type Natriuretic Peptide and Late Left Ventricular Reverse Remodeling in Coronary Artery Bypass Grafting Patients with Low Ejection Fraction

Hatemi¹,

Gürsoy²,

Işiksungur³

et al. 2011

Turkiye Klinikleri J Med Sci

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A AB BS S T TR RA AC CT T O Ob b j je ec c t ti i v ve e: : Left ven tri cu lar re mo de ling ac ce le ra tes the co ur se of car di ac fa i lu re by aggra va ting ven tri cu lar dysfunc ti on fol lo wing myo car di al in farc ti on. Thus, pre dic ti on and pre ven tion of left ven tri cu lar re mo de ling is cru ci al. The aim of this study was to eva lu a te the pre dic ti ve va lu e of pe ri o pe ra ti ve plas ma NT-proBNP le vels for pos to pe ra ti ve left ven tri cu lar re ver se re mo deling and ejec ti on frac ti on in pa ti ents who un der went co ro nary ar tery bypass graf ting. M Ma a t te e r ri i a al l a an nd d M Me et t h ho od ds s: : Forty pa ti ents with myo car di al in farc ti on inprevious thre e months we re en rol led in the study. All pa ti ents with mo de ra te left ven tri cu lar dysfunc ti on (EF ≤40%) un der went on pump coro nary ar tery bypass graf ting (CABG) ope ra ti on. Pa ti ents' pre o pe ra ti ve left ven tric le vo lu mes and in de xes, ejec ti on frac ti ons, and NT-proBNP le vels we re com pa red to the pos to pe ra ti ve va lu es. R Re e--s su ul lt ts s: : Pre o pe ra ti ve NT-proBNP le vels we re sig ni fi cantly re la ted to pre o pe ra ti ve and pos to pe ra ti ve ejec ti on frac ti ons, and pos to pe ra ti ve left ven tri cu lar re ver se re mo de ling (p= 0.037, p= 0.033, p= 0.014, res pec ti vely). C Co on nc c l lu u s si i o on n: : The pre o pe ra ti ve N-ter mi nal proBNP may help to as sess the pos to pe ra ti ve ejec ti on frac ti on and ven tri cu lar re mo de ling. Ami no ter mi nal proBNP is a sa fe, ava i lable and ef fec ti ve to ol to pre dict the pos to pe ra ti ve func ti o nal and struc tu ral chan ges of the left ven tric le. K Ke ey y W Wo or rd ds s: : Pro-bra in nat ri u re tic pep ti de (1-76); ven tri cu lar re mo de ling; co ro nary ar tery bypass; ec ho car di og raphy; stro ke vo lu me Ö ÖZ ZE ET T A Am ma aç ç: : İnfark tüs son ra sı dö nem de ki sol ven tri kü lün ye ni den şekil len me si (re mo del ling) kalp yet mez li ği ne gö tü ren kö tü prog noz için güç lü bir gös ter ge dir. Bu ça lış ma nın ama cı pe ri o pera tif plaz ma NT-proBNP dü ze yi nin cer ra hi re vas kü la ri zas yon son ra sı sol ven tri kül re vers re model lin gi ve ejek si yon frak si yo nu yö nün den pre dik tif de ğe ri ni in ce le mek tir. G Ge e r re eç ç v ve e Y Yö ön n t te em m l le er r: : Son üç ay için de mi yo kard en fark tü sü ge çi ren ve or ta dü zey de sol ven tri kül (LV) dis fonk si yo nu olan 40 has ta ça lış ma ya alın dı. Bü tün has ta la ra pom pa yar dım lı ko ro ner ar ter bay pas greft le me (CABG) ope ras yo nu ya pıl mış tı. Has ta lar da pre o pe ra tif sol ven tri kül ha cim le ri ve in deks le ri, ejeksi yon frak si yon la rı ve NT-proBNP dü zey le ri pos to pe ra tif de ğer ler le kar şı laş tı rıl dı. B Bu ul l g gu u l la ar r: : Preo pe ra tif NT-ProBNP dü zey le ri pre o pe ra tif ve pos to pe ra tif ejek si yon frak si yon la rı ve pos to pe ra tif sol ven tri kül re vers re mo del ling ile (sı ra sıy la p= 0.037, p= 0.033, p=...

show abstract

Pretreatment with B-type Natriuretic Peptide Protects the Heart From Ischemia-Reperfusion Injury by Inhibiting Myocardial Apoptosis

Cited by 24 publications

References 27 publications

Lebetin 2, a Snake Venom-Derived Natriuretic Peptide, Attenuates Acute Myocardial Ischemic Injury through the Modulation of Mitochondrial Permeability Transition Pore at the Time of Reperfusion

Lebetin 2, a Snake Venom-Derived Natriuretic Peptide, Attenuates Acute Myocardial Ischemic Injury through the Modulation of Mitochondrial Permeability Transition Pore at the Time of Reperfusion

Natriuretic Peptide Receptor B modulates the proliferation of the cardiac cells expressing the Stem Cell Antigen-1

Amino Terminal Pro-B-Type Natriuretic Peptide and Late Left Ventricular Reverse Remodeling in Coronary Artery Bypass Grafting Patients with Low Ejection Fraction

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