Expression of Heme Oxygenase-1 in Response to Myocardial Infarction in Rats

2002 ◽  
Vol 34 (10) ◽  
pp. 1357-1365 ◽  
Author(s):  
Päivi Lakkisto ◽  
Eeva Palojoki ◽  
Tom Bäcklund ◽  
Antti Saraste ◽  
Ilkka Tikkanen ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heme Oxygenase ◽  
Heme Oxygenase 1

Stimulation of haematopoiesis in murine model of myocardial infarction. Role of heme oxygenase 1

2016 ◽  
Vol 33 ◽  
pp. S77-S78
Author(s):  
Mateusz Tomczyk ◽  
Krzysztof Szade ◽  
Izabela Kraszewska ◽  
Karolina Bukowska-Strakova ◽  
Alicja Józkowicz ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heme Oxygenase ◽  
Murine Model ◽  
Heme Oxygenase 1 ◽  
Stimulation Of

Heme oxygenase-1 induction protects the heart and modulates cellular and extracellular remodelling after myocardial infarction in rats

2011 ◽  
Vol 236 (12) ◽  
pp. 1437-1448 ◽  
Author(s):  
Päivi Lakkisto ◽  
Juha-Matti Siren ◽  
Ville Kytö ◽  
Hanna Forsten ◽  
Mika Laine ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heme Oxygenase ◽  
Heme Oxygenase 1

scholarly journals Effects of heme oxygenase-1 upregulation on isoproterenol-induced myocardial infarction

2019 ◽  
Vol 23 (3) ◽  
pp. 203 ◽  
Author(s):  
Somaia A.G. Eltobshy ◽  
Abdelaziz M. Hussein ◽  
Asaad A. Elmileegy ◽  
Mona H. Askar ◽  
Yomna Khater ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heme Oxygenase ◽  
Heme Oxygenase 1

Abstract 648: Heme-oxygenase-1 Gene Expression Ameliorates Cardiac Dysfunction Following Myocardial Infarction In C57 Mice By Recruitment Of Angiogenic Factors And Angiogenesis In C57 Mice

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
David Sacerdoti ◽  
Sumit R Monu ◽  
Paola Pesce ◽  
Stephen J Peterson ◽  
Komal Sodhi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Myocardial Infarction ◽  
Cardiac Function ◽  
Heme Oxygenase ◽  
Angiogenic Factors ◽  
Heme Oxygenase 1 ◽  
Artery Ligation ◽  
Capillary Formation ◽  
Beneficial Effects ◽  
Angiogenic Proteins

Rational: Angiogenesis is essential in order to increase blood circulation in infarcted tissue of MI (Myocardial infarction). Increased Heme-Oxygenase (HO)-1 gene expression increases angiogenic proteins, e.g. VEGF, bFGF, EGF, angiopoietin and adiponectin. Objective: To investigate whether increased levels of HO-1, after the occurrence of a MI, improves angiogenesis and capillary formation in ischemic myocardium, thereby improving cardiac function. METHODS: Experimental MI was induced by LAD (Left anterior descending artery) ligation. C57BL6 mice were divided into 4 groups: Sham; MI; 5 days after MI treated with the HO-1 inducer, cobalt protoporphyrinIX (CoPP); and, CoPP in the presence of the HO activity inhibitor, Stannous Mesoporphyrin (SnMP). HO-1 downstream signaling proteins were determined including VEGF, CD31 and adiponectin. Echocardiography was performed weekly for 4 weeks after surgery. Results: 5 days after MI, CoPP treatment significantly increased VEGF (p<0.05 vs.MI), CD31 (p<0.05 vs.MI), and adiponectin levels (p<0.05 vs.MI). These findings were associated with a significant increase in capillary formation and blood flow in CoPP-treated animals (p<0.05 vs.MI). Echocardiography showed that left ventricle dilatation, measured as end diastolic area (EDA), was significantly reduced in CoPP- treated animals compared to MI groups (EDA: MI: 0.216±0.02cm2; MI+CoPP: 0.172±0.03 cm2; (-13%) p<0.01). This was associated with a significant decrease in apoptosis and fibrosis (P<0.05). These beneficial effects were reversed by SnMP administration. Conclusion: HO-1 improved cardiac function and enhanced angiogenesis via the recruitment of pro-angiogenic factors.

Abstract 395: Heme Oxygenase-1-mediated PPARd Improves Cardiac Fibrosis and Inflammation in SCID Mice via Induction of T Reg Cells

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Robert Touchon ◽  
Ellen Thompson ◽  
Komal Sodhi ◽  
Nitin Puri ◽  
Gaia Favero ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heme Oxygenase ◽  
Cardiac Fibrosis ◽  
Treg Cells ◽  
Scid Mice ◽  
Heme Oxygenase 1 ◽  
Coronary Artery Ligation ◽  
Cardiac Tissues ◽  
Renal Vasoconstriction ◽  
Immunosuppressed Mice

Introduction: Post-infarcted cardiac failure is the consequence of pathological remodeling after myocardial infarction (MI). A subtype of T lymphocytes, regulatory T (Treg) cells play an important role in improving cardiac function after MI via inhibition of inflammation and direct protection of cardiomyocytes. Heme oxygenase (HO)-1 induction improves heart function after ischemic damage by its anti-inflammatory, anti-oxidative and anti-fibrotic effects. To assess the role of Treg cells in post infarcted myocardium and on renal arteriolar vasoconstriction in immunosuppressed mice via the interplay of HO-1-PPAR δ axis. Methods: We examined the effect of HO-1 induction on post-ischemic heart failure induced by left anterior descending coronary artery ligation, in T-lymphocyte immunosuppressive (BALB SCID) mice. Mice were divided into 4 groups: sham, myocardial infarction (MI), MI treated with the HO-1 inducer cobalt protoporphyrin (CoPP) with and without the HO activity inhibitor stannous mesoporphyrin (SnMP). Thirty days after surgery all mice underwent cardiac and renal Doppler sonography. Cardiac fibrosis and necrosis were analyzed and densitometry analysis of HO-1, PPAR δ and thromboxane synthase (TxA2) in cardiac tissues was done. Results: Mice with MI had increased levels of cardiac fibrosis and necrosis (p<0.05) compared to sham operated controls. Echocardiography showed that fractional area shortening (FAS) was increased in the CoPP−MI group compared to the MI group (p<0.01). Renal pulsatiltiy index was increased in the MI group compared to the sham operated group (sham 0.72 ±0.08, MI 1.37±0.37, p<0.05). CoPP improved renal vasoconstriction as compared to the MI group (p<0.05). Increased expression of HO-1, PPAR-δ, pAMPK and pAKT and decreased expression of TxA2 was detected in cardiac tissues in CoPP-treated animals (p<0.02) as compared to the MI group. All these beneficial effects were reversed by SnMP. Conclusion: Upregulation of HO-1 attenuates post myocardial fibrosis and inflammation and renal vasoconstriction in immunosuppressed mice via recruitment of Treg lymphocytes and PPAR delta activation.

Hsp60 and heme oxygenase-1 (Hsp32) in acute myocardial infarction

2011 ◽  
Vol 157 (5) ◽  
pp. 285-292 ◽  
Author(s):  
Giuseppina Novo ◽  
Francesco Cappello ◽  
Manfredi Rizzo ◽  
Giovanni Fazio ◽  
Sabrina Zambuto ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Heme Oxygenase ◽  
Heme Oxygenase 1

Preemptive heme oxygenase-1 gene delivery reveals reduced mortality and preservation of left ventricular function 1 yr after acute myocardial infarction

2007 ◽  
Vol 293 (1) ◽  
pp. H48-H59 ◽  
Author(s):  
Xiaoli Liu ◽  
Jeremy A. Simpson ◽  
Keith R. Brunt ◽  
Christopher A. Ward ◽  
Sean R. R. Hall ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Gene Delivery ◽  
Heme Oxygenase ◽  
Left Ventricular ◽  
Heme Oxygenase 1 ◽  
Term Survival ◽  
Long Term Survival ◽  
Lv Remodeling

We reported previously that predelivery of heme oxygenase-1 (HO-1) gene to the heart by adeno-associated virus-2 (AAV-2) markedly reduces ischemia and reperfusion (I/R)-induced myocardial injury. However, the effect of preemptive HO-1 gene delivery on long-term survival and prevention of postinfarction heart failure has not been determined. We assessed the effect of HO-1 gene delivery on long-term survival, myocardial function, and left ventricular (LV) remodeling 1 yr after myocardial infarction (MI) using echocardiographic imaging, pressure-volume (PV) analysis, and histomorphometric approaches. Two groups of Lewis rats were injected with 2 × 1011 particles of AAV-LacZ (control) or AAV-human HO-1 (hHO-1) in the anterior-posterior apical region of the LV wall. Six weeks after gene transfer, animals were subjected to 30 min of ischemia by ligation of the left anterior descending artery followed by reperfusion. Echocardiographic measurements and PV analysis of LV function were obtained at 2 wk and 12 mo after I/R. One year after acute MI, mortality was markedly reduced in the HO-1-treated animals compared with the LacZ-treated animals. PV analysis demonstrated significantly enhanced LV developed pressure, elevated maximal dP/d t, and lower end-diastolic volume in the HO-1 animals compared with the LacZ animals. Echocardiography showed a larger apical anterior-to-posterior wall ratio in HO-1 animals compared with LacZ animals. Morphometric analysis revealed extensive myocardial scarring and fibrosis in the infarcted LV area of LacZ animals, which was reduced by 62% in HO-1 animals. These results suggest that preemptive HO-1 gene delivery may be useful as a therapeutic strategy to reduce post-MI LV remodeling and heart failure.

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