Heme oxygenase-1 overexpression exacerbates heart failure with aging and pressure overload but is protective against isoproterenol-induced cardiomyopathy in mice

Allwood, Melissa A.; Kinobe, Robert T.; Ballantyne, Laurel L.; Romanova, Nadya; Melo, Luis G.; Ward, Christopher A.; Brunt, Keith R.; Simpson, Jeremy A.

doi:10.1016/j.carpath.2014.03.007

Cited by 30 publications

(21 citation statements)

References 43 publications

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“…It is widely considered to be cyto-protective, since chemical induction of HO-1 attenuates obesity and diabetes [41,42]. In contrast, several studies have identified pathological effects of its celltype specific deletion [17] as well as of its overexpression [43]. The role of HO-1 in bone is also controversial.…”

Section: Discussionmentioning

confidence: 96%

MicroRNA-183 increases osteoclastogenesis by repressing heme oxygenase-1

Sul

Rajasekaran

et al. 2015

Bone

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Section: Discussionmentioning

confidence: 96%

MicroRNA-183 increases osteoclastogenesis by repressing heme oxygenase-1

Sul

Rajasekaran

et al. 2015

Bone

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“…; Allwood et al . ). HMOX‐derived carbon monoxide is a potent vasodilator, similar to NO, and is involved in regulating vascular tone (Thorup et al .…”

Section: Discussionmentioning

confidence: 97%

“…The results of the present study demonstrate that both moderate and severe hypoxia are associated with corresponding increases in HMOX1 mRNA and protein. HMOX1 is an inducible enzyme responsible for catabolizing haeme into ferrous iron, biliverdin and carbon monoxide Brunt et al 2009;Allwood et al 2014). HMOX-derived carbon monoxide is a potent vasodilator, similar to NO, and is involved in regulating vascular tone (Thorup et al 1999).…”

Section: Discussionmentioning

confidence: 99%

Moderate and severe hypoxia elicit divergent effects on cardiovascular function and physiological rhythms

Allwood

Edgett

Eadie

et al. 2018

The Journal of Physiology

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Hypoxia is both a consequence and cause of many acute and chronic diseases. Severe hypoxia causes hypertension with cardiovascular sequelae; however, the rare studies using moderate severities of hypoxia indicate that it can be beneficial, suggesting that hypoxia may not always be detrimental. Comparisons between studies are difficult because of the varied classifications of hypoxic severities, methods of delivery and use of anaesthetics. Thus, to investigate the long-term effects of moderate hypoxia on cardiovascular health, radiotelemetry was used to obtain in vivo physiological measurements in unanaesthetized mice during 24 h of either moderate or severe hypoxia, followed by 72 h of normoxic recovery. Systolic blood pressure was decreased during recovery following moderate hypoxia but increased following severe hypoxia. Moderate and severe hypoxia increased haeme oxygenase-1 expression during recovery, suggesting parity in hypoxic stress at the level of the artery. Severe but not moderate hypoxia increased the low/high frequency ratio of heart rate variability 72 h post-hypoxia, indicating a shift in sympathovagal balance. Moderate hypoxia dampened the amplitude of circadian rhythm, whereas severe disrupted rhythm during the entire insult, with perturbations persisting throughout normoxic recovery. Thus, hypoxic severity differentially regulates circadian blood pressure.

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“…Transverse aortic constriction was performed as previously described (4). In brief, 9-wk-old mice (ϳ35 g body wt) were anesthetized with a minimum alveolar concentration (MAC) of 5% isoflurane in 100% O 2 and were maintained in the surgical plane of anesthesia with a MAC of 2% isoflurane in 100% O2.…”

Section: Methodsmentioning

confidence: 99%

Dissecting the role of the myofilament in diaphragm dysfunction during the development of heart failure in mice

Gillis

Klaiman

Foster

et al. 2016

American Journal of Physiology-Heart and Circulatory Physiology

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Gillis TE, Klaiman JM, Foster A, Platt MJ, Huber JS, Corso MY, Simpson JA. Dissecting the role of the myofilament in diaphragm dysfunction during the development of heart failure in mice. Am J Physiol Heart Circ Physiol 310: H572-H586, 2016. First published December 23, 2015 doi:10.1152/ajpheart.00773.2015.-Dyspnea and reduced exercise capacity, caused, in part, by respiratory muscle dysfunction, are common symptoms in patients with heart failure (HF). However, the etiology of diaphragmatic dysfunction has not been identified. To investigate the effects of HF on diaphragmatic function, models of HF were surgically induced in CD-1 mice by transverse aortic constriction (TAC) and acute myocardial infarction (AMI), respectively. Assessment of myocardial function, isolated diaphragmatic strip function, myofilament force-pCa relationship, and phosphorylation status of myofilament proteins was performed at either 2 or 18 wk postsurgery. Echocardiography and invasive hemodynamics revealed development of HF by 18 wk postsurgery in both models. In vitro diaphragmatic force production was preserved in all groups while morphometric analysis revealed diaphragmatic atrophy and fibrosis in 18 wk TAC and AMI groups. Isometric force-pCa measurements of myofilament preparations revealed reduced Ca 2ϩ sensitivity of force generation and force generation at half-maximum and maximum Ca 2ϩ activation in 18 wk TAC. The rate of force redevelopment (k tr) was reduced in all HF groups at high levels of Ca 2ϩ activation. Finally, there were significant changes in the myofilament phosphorylation status of the 18 wk TAC group. This includes a decrease in the phosphorylation of troponin T, desmin, myosin light chain (MLC) 1, and MLC 2 as well as a shift in myosin isoforms. These results indicate that there are multiple changes in diaphragmatic myofilament function, which are specific to the type and stage of HF and occur before overt impairment of in vitro force production.calcium-activated force generation; diaphragm function; heart failure; myofilament proteins; protein phosphorylation HEART FAILURE (HF) is a global health problem and is one of the most prevalent causes of morbidity in all ages (15,46). Patients with HF are frequently limited in their daily activities by dyspnea and exertional fatigue. One potential cause is inspiratory muscle (primarily the diaphragm) dysfunction. De Troyer and colleagues (11) first noted compromised inspiratory muscle function in patients with cardiac dysfunction. Respiratory muscle dysfunction is now considered a salient feature of patients (11,21,23,35,36,62) and animals (7-9, 24, 28, 53, 58) with HF. Currently, little is known about the development of respiratory muscle dysfunction during the early onset of HF.In patients with HF, eupneic pressure generation is increased (28, 58), which is considered to impose a stress on the diaphragm. This chronic workload on the diaphragm is thought to overwork the muscle leading to development of a myopathy characterized by a shift in fiber type, atrophy, and co...

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Heme oxygenase-1 overexpression exacerbates heart failure with aging and pressure overload but is protective against isoproterenol-induced cardiomyopathy in mice

Cited by 30 publications

References 43 publications

MicroRNA-183 increases osteoclastogenesis by repressing heme oxygenase-1

MicroRNA-183 increases osteoclastogenesis by repressing heme oxygenase-1

Moderate and severe hypoxia elicit divergent effects on cardiovascular function and physiological rhythms

Dissecting the role of the myofilament in diaphragm dysfunction during the development of heart failure in mice

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