Zinc deficiency exacerbates while zinc supplement attenuates cardiac hypertrophy in high-fat diet-induced obese mice through modulating p38 MAPK-dependent signaling

Wang, Shudong; Luo, Manyu; Zhang, Zhiguo; Gu, Junlian; Chen, Jing; Payne, Kristen Mc Clung; Tan, Yi; Wang, Yuehui; Xia, Yin; Zhang, Xiang; Liu, Gilbert C.; Wintergerst, Kupper A.; Liu, Quan; Zheng, Yang; Cai, Lu

doi:10.1016/j.toxlet.2016.06.020

Cited by 32 publications

(33 citation statements)

References 48 publications

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“…Overall, decreased NO bioavailability with increased production of reactive nitrogen species as reported in animal and human studies of diabetes, supports a role for platelets in diabetes-induced endothelial and pulmonary injury (Figure 3). Studies in our laboratory have previously shown that genetically-induced antioxidant pathways, such as metallothionein (MT) or Nrf 2 (nuclear factor erythroid-related factor 2) overexpression, or pharmacological induction of these pathways by zinc administration (to induce MT) or sulforaphane (to induce Nrf2) alleviate DM-induced cardiac inflammation oxidative stress and fibrosis [2,84,85,86,87,88,89]. Ongoing similar studies are in progress in our laboratory to determine the role of this pathway in inducing platelet hyperreactivity and DM-induced lung fibrosis.…”

Section: Putative Signaling Mediating Diabetes-induced Microvasculmentioning

confidence: 99%

Diabetic Microvascular Disease and Pulmonary Fibrosis: The Contribution of Platelets and Systemic Inflammation

Jagadapillai

Rane

Lin

et al. 2016

IJMS

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Diabetes is strongly associated with systemic inflammation and oxidative stress, but its effect on pulmonary vascular disease and lung function has often been disregarded. Several studies identified restrictive lung disease and fibrotic changes in diabetic patients and in animal models of diabetes. While microvascular dysfunction is a well-known complication of diabetes, the mechanisms leading to diabetes-induced lung injury have largely been disregarded. We described the potential involvement of diabetes-induced platelet-endothelial interactions in perpetuating vascular inflammation and oxidative injury leading to fibrotic changes in the lung. Changes in nitric oxide synthase (NOS) activation and decreased NO bioavailability in the diabetic lung increase platelet activation and vascular injury and may account for platelet hyperreactivity reported in diabetic patients. Additionally, the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway has been reported to mediate pancreatic islet damage, and is implicated in the onset of diabetes, inflammation and vascular injury. Many growth factors and diabetes-induced agonists act via the JAK/STAT pathway. Other studies reported the contribution of the JAK/STAT pathway to the regulation of the pulmonary fibrotic process but the role of this pathway in the development of diabetic lung fibrosis has not been considered. These observations may open new therapeutic perspectives for modulating multiple pathways to mitigate diabetes onset or its pulmonary consequences.

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Section: Putative Signaling Mediating Diabetes-induced Microvasculmentioning

confidence: 99%

Diabetic Microvascular Disease and Pulmonary Fibrosis: The Contribution of Platelets and Systemic Inflammation

Jagadapillai

Rane

Lin

et al. 2016

IJMS

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“…Volume Pressure Recording (VPR) sensor technology for tail‐cuff, presently one of the most widely used, was validated by Feng et al 10. It is commonly cited that they found negligible difference between telemetry and the VPR systems,25, 26 despite an apparent difference in individual recordings or lack of consistent results across the whole range of blood pressure recordings.…”

Section: Introductionmentioning

confidence: 99%

Tail‐Cuff Technique and Its Influence on Central Blood Pressure in the Mouse

Wilde

Aubdool

Thakore

et al. 2017

JAHA

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BackgroundReliable measurement of blood pressure in conscious mice is essential in cardiovascular research. Telemetry, the “gold‐standard” technique, is invasive and expensive and therefore tail‐cuff, a noninvasive alternative, is widely used. However, tail‐cuff requires handling and restraint during measurement, which may cause stress affecting blood pressure and undermining reliability of the results.Methods and ResultsC57Bl/6J mice were implanted with radio‐telemetry probes to investigate the effects of the steps of the tail‐cuff technique on central blood pressure, heart rate, and temperature. This included comparison of handling techniques, operator's sex, habituation, and influence of hypertension induced by angiotensin II. Direct comparison of measurements obtained by telemetry and tail‐cuff were made in the same mouse. The results revealed significant increases in central blood pressure, heart rate, and core body temperature from baseline following handling interventions without significant difference among the different handling technique, habituation, or sex of the investigator. Restraint induced the largest and sustained increase in cardiovascular parameters and temperature. The tail‐cuff readings significantly underestimated those from simultaneous telemetry recordings; however, “nonsimultaneous” telemetry, obtained in undisturbed mice, were similar to tail‐cuff readings obtained in undisturbed mice on the same day.ConclusionsThis study reveals that the tail‐cuff technique underestimates the core blood pressure changes that occur simultaneously during the restraint and measurement phases. However, the measurements between the 2 techniques are similar when tail‐cuff readings are compared with telemetry readings in the nondisturbed mice. The differences between the simultaneous recordings by the 2 techniques should be recognized by researchers.

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“…In fact, many researchers have realized the association of mitogen-activated protein kinase (MAPK) involvement during DCM development. MAPK signaling pathways, such as extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal protein kinase (JNK) and p38 MAP kinase, are demonstrated to be actively involved in myocardial dysfunction [9,10], hypertrophy [11,12,13], fibrosis [14,15,16] and heart failure [17,18,19]. As one MAPK family member, ERK1/2 has been known to be involved in cardiac hypertrophy [20,21].…”

Section: Introductionmentioning

confidence: 99%

The Role of ERK1/2 in the Development of Diabetic Cardiomyopathy

Sun

Tong

et al. 2016

IJMS

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Diabetes mellitus is a chronic metabolic condition that affects carbohydrate, lipid and protein metabolism and may impair numerous organs and functions of the organism. Cardiac dysfunction afflicts many patients who experience the oxidative stress of the heart. Diabetic cardiomyopathy (DCM) is one of the major complications that accounts for more than half of diabetes-related morbidity and mortality cases. Chronic hyperglycemia and hyperlipidemia from diabetes mellitus cause cardiac oxidative stress, endothelial dysfunction, impaired cellular calcium handling, mitochondrial dysfunction, metabolic disturbances, and remodeling of the extracellular matrix, which ultimately lead to DCM. Although many studies have explored the mechanisms leading to DCM, the pathophysiology of DCM has not yet been fully clarified. In fact, as a potential mechanism, the associations between DCM development and mitogen-activated protein kinase (MAPK) activation have been the subjects of tremendous interest. Nonetheless, much remains to be investigated, such as tissue- and cell-specific processes of selection of MAPK activation between pro-apoptotic vs. pro-survival fate, as well as their relation with the pathogenesis of diabetes and associated complications. In general, it turns out that MAPK signaling pathways, such as extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal protein kinase (JNK) and p38 MAP kinase, are demonstrated to be actively involved in myocardial dysfunction, hypertrophy, fibrosis and heart failure. As one of MAPK family members, the activation of ERK1/2 has also been known to be involved in cardiac hypertrophy and dysfunction. However, many recent studies have demonstrated that ERK1/2 signaling activation also plays a crucial role in FGF21 signaling and exerts a protective environment of glucose and lipid metabolism, therefore preventing abnormal healing and cardiac dysfunction. The duration, extent, and subcellular compartment of ERK1/2 activation are vital to differential biological effects of ERK1/2. Moreover, many intracellular events, including mitochondrial signaling and protein kinases, manipulate signaling upstream and downstream of MAPK, to influence myocardial survival or death. In this review, we will summarize the roles of ERK1/2 pathways in DCM development by the evidence from current studies and will present novel opinions on “differential influence of ERK1/2 action in cardiac dysfunction, and protection against myocardial ischemia-reperfusion injury”.

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Zinc deficiency exacerbates while zinc supplement attenuates cardiac hypertrophy in high-fat diet-induced obese mice through modulating p38 MAPK-dependent signaling

Cited by 32 publications

References 48 publications

Diabetic Microvascular Disease and Pulmonary Fibrosis: The Contribution of Platelets and Systemic Inflammation

Diabetic Microvascular Disease and Pulmonary Fibrosis: The Contribution of Platelets and Systemic Inflammation

Tail‐Cuff Technique and Its Influence on Central Blood Pressure in the Mouse

The Role of ERK1/2 in the Development of Diabetic Cardiomyopathy

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