EMMPRIN mediates β-adrenergic receptor-stimulated matrix metalloproteinase activity in cardiac myocytes

Siwik, Deborah A.; Kuster, Gabriela M.; Brahmbhatt, Jamin; Zaidi, Zaheer; Malik, Julia; Ooi, Henry; Ghorayeb, Ghassan

doi:10.1016/j.yjmcc.2007.07.054

Cited by 53 publications

(38 citation statements)

References 53 publications

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“…35 In addition, it has been reported that cardiomyocytederived Bsg induces MMPs expressions and activities by oxidative stress and β-adrenergic stimuli. 36 These findings indicate important role of cardiomyocyte-derived Bsg in the development of pressure overload-induced cardiac fibrosis and failure. It is important to elucidate the role of BM-derived Bsg for the development of cardiac hypertrophy and fibrosis.…”

Section: Bsg In Cardiac Tissues Promotes Hypertrophy Fibrosis and Hmentioning

confidence: 86%

Basigin Promotes Cardiac Fibrosis and Failure in Response to Chronic Pressure Overload in Mice

Suzuki

Satoh

Ikeda

et al. 2016

ATVB

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Objective— Basigin (Bsg) is a transmembrane glycoprotein that activates matrix metalloproteinases and promotes inflammation. However, the role of Bsg in the pathogenesis of cardiac hypertrophy and failure remains to be elucidated. We examined the role of Bsg in cardiac hypertrophy and failure in mice and humans. Approach and Results— We performed transverse aortic constriction in Bsg +/– and in wild-type mice. Bsg +/– mice showed significantly less heart and lung weight and cardiac interstitial fibrosis compared with littermate controls after transverse aortic constriction. Both matrix metalloproteinase activities and oxidative stress in loaded left ventricle were significantly less in Bsg +/– mice compared with controls. Echocardiography showed that Bsg +/– mice showed less hypertrophy, less left ventricular dilatation, and preserved left ventricular fractional shortening compared with littermate controls after transverse aortic constriction. Consistently, Bsg +/– mice showed a significantly improved long-term survival after transverse aortic constriction compared with Bsg +/+ mice, regardless of the source of bone marrow ( Bsg +/+ or Bsg +/– ). Conversely, cardiac-specific Bsg-overexpressing mice showed significantly poor survival compared with littermate controls. Next, we isolated cardiac fibroblasts and examined their responses to angiotensin II or mechanical stretch. Both stimuli significantly increased Bsg expression, cytokines/chemokines secretion, and extracellular signal–regulated kinase/Akt/JNK activities in Bsg +/+ cardiac fibroblasts, all of which were significantly less in Bsg +/– cardiac fibroblasts. Consistently, extracellular and intracellular Bsg significantly promoted cardiac fibroblast proliferation. Finally, serum levels of Bsg were significantly elevated in patients with heart failure and predicted poor prognosis. Conclusions— These results indicate the crucial roles of intracellular and extracellular Bsg in the pathogenesis of cardiac hypertrophy, fibrosis, and failure in mice and humans.

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Section: Bsg In Cardiac Tissues Promotes Hypertrophy Fibrosis and Hmentioning

confidence: 86%

Basigin Promotes Cardiac Fibrosis and Failure in Response to Chronic Pressure Overload in Mice

Suzuki

Satoh

Ikeda

et al. 2016

ATVB

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“…Basigin has been most extensively investigated with respect to tumor invasion and metastasis, and it has been implicated as a factor contributing to the induction of MMP expression by autocrine or paracrine mechanisms (10,(24)(25)(26). It has been demonstrated that basigin is expressed on cardiac myocytes (13,14), and is involved with the human left ventricle, following acute myocardial infarction, heart failure myocardium and the ventricle of ischemic cardiomyopathies (13,15,18). These results strongly suggested that basigin may be involved in myocardial injury.…”

Section: Discussionmentioning

confidence: 99%

“…Basigin is also involved in tissue remodeling in numerous physiological and pathological conditions. Previously, certain studies have demonstrated that basigin is expressed in cardiac myocytes, but not in cardiac microvascular endothelial cells or cardiac fibroblasts (13,14), and basigin protein expression levels are significantly elevated in acute infarcted myocardium (15,16), destabilizing atheroma (17), human heart failure myocardium (13) and the ventricle of ischemic cardiomyopathy (18). A limited number of studies had investigated the theory that basigin mRNA and protein were expressed in AMI within 1 h. In the present study, we investigated the temporal and spatial expression patterns of basigin in the early phase of AMI during different ischemic periods, as basigin is a known differentially expressed gene potentially related to the early phase of AMI.…”

Section: Introductionmentioning

confidence: 99%

Expression of basigin in the early phase of acute myocardial ischemia in rats

Liu

Liang

Zhang

et al. 2013

Molecular Medicine Reports

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Abstract. Basigin may be involved in cardiovascular disease. In our previous study, suppression subtractive hybridization results indicated that basigin may be associated with the early phase of acute myocardial ischemia (AMI) within 1 h. However, little is known regarding the expression of basigin in the early phase of AMI. The aim of the present study was to evaluate the temporal and spatial expression patterns of basigin mRNA and protein levels in AMI in rats. We constructed an AMI model in rats that received left anterior descending coronary artery ligation for 0, 15, 30, 60, 120 or 240 min. Real-time quantitative PCR and in situ hybridization (ISH) were conducted to reveal the basigin mRNA levels in the early ischemic myocardium (EIM) and non-ischemic myocardium (NIM). The expression levels of basigin protein were detected using western blot analysis and immunohistochemistry. The expression levels of basigin mRNA and protein significantly changed in the EIM as early as 30 min from ischemia, and the changes continued to be present throughout the ischemic period (P<0.05). The expression levels of basigin mRNA were significantly reduced, whilst those of the protein underwent a significant ~2-fold increase in the EIM. However, there were no significant differences in the basigin mRNA or protein expression levels from 0-240 min in the NIM (P>0.05). We failed to detect a signal for basigin mRNA in the myocardium by ISH. Our findings indicated that basigin may be involved in acute myocardial ischemia following continual ischemia for >30 min.

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“…Это уменьшает энергетические затраты и потребление кислорода, связанные с осуществлением насосной функции. Соответственно, при умеренной гипертрофии миокарда, индуцированной путем хронического введения адренергического агониста, его сократительная функция хорошо сохранена или даже повышена [27,28] [33,34]. Данные ферменты осуществляют протеолиз коллагеновых фибрил, образующих поперечные каркасные связи ("сшивку") между соседними пучками мышечных волокон в стенке левого желудочка.…”

Section: сократительная дисфункцияunclassified

Role of Sustained Sympathetic Overactivation in the Development of Structural and Functional Myocardial Changes in Heart Failure

Osadchii¹

2018

Kuban. nauсh. med. vestnik

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АННОТАЦИЯРазвитие сердечной недостаточности сопровождается выраженной активацией симпатической нервной системы, которая изначально осуществляется как компенсаторный эффект, необходимый для поддержания насосной функции сердца. Тем не менее, на долговременной основе, симпатическая активация вызывает ряд негативных структурно-функциональных изменений миокарда, которые способствуют прогрессированию сократительной дисфункции, и определяют неблагоприятный клинический прогноз. Природа данных изменений и их механизмы были изучены с помощью модели сердечной недостаточности, полученной при хроническом введении норадреналина или его аналогов экспериментальным животным. В данной модели aдренергическая активация приводит к гипертрофии сердца в связи с усилением синтеза сократительных белков в кардиомиоцитах, а также вызывает фиброзные изменения миокарда посредством увеличения образования коллагена фибробластами сердца. Параллельно с этим происходит гибель кардиомиоцитов за счет некроза и апоптоза, что связано с их перегрузкой ионами кальция и повреждением митохондрий в результате образования свободнорадикальных форм кислорода. Адренергическая стимуляция повышает активность матриксных протеиназ, которые разрушают коллагеновые связи между пучками мышечных волокон, что вызывает смещение интрамуральных слоев миокарда, и как следствие -дилатацию полости левого желудочка. Чрезмерная адренергическая стимуляция также приводит к истощению запасов катехоламинов в симпатических терминалях сердца, а на клеточном уровне -к выраженным нарушениям кальциевого гомеостаза. К числу последних относится "утечка" кальция из саркоплазматического ретикулума в связи с дисфункцией рианодинового рецептора, а также уменьшение обратного поступления кальция из цитозоля в саркоплазматический ретикулум во время диастолы в результате угнетения Са 2+ АТФазы (SERCA2a). Сочетанное действие этих факторов играет ключевую роль в снижении сократительных резервов сердца. Структурно-функциональные изменения миокарда в условиях хронической активации симпатической нервной системы опосредованы стимуляцией образования ангиотензина II и альдостерона, а также локальных факторов роста, и повышением экспрессии цитокинов. На субклеточном уровне эти изменения реализуются за счет стимуляции митоген-активируемых протеинкиназ, которые в свою очередь активируют гены "раннего ответа", и таким образом инициируют процессы транскрипции, ведущие к увеличению белкового синтеза, образованию новых саркомеров, и их включению в структуру кардиомиоцитов.Ключевые слова: симпатическая активация, структурно-функциональные изменения миокарда, сердечная не-достаточность Для цитирования: Осадчий О.Е. Роль активации симпатической нервной системы в развитии структур-но-функциональных изменений миокарда при сердечной недостаточности. Кубанский научный медицинский вест-ник. 2018; 25(1): 180-188. DOI: 10.25207 / 1608 25(1): 180-188. DOI: 10.25207 / -6228-2018 For citation: Oleg E. Osadchii. Role of sustained sympathetic overactivation in the development of structural and functional myocardial changes...

show abstract

EMMPRIN mediates β-adrenergic receptor-stimulated matrix metalloproteinase activity in cardiac myocytes

Cited by 53 publications

References 53 publications

Basigin Promotes Cardiac Fibrosis and Failure in Response to Chronic Pressure Overload in Mice

Basigin Promotes Cardiac Fibrosis and Failure in Response to Chronic Pressure Overload in Mice

Expression of basigin in the early phase of acute myocardial ischemia in rats

Role of Sustained Sympathetic Overactivation in the Development of Structural and Functional Myocardial Changes in Heart Failure

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