Time-dependent changes of decorin in the infarct zone after experimentally induced myocardial infarction in rats: Comparison with biglycan

Doi, Masayuki; Kusachi, Shozo; Murakami, Takashi; Ninomiya, Yoshifumi; Murakami, Masahirô; Nakahama, Makoto; Takeda, Kenji; Komatsubara, Issei; Naito, Ichiro; Tsuji, Takao

doi:10.1016/s0344-0338(00)80018-7

Cited by 28 publications

(24 citation statements)

References 22 publications

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“…10,11 Interestingly, the upregulation was transient, peaking at 7 days, at the same time that collagen content also is highest. 2 Using immunohistochemistry, we found biglycan in the infarct scar and border zone of the infarct at 7 and 14 days after MI, in line with a role of biglycan in collagen remodeling.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, at 7 days after MI, fibroblasts and inflammatory cells were detected in areas enriched with biglycan (online Data Supplement), in line with previous results in rats. 10,11 At 14 days after MI, bgn mRNA levels were still 5-fold higher than in sham animals ( Figure 1A), and biglycan immunostaining was still increased in the infarct and peri-infarct zones ( Figure 1D). …”

Section: Increased Biglycan Expression After MImentioning

confidence: 96%

“…It has been reported previously that biglycan and decorin are induced after MI in rats and that biglycan associates with cardiac fibroblasts in the infarcted myocardium. 10,11 bgn Ϫ/0 mice have reduced skeletal growth and develop an osteoporosis-like phenotype resulting from a defect in bone formation. 12 Furthermore, the diameter of collagen fibrils was reduced in bgn Ϫ/0 mice.…”

Section: Clinical Perspective P 1276mentioning

confidence: 99%

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Biglycan Is Required for Adaptive Remodeling After Myocardial Infarction

Westermann

Mersmann²,

Melchior³

et al. 2008

Circulation

112

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Background-After myocardial infarction (MI), extensive remodeling of extracellular matrix contributes to scar formation and preservation of hemodynamic function. On the other hand, adverse and excessive extracellular matrix remodeling leads to fibrosis and impaired function. The present study investigates the role of the small leucine-rich proteoglycan biglycan during cardiac extracellular matrix remodeling and cardiac hemodynamics after MI. Methods and Results-Experimental MI was induced in wild-type (WT) and bgn Ϫ/0 mice by permanent ligation of the left anterior descending coronary artery. Biglycan expression was strongly increased at 3, 7, and 14 days after MI in WT mice. bgn Ϫ/0 mice showed increased mortality rates after MI as a result of frequent left ventricular (LV) ruptures. Furthermore, tensile strength of the LV derived from bgn Ϫ/0 mice 21 days after MI was reduced as measured ex vivo. Collagen matrix organization was severely impaired in bgn Ϫ/0 mice, as shown by birefringence analysis of Sirius red staining and electron microscopy of collagen fibrils. At 21 days after MI, LV hemodynamic parameters were assessed by pressure-volume measurements in vivo to obtain LV end-diastolic pressure, end-diastolic volume, and end-systolic volume. bgn Ϫ/0 mice were characterized by aggravated LV dilation evidenced by increased LV end-diastolic volume (bgn

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Section: Discussionmentioning

confidence: 99%

Section: Increased Biglycan Expression After MImentioning

confidence: 96%

Section: Clinical Perspective P 1276mentioning

confidence: 99%

See 1 more Smart Citation

Biglycan Is Required for Adaptive Remodeling After Myocardial Infarction

Westermann

Mersmann²,

Melchior³

et al. 2008

Circulation

112

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“…Previous reports revealed that versican was inducible in various cells, including vascular smooth muscle cells and endothelial cells under stimulation with growth factors [20][21][22][23][24][25][26][27][28][29][30][31][32][33][34]. The significance of the V0/V1 splicing form in the infarcted heart will be investigated in future studies.…”

Section: Discussionmentioning

confidence: 99%

“…Immunohistochemical analysis was performed as previously reported [12][13][14][15][16][17][18][19][20][21][22][23][24][25].…”

Section: Immunohistochemistrymentioning

confidence: 99%

Versican is induced in infiltrating monocytes in myocardial infarction

et al. 2005

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Abbreviations: bp, base pairs; hr, hours; kbp, kilo base pairs; min, minutes; RNA, ribonucleic acid; sec, seconds Toeda et al, Versican expression in myocardial infarction 2 AbstractVersican, a large chondroitin sulfate proteoglycan, plays a role in conditions such as wound healing and tissue remodeling.To test the hypothesis that versican is transiently expressed and plays a role in the infarcted heart, we examined its expression in a rat model of myocardial infarction.Northern blot analysis demonstrated increased expression of versican mRNA. Quantitative real-time RT-PCR analysis revealed that versican mRNA began to increase as early as 6 hours and reached its maximal level 2 days after coronary artery ligation. Versican mRNA then gradually decreased, while the mRNA of decorin, another small proteoglycan, increased thereafter. gene by monocytes in the infarcted heart. We suggest that upregulation of versican in the infarcted myocardium may have a role in the inflammatory reaction, which mediates subsequent chemotaxis in the infarcted heart.

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Extracellular Matrix Communication and Turnover in Cardiac Physiology and Pathology

Takawale

Sakamuri

Kassiri

2015

Comprehensive Physiology

100

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Despite significant advances in treating heart disease, heart failure remains a major cause of morbidity and mortality. Regardless of the initiating cause(s), heart failure is associated with disruptions in the myocardial extracellular matrix (ECM). ECM is a dynamic structure and its physiological turnover is mediated by matrix metalloproteinases (MMPs) and their inhibitors (TIMPs). Research in the past two decades has revealed that the function of ECM extends beyond its role in providing structural support. Similarly, ECM regulatory proteins, MMPs and TIMPs, have been demonstrated to play diverse and ECM-independent roles in tissue remodeling and homeostasis. ECM is a network structure that in addition to providing structural support, serves as an extracellular reservoir for a number of growth factors and cytokines, and plays a central role in interstitial transport of different molecules (hormones, growth factors, drugs, etc.). This is mainly through the action of nonstructural ECM components, proteoglycans and matricellular proteins, which are also critical in cell-ECM interactions and overall ECM remodeling. As such, sustaining the ECM integrity is not only critical in preserving cardiac geometry and function, it is essential in ensuring optimal delivery of different molecules to their site of action. Further, ECM composition and integrity in disease should be considered in designing drugs with a specific site of action. In this review article, we provide an overview of the ECM structure, components, its function in interstitial transport, heart disease-dependent ECM remodeling, and the potential therapeutic approaches in preserving the diseased myocardial ECM and cardiac function.

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Time-dependent changes of decorin in the infarct zone after experimentally induced myocardial infarction in rats: Comparison with biglycan

Cited by 28 publications

References 22 publications

Biglycan Is Required for Adaptive Remodeling After Myocardial Infarction

Biglycan Is Required for Adaptive Remodeling After Myocardial Infarction

Versican is induced in infiltrating monocytes in myocardial infarction

Extracellular Matrix Communication and Turnover in Cardiac Physiology and Pathology

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