Thrombospondin-4 expression is rapidly upregulated by cardiac overload

Mustonen, Erno; Aro, Jani; Puhakka, Jutta; Ilves, Mika; Soini, Ylermi; Leskinen, Hanna; Ruskoaho, Heikki; Rysä, Jaana

doi:10.1016/j.bbrc.2008.05.164

Cited by 54 publications

(65 citation statements)

References 30 publications

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“…The proteins appear to be unstable after they are secreted, stressing the importance of timely elimination of TSPs from the ECM and cell environment (41-43). In adult organisms, upregulation of TSPs is associated with specific stages of wound healing [e.g., (36, 44-48)] and tissue remodeling [e.g., (13, 24, 25, 49-52)], in which it can be either protective and beneficial or detrimental.…”

Section: Introductionmentioning

confidence: 99%

“…There is very little information about the transcriptional regulation of TSP-4 and TSP-5 genes, despite their reported importance in several physiological and pathological processes (13, 24-26, 29, 52, 107, 108). The promoter of TSP-5 (COMP) has been analyzed, and a region required for the activity in chondrocytes was identified within 375 bp of the translational start site, as well as enhancer elements between −1.0 kb and −1.7 kb (109).…”

Section: Introductionmentioning

confidence: 99%

“…TSP-4 is upregulated in the mouse heart in response to pressure overload and in human hypertrophied hearts. It has a protective function regulating cardyomyocyte function and production of extracellular matrix (24-26, 52, 130-132). TSP-4 is expressed in atherosclerotic lesions and promotes atherosclerotic process by attracting and retaining macrophages in the lesion (13).…”

Section: Introductionmentioning

confidence: 99%

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Invoking the power of thrombospondins: Regulation of thrombospondins expression

Stenina‐Adognravi¹

2014

Matrix Biology

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Increasing evidence suggests critical functions of thrombospondins (TSPs) in a variety of physiological and pathological processes. With the growing understanding of the importance of these matricellular proteins, the need to understand the mechanisms of regulation of their expression and potential approaches to modulate their levels is also increasing. The regulation of TSPs expression is multi-leveled, cell- and tissue-specific, and very precise. However, the knowledge of mechanisms modulating the levels of TSPs is fragmented and incomplete. This review discusses the known mechanisms of regulation of TSPs levels and the gaps in our knowledge that prevent us from developing strategies to modulate the expression of these physiologically important proteins.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Invoking the power of thrombospondins: Regulation of thrombospondins expression

Stenina‐Adognravi¹

2014

Matrix Biology

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“…[108][109][110][111] Thrombospondin-1, thrombospondin-2, thrombospondin-3, and thrombospondin-4 are increased during hypertensive cardiomyopathy and contribute to cardiac remodeling. [112][113][114][115][116][117][118] Thrombospondin-1 can trigger ECM synthesis by activating TGFβ in vitro and in vivo by releasing the ECM-bound latent TGFβ. [119][120][121] Inhibition of thrombospondin-1-mediated TGFβ1 activation improved myocardial fibrosis and function after pressure overload, 119 highlighting the central role of thrombospondin-1 in this process.…”

Section: Ecm-cell Interactions Are Critical In Cell Response To Extramentioning

confidence: 99%

“…124 Thrombospondin-2-deficient mice exhibit a significant rate of cardiac rupture after angiotensin II infusion indicating the critical role of thrombospondin-2 in optimal assembly of ECM in the myocardium. 114 Thrombospondins can inhibit a broad spectrum of proteases, 105,125,126 including MMP2 114,115 and MMP9, 127 which could underlie their ability to protect and stabilize newly formed ECM during tissue remodeling. This could also underlie their antiangiogenic function, 112,128 although the N-terminal fragment of thrombospondin-1 (25 kDa) is proangiogenic through its interaction with syndecan-4 of endothelial cells.…”

Section: Ecm-cell Interactions Are Critical In Cell Response To Extramentioning

confidence: 99%

Matrix as an Interstitial Transport System

Fan

Creemers²,

Kassiri³

2014

Circulation Research

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T he extracellular space, or the interstitium, can be broadly divided into a fluid phase (water, electrolytes, nutrients, and some plasma proteins) and the extracellular matrix (ECM). In the heart, the ECM comprises structural proteins (primarily collagen types I and III) that form the fibrillar structure of the matrix; the basement membrane that forms an interface between the cardiomyocytes and the interstitial space as well as the molecules that mediate the cell-ECM connection; and the nonstructural proteins such as proteoglycans. Molecules traveling in the extracellular space come in contact with different ECM components, and these interactions determine the direction, speed, and distance of their transport, whereas the ECM can also provide a reservoir for several growth factors and cytokines. Moreover, the cell-ECM connection allows for transmission of signals across the cell membrane. Therefore, in addition to the classical role of ECM in providing structural support, it contributes to a multitude of intra-and extracellular events. Several thorough reviews have been published recently on the structural properties of the ECM and its remodeling in heart disease. [1][2][3] In this review, we will discuss less explored aspects of ECM function, such as its conductivity in extracellular transportation, its role in cell-cell interactions, and different modes of cell-cell communication through the extracellular space.

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Insider trading: Extracellular matrix proteins and their non‐canonical intracellular roles

Hellewell

Adams

2015

BioEssays

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General rightsThis document is made available in accordance with publisher policies. Please cite only the published version using the reference above. Full terms of use are available: http://www.bristol.ac.uk/pure/about/ebr-terms Graphical AbstractIt is a given that ECM proteins function outside cells. We evaluate emerging data that implicate noncanonical roles in the cytoplasm or nucleus. We discuss the conceptual and experimental challenges that will need to be met to investigate this under-studied area of ECM biology more rigorously. SummaryIn metazoans, the extracellular matrix (ECM) provides a dynamic, heterogeneous microenvironment that has important supportive and instructive roles. Although the primary site of action of ECM proteins is extracellular, evidence is emerging for noncanonical intracellular roles. Examples include osteopontin, thrombospondins, IGF-binding protein 3 and biglycan, and relate to roles in transcription, cell-stress responses, autophagy and cancer. These findings pose conceptual problems on how proteins signalled for secretion can be routed to the cytosol or nucleus, or can function in environments with diverse redox, pH and ionic conditions. We review evidence for intracellular locations and functions of ECM proteins, and current knowledge of the mechanisms by which they may enter intracellular compartments. We evaluate the experimental methods that are appropriate to obtain rigorous evidence for intracellular localisation and function. Better insight into this under-researched topic is needed to decipher the complete spectrum of physiological and pathological roles of ECM proteins.

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Thrombospondin-4 expression is rapidly upregulated by cardiac overload

Cited by 54 publications

References 30 publications

Invoking the power of thrombospondins: Regulation of thrombospondins expression

Invoking the power of thrombospondins: Regulation of thrombospondins expression

Matrix as an Interstitial Transport System

Insider trading: Extracellular matrix proteins and their non‐canonical intracellular roles

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