The Role of ADAMTS1 and Versican in Human Myocardial Infarction: A Postmortem Study

Pehlivan, Sultan; Gürses, Murat Serdar; Ural, Mustafa; Akyol, Sümeyya; Eren, Filiz; İnanır, Nursel Türkmen; Güleç, Mehmet Akif; Eren, Bülent; Fedakar, Recep; Demircan, Kadir; Akyol, Ömer

doi:10.1093/labmed/lmw022

Cited by 3 publications

(2 citation statements)

References 24 publications

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“…In contrast, the detectable potential pro-inflammatory proteins MX2, SPP1 and PIBF1 were found to be down-regulated ( Figure 3 B, red), whereas the rather anti-inflammatory proteins ANXA1, LTBP1, SERPINA4 and TXN were found to be up-regulated in MB samples ( Figure 3 B, orange). Remarkable was the detection of a distinct molecular signature indicative for hypoxia, represented by the up-regulated proteins ADAMTS1 [ 38 ], GAP43 [ 39 ] and GPR37 [ 40 ] ( Figure 3 B, blue). The detailed classification of proteins is documented in Table S6 .…”

Section: Resultsmentioning

confidence: 99%

Determination of a Tumor-Promoting Microenvironment in Recurrent Medulloblastoma: A Multi-Omics Study of Cerebrospinal Fluid

Reichl

Niederstaetter

Boegl

et al. 2020

Cancers

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Molecular classification of medulloblastoma (MB) is well-established and reflects the cell origin and biological properties of tumor cells. However, limited data is available regarding the MB tumor microenvironment. Here, we present a mass spectrometry-based multi-omics pilot study of cerebrospinal fluid (CSF) from recurrent MB patients. A group of age-matched patients without a neoplastic disease was used as control cohort. Proteome profiling identified characteristic tumor markers, including FSTL5, ART3, and FMOD, and revealed a strong prevalence of anti-inflammatory and tumor-promoting proteins characteristic for alternatively polarized myeloid cells in MB samples. The up-regulation of ADAMTS1, GAP43 and GPR37 indicated hypoxic conditions in the CSF of MB patients. This notion was independently supported by metabolomics, demonstrating the up-regulation of tryptophan, methionine, serine and lysine, which have all been described to be induced upon hypoxia in CSF. While cyclooxygenase products were hardly detectable, the epoxygenase product and beta-oxidation promoting lipid hormone 12,13-DiHOME was found to be strongly up-regulated. Taken together, the data suggest a vicious cycle driven by autophagy, the formation of 12,13-DiHOME and increased beta-oxidation, thus promoting a metabolic shift supporting the formation of drug resistance and stem cell properties of MB cells. In conclusion, the different omics-techniques clearly synergized and mutually supported a novel model for a specific pathomechanism.

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Section: Resultsmentioning

confidence: 99%

Determination of a Tumor-Promoting Microenvironment in Recurrent Medulloblastoma: A Multi-Omics Study of Cerebrospinal Fluid

Reichl

Niederstaetter

Boegl

et al. 2020

Cancers

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“…Another interesting function attractive for researchers r e g a r d s A D A M T S 1 a n d A D A M T S 4 w h i c h a r e capable to cleave versican, the primary proteoglycan component of the vasculature. In the cardiovascular context, ADAMTS1 and ADAMTS4 ability in ECM rearrangement results crucially detrimental both for the ventricular remodelling after MI and the regulation of fibrous cap stability in atherosclerotic plaque (117,130). The damaging role of ADAMTS1 is basically due to its cleavage activity of versican that, once cleaved, stimulates vascular smooth muscle cell migrations (131).…”

Section: The Adamts Proteinsmentioning

confidence: 99%

Cardiac fibrosis in regenerative medicine: destroy to rebuild

Perrucci¹,

Rurali²,

Pompilio³

2018

J. Thorac. Dis.

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The major limitations for cardiac regeneration in patients after myocardial infarction (MI) are the wide loss of cardiomyocytes and the adverse structural alterations of extracellular matrix (ECM). Cardiac fibroblast differentiation into myofibroblasts (MFB) leads to a huge deposition of ECM and to the subsequent loss of ventricular structural integrity. All these molecular events depict the fundamental features at the basis of the post-MI fibrosis and deserve in depth cellular and molecular studies to fill the gap in the clinical practice. Indeed, to date, there are no effective therapeutic approaches to limit the post-MI massive fibrosis development. In this review we describe the involvement of integrins and a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)/ADAMTS-like (ADAMTSL) proteins in cardiac reparative pro-fibrotic response after MI, proposing some of them as novel potential pharmacological tools.

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ADAM and ADAMTS disintegrin and metalloproteinases as major factors and molecular targets in vascular malfunction and disease

Yang

Khalil

2022

Advances in Pharmacology

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The Role of ADAMTS1 and Versican in Human Myocardial Infarction: A Postmortem Study

Abstract: Similar localizations of ADAMTS and fragmented versican in human heart tissue indicate that versican presumably is cleaved by ADAMTS1. Hence, ADAMTS1 can be regarded as a new marker for postmortem differential diagnosis of MI.

Cited by 3 publications

References 24 publications

Determination of a Tumor-Promoting Microenvironment in Recurrent Medulloblastoma: A Multi-Omics Study of Cerebrospinal Fluid

Determination of a Tumor-Promoting Microenvironment in Recurrent Medulloblastoma: A Multi-Omics Study of Cerebrospinal Fluid

Cardiac fibrosis in regenerative medicine: destroy to rebuild

ADAM and ADAMTS disintegrin and metalloproteinases as major factors and molecular targets in vascular malfunction and disease

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