Urinary matrix metalloproteinases-2/9 in healthy infants and haemangioma patients prior to and during propranolol therapy

Kleber, Christian; Spiess, Alexander; Kleber, Johann-Baptist; Hinz, Ulf; Holland‐Cunz, Stefan; Weiß, Johanna

doi:10.1007/s00431-011-1660-x

Cited by 14 publications

(15 citation statements)

References 24 publications

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“…This reduced residuum could result from depletion of the MSC population, inhibition of their differentiation, or enhanced degradation of the basement membrane that normally develops during involution. 23 However, it cannot be discounted that the degranulation observed here is a consequence of ulceration of the lesions, rather than a consequence of propranolol treatment. 1, http://links.lww.com/PAT/A19) to identify the perivascular MSC population did not identify any differences in the number of CD90 staining cells between the samples, suggesting that propranolol does not induce depletion of adipocyte precursors.…”

Section: Discussionmentioning

confidence: 66%

Increased apoptosis and secretion of tryptase by mast cells in infantile haemangioma treated with propranolol

Steel

Day

2014

Pathology

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Section: Discussionmentioning

confidence: 66%

Increased apoptosis and secretion of tryptase by mast cells in infantile haemangioma treated with propranolol

Steel

Day

2014

Pathology

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“…In a study reported by Marler et al, elevation of urinary MMP-2, MMP-9, bFGF or VEGF was not observed in children with infantile hemangioma, but they did identify 2 high molecular weight matrix metalloproteases in 60% of children with hemangiomas (27). Kleber et al monitored urinary MMP-2 and MMP-9 levels in response to propranolol treatment of hemangiomas and found increased MMP-2 levels, but no changes in MMP-9 levels (28). However, MMP-2 and MMP-9 are found in the urine of healthy children in response to normal tissue remodeling, so the levels of these proteins are not necessarily specific for hemangioma growth (29).…”

Section: Discussionmentioning

confidence: 99%

Urinary Excretion of MicroRNA-126 Is a Biomarker for Hemangioma Proliferation

Biswas

Pan

Meyer

et al. 2017

Plastic &Amp; Reconstructive Surgery

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Background Hemangiomas are unique endothelial cell tumors that spontaneously involute, which makes it difficult to interpret response to therapies. The objective of this work was to identify a potential biomarker in the urine of children with infantile hemangiomas that would facilitate testing new therapies. Methods A prospective longitudinal study in children with hemangiomas and age matched healthy controls was performed to determine whether microRNA (miR)-126, which is highly abundant in fetal endothelial cells, was more abundant in the urine of affected children. Prospective ultrasound measurements of hemangioma size and blood flow velocity were obtained as secondary endpoints to document longitudinal changes in untreated hemangiomas. Results Urinary miR-126 levels were significantly elevated in children with proliferating hemangiomas and relative levels of urinary miR abundance correlated with hemangioma size. Hemangiomas had elevated levels of miR abundance compared to healthy controls. Ultrasound data revealed that hemangioma proliferation typically stopped between 6 to 9 months of age. When hemangioma proliferation stopped urinary miR-126 levels in children with hemangiomas dropped to levels observed in healthy age matched controls. Conclusions These are the first reported results to identify a potential miR biomarker in the urine of children with hemangiomas. Measurement of urinary levels of miR-126 could potentially be used to monitor hemangioma response to therapies.

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“…Taking into account the above‐mentioned literature, as well as the results presented by Kleber et al, the correlation between MMPs, proliferation, and regression of hemangiomas and propranolol remains unclear .…”

Section: Mechanism Of Action Of Beta‐blockersmentioning

confidence: 99%

Infantile hemangioma: pathogenesis and mechanisms of action of propranolol

Rotter

Oliveira

2017

J Deutsche Derma Gesell

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SummaryInfantile hemangioma (IH) is the most common benign tumor of childhood, with a prevalence of 4 % to 10 %. It is characterized by a proliferative rapid growth phase, which starts after a few weeks of life, followed by a slow regression phase. In IH cases that are potentially disfiguring or life-threatening (10 % to 15 % of all cases), systemic therapy should be promptly initiated. Data source: The present study reviews published scientific articles available in reliable electronic databases. Selected were all studies that evaluated the pathogenesis of IH and the mechanisms of action of propranolol. Conclusions: The pathogenesis of IH has not been fully elucidated. Studies show that, in the proliferative phase of IH, there is an imbalance of angiogenic factors and an increase in the levels of vascular endothelial growth factor and matrix metalloproteinases 2 and 9. In the regression phase, the levels of these factors decrease, whereas those of antiangiogenic factors, including tissue inhibitors of matrix metalloproteinases, increase. Since 2008, propranolol has become the drug of choice in the treatment of IH, targeting vascular tone, angiogenesis, and apoptosis. Current insights into the pathogenesis of IH allow for the development of new therapeutic strategies.

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Urinary matrix metalloproteinases-2/9 in healthy infants and haemangioma patients prior to and during propranolol therapy

Cited by 14 publications

References 24 publications

Increased apoptosis and secretion of tryptase by mast cells in infantile haemangioma treated with propranolol

Increased apoptosis and secretion of tryptase by mast cells in infantile haemangioma treated with propranolol

Urinary Excretion of MicroRNA-126 Is a Biomarker for Hemangioma Proliferation

Infantile hemangioma: pathogenesis and mechanisms of action of propranolol

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