Peripheral blood mononuclear cells from patients with systemic sclerosis spontaneously secrete increased amounts of vascular endothelial growth factor (VEGF) already in the early stage of the disease

Bielecki, M; Kowal, Krzysztof; Lapinska, Anna; Chwieśko-Minarowska, Sylwia; Chyczewski, L; Kowal-Bielecka, Otylia

doi:10.2478/v10039-011-0025-z

Cited by 21 publications

(13 citation statements)

References 31 publications

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“…Presumably, a critical element of angiogenesis is either absent or blocked in SSc. Surprisingly, several studies have demonstrated enhanced expression of the proangiogenic factor VEGF‐A in both the skin and the circulation of SSc patients (). The paradox is that VEGF levels, rather than being associated with evidence of angiogenesis, actually correlate with progressive microvascular loss and disease progression.…”

Section: Pathologic Modification and Vascular Pathogenesismentioning

confidence: 99%

Review: Evidence That Systemic Sclerosis Is a Vascular Disease

Matucci‐Cerinic

Kahaleh

Wigley

2013

Arthritis & Rheumatism

377

263

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Section: Pathologic Modification and Vascular Pathogenesismentioning

confidence: 99%

Review: Evidence That Systemic Sclerosis Is a Vascular Disease

Matucci‐Cerinic

Kahaleh

Wigley

2013

Arthritis & Rheumatism

377

263

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“…Besides TGF- β , the most important growth factor, involved in SSc tissue fibrosis and in EndoMT, other growth factors and profibrogenic molecules, including platelet derived growth factors [167], vascular endothelial growth factor [168], and insulin-derived growth factor [169], may also participate in EndoMT although their role in this process has not been studied to our knowledge. However, some studies that examined the role of other profibrotic growth factors have been described.…”

Section: Molecular Mechanisms Of Endomtmentioning

confidence: 99%

Role of Endothelial to Mesenchymal Transition in the Pathogenesis of the Vascular Alterations in Systemic Sclerosis

2013

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The pathogenesis of Systemic Sclerosis (SSc) is extremely complex, and despite extensive studies, the exact mechanisms involved are not well understood. Numerous recent studies of early events in SSc pathogenesis have suggested that unknown etiologic factors in a genetically receptive host trigger structural and functional microvascular endothelial cell abnormalities. These alterations result in the attraction, transmigration, and accumulation of immune and inflammatory cells in the perivascular tissues, which in turn induce the phenotypic conversion of endothelial cells and quiescent fibroblasts into activated myofibroblasts, a process known as endothelial to mesenchymal transition or EndoMT. The activated myofibroblasts are the effector cells responsible for the severe and frequently progressive fibrotic process and the fibroproliferative vasculopathy that are the hallmarks of SSc. Thus, according to this hypothesis the endothelial and vascular alterations, which include the phenotypic conversion of endothelial cells into activated myofibroblasts, play a crucial role in the development of the progressive fibrotic process affecting skin and multiple internal organs. The role of endothelial cell and vascular alterations, the potential contribution of endothelial to mesenchymal cell transition in the pathogenesis of the tissue fibrosis, and fibroproliferative vasculopathy in SSc will be reviewed here.

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“…In SSc, panVEGF-A and VEGF-A165b is expressed in fibroblasts, endothelial and perivascular inflammatory cells [11,12] with additional expression of VEGF-A165b in vascular smooth muscle cells in ex vivo lesional skin [12]. Circulating mononuclear cells [89] and skin keratinocytes [8,11] also produce increased panVEGF-A levels.…”

Section: What Is the Potential Cellular Source Of Vegf-a Isoforms In mentioning

confidence: 99%

“…Figure 3 demonstrates the pathway of hypoxia induced VEGF-A induction via HIF and hypoxia mRNA stabilization [32,43,53,104]. Known cellular sources of VEGF-A in SSc are illustrated based on available evidence (panVEGF-A = (a), VEGF-A165b = (b)) [11,12,89,91,92,103,111,114,131]. *TGFβ and HIF1α synergistically increase VEGF-A in endothelial cells [104].…”

Section: Figure Legendsmentioning

confidence: 99%

The Role of Vascular Endothelial Growth Factor in Systemic Sclerosis

Flower

Barratt

Ward

et al. 2019

CRR

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The pathological hallmarks of Systemic sclerosis (SSc) constitute an inter-related triad of autoimmunity, vasculopathy and tissue remodeling. Many signaling mediators have been implicated in SSc pathology; most focusing on individual components of this pathogenic triad and current treatment paradigms tend to approach management of such as distinct entities. The present review shall examine the role of vascular endothelial growth factor (VEGF) in SSc pathogenesis. We shall outline potential mechanisms whereby differential vascular endothelial growth factor-A (VEGF-A) isoform expression (through conventional and alternative VEGF-A splicing,) may influence the relevant burden of vasculopathy and fibrosis offering novel insight into clinical heterogeneity and disease progression in SSc. Emerging therapeutic approaches targeting VEGF signaling pathways might play an important role in the management of SSc, and differential VEGF-A splice isoform expression may provide a tool for personalized medicine approaches to disease management.

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Peripheral blood mononuclear cells from patients with systemic sclerosis spontaneously secrete increased amounts of vascular endothelial growth factor (VEGF) already in the early stage of the disease

Cited by 21 publications

References 31 publications

Review: Evidence That Systemic Sclerosis Is a Vascular Disease

Review: Evidence That Systemic Sclerosis Is a Vascular Disease

Role of Endothelial to Mesenchymal Transition in the Pathogenesis of the Vascular Alterations in Systemic Sclerosis

The Role of Vascular Endothelial Growth Factor in Systemic Sclerosis

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