Non-Bone Marrow Origin of Neointimal Smooth Muscle Cells in Experimental In-Stent Restenosis in Rats

Groenewegen, Hendrik C.; Onuta, Geanina; Goris, Maaike; Zandvoort, Andre; Zijlstra, Felix; Gilst, Wiek H. van; Rozing, Jan; Smet, Bart J. G. L. de; Roks, Anton J.M.; Hillebrands, Jan-Luuk

doi:10.1159/000127440

Cited by 6 publications

(3 citation statements)

References 43 publications

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“…Although we did not study the underlying mechanism(s) of enhanced ISR in diabetic BBDP rats yet, we suggest that long-term diabetes increases the proliferative and migratory capacity of medial and neointimal smooth muscle cells, thereby facilitating neointima formation [36, 37]. In addition, reduced endothelial repair capacity in diabetic BBDP rats might have contributed to enhanced ISR [38], but this needs to be determined.…”

Section: Discussionmentioning

confidence: 99%

Long‐Term Type 1 Diabetes Enhances In‐Stent Restenosis after Aortic Stenting in Diabetes‐Prone BB Rats

Onuta

Groenewegen

Klatter

et al. 2011

BioMed Research International

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Type 1 diabetic patients have increased risk of developing in-stent restenosis following endovascular stenting. Underlying pathogenetic mechanisms are not fully understood partly due to the lack of a relevant animal model to study the effect(s) of long-term autoimmune diabetes on development of in-stent restenosis. We here describe the development of in-stent restenosis in long-term (~7 months) spontaneously diabetic and age-matched, thymectomized, nondiabetic Diabetes Prone BioBreeding (BBDP) rats (n = 6-7 in each group). Diabetes was suboptimally treated with insulin and was characterized by significant hyperglycaemia, polyuria, proteinuria, and increased HbA1c levels. Stented abdominal aortas were harvested 28 days after stenting. Computerized morphometric analysis revealed significantly increased neointima formation in long-term diabetic rats compared with nondiabetic controls. In conclusion, long-term autoimmune diabetes in BBDP rats enhances in-stent restenosis. This model can be used to study the underlying pathogenetic mechanisms of diabetes-enhanced in-stent restenosis as well as to test new therapeutic modalities.

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Section: Discussionmentioning

confidence: 99%

Long‐Term Type 1 Diabetes Enhances In‐Stent Restenosis after Aortic Stenting in Diabetes‐Prone BB Rats

Onuta

Groenewegen

Klatter

et al. 2011

BioMed Research International

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“…Therefore VSMClike cells originating from the BM, and perhaps also from adipose tissue, may play a pro-inflammatory role, rather than representing a pool of progenitor cells that will permanently differentiate into adult VSMCs. This might explain why we found that all BM-derived cells in the neointima after stenting expressed inflammatory cell markers [178]. The importance of such cells may of course be significant: the effect of AngII on stimulating the development of the VSMC-like cells that support or possess traits of inflammatory cells may be another example of the versatility of this peptide as a proinflammatory factor.…”

Section: Mscs With Vsmc Traitsmentioning

confidence: 91%

The renin–angiotensin system, bone marrow and progenitor cells

Durik¹,

Pessôa²,

Roks³

2012

Clinical Science

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Modulation of the RAS (renin–angiotensin system), in particular of the function of the hormones AngII (angiotensin II) and Ang-(1–7) [angiotensin-(1–7)], is an important target for pharmacotherapy in the cardiovascular system. In the classical view, such modulation affects cardiovascular cells to decrease hypertrophy, fibrosis and endothelial dysfunction, and improves diuresis. In this view, excessive stimulation of AT1 receptors (AngII type 1 receptors) fulfils a detrimental role, as it promotes cardiovascular pathogenesis, and this is opposed by stimulation of the AT2 receptor (angiotensin II type 2 receptor) and the Ang-(1–7) receptor encoded by the Mas proto-oncogene. In recent years, this view has been broadened with the observation that the RAS regulates bone marrow stromal cells and stem cells, thus involving haematopoiesis and tissue regeneration by progenitor cells. This change of paradigm has enlarged the field of perspectives for therapeutic application of existing as well as newly developed medicines that alter angiotensin signalling, which now stretches beyond cardiovascular therapy. In the present article, we review the role of AngII and Ang-(1–7) and their respective receptors in haematopoietic and mesenchymal stem cells, and discuss possible pharmacotherapeutical implications.

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“…Progenitor cells isolated from the tunica media of mouse aortas by flow cytometry could acquire the phenotype of SMC in culture as measured by positivity for calponin, α-SMA and SM MHC [37]. The possibility of a stem cell niche in the vessel wall could be of importance in studies that report a non-BM-derived origin for cells in the neointima [5, 25-27, 29, 30, 38]. …”

Section: Origin Of Smc In Vascular Disease: Role Of Bm-derived Spcmentioning

confidence: 99%

Smooth Muscle Progenitor Cells: Friend or Foe in Vascular Disease?

Oostrom¹,

Fledderus²,

Kleijn³

et al. 2009

CSCR

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The origin of vascular smooth muscle cells that accumulate in the neointima in vascular diseases such as transplant arteriosclerosis, atherosclerosis and restenosis remains subject to much debate. Smooth muscle cells are a highly heterogeneous cell population with different characteristics and markers, and distinct phenotypes in physiological and pathological conditions. Several studies have reported a role for bone marrow-derived progenitor cells in vascular maintenance and repair. Moreover, bone marrow-derived smooth muscle progenitor cells have been detected in human atherosclerotic tissue as well as in in vivo mouse models of vascular disease. However, it is not clear whether smooth muscle progenitor cells can be regarded as a ‘friend’ or ‘foe’ in neointima formation. In this review we will discuss the heterogeneity of smooth muscle cells, the role of smooth muscle progenitor cells in vascular disease, potential mechanisms that could regulate smooth muscle progenitor cell contribution and the implications this may have on designing novel therapeutic tools to prevent development and progression of vascular disease.

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Non-Bone Marrow Origin of Neointimal Smooth Muscle Cells in Experimental In-Stent Restenosis in Rats

Cited by 6 publications

References 43 publications

Long‐Term Type 1 Diabetes Enhances In‐Stent Restenosis after Aortic Stenting in Diabetes‐Prone BB Rats

Long‐Term Type 1 Diabetes Enhances In‐Stent Restenosis after Aortic Stenting in Diabetes‐Prone BB Rats

The renin–angiotensin system, bone marrow and progenitor cells

Smooth Muscle Progenitor Cells: Friend or Foe in Vascular Disease?

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