Vascular Remodeling and Altered Protein Expression During Growth of Coronary Collateral Arteries

Wolf, Claudia; Cai, Wenju; Vosschulte, Regina; Koltai, Sofie; Mousavipour, Dehim; Scholz, Dimitri; Afsah-Hedjri, Abdollah; Schäper, Wolfgang; Schaper, Jutta

doi:10.1006/jmcc.1998.0790

Cited by 126 publications

(95 citation statements)

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“…3) Extracellular matrix deposits induce mature collaterals. [22][23][24][25][26][27][28] A number of experimental and clinical arteriogenic therapies have been attempted using topical transplantation of growth factors or stem cells/precursors, with favorable results. 5,11,12) Although studies have demonstrated capillary formation (vasculogenesis/angiogenesis) by transplanted cells, 11,12) they could not confirm that transplanted cells migrating into pre-existing vessel walls became SMCs or ECs or their incorporation into vessels to enlarge them.…”

Section: Discussionmentioning

confidence: 99%

Migration of Mononuclear Cells Expressing β-Actin Through the Adventitia into Media and Intima in Coronary Arteriogenesis and Venogenesis in Ischemic Myocardium

Uchida

Maezawa

et al. 2012

Int. Heart J.

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SummaryIt was previously thought that arteriogenesis and venogenesis are induced not only by proliferation of vessel-resident smooth muscle cells (SMCs) and endothelial cells (ECs) but also by migration of their precursors. However, it is not well understood through what route(s) the precursors migrate into the existing vessels.We examined through what route or routes circulating mononuclear cells expressing β-actin (β-MNCs), which we identified in canine coronary vessels, migrate into coronary vessel walls and cause arteriogenesis and venogenesis at 1, 2, 4 and 8 weeks after induction of myocardial infarction.The following changes were observed: (1) The β-MNCs migrated via coronary microvessels to the interstitial space at one week; (2) β-MNCs traversed the adventitia into the media and settled in parallel with pre-existing smooth muscle cells (SMCs) in arterioles and arteries and lost β-actin and acquired α-smooth muscle actin (α-SMA) to become mature SMCs at 2-4 weeks; (3) at the same time, other β-MNCs migrated across the adventitia and media into the intima and settled in parallel with pre-existing endothelial cells (ECs) and lost β-actin, while acquiring CD 31 , to become mature ECs, resulting in arteriogenesis; (4) Similarly, β-MNCs migrated into venular and venous walls and became SMCs or ECs, resulting in venogenesis.β-MNCs in the interstitial space expressed CD 34 but not other major vascular cell markers. β-MNCs, possibly a vascular progenitor, migrate not from the lumen but across the adventitia into the media or intima of coronary vessels and transit to SMCs or ECs, and participate in arteriogenesis and venogenesis in ischemic myocardium. (Int Heart J 2012; 53: 54-63)

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Section: Discussionmentioning

confidence: 99%

Migration of Mononuclear Cells Expressing β-Actin Through the Adventitia into Media and Intima in Coronary Arteriogenesis and Venogenesis in Ischemic Myocardium

Uchida

Maezawa

et al. 2012

Int. Heart J.

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“…The protocol for preparation of this animal model has been previously described (29). Briefly, six adult mongrel dogs weighing 18-20 kg were anesthetized with pentobarbital (138 mM/kg body wt).…”

Section: Methodsmentioning

confidence: 99%

“…The mechanism of collateral vessel growth is only partially understood. Many factors or events have been indicated to make contributions to this process, e.g., increased shear stress, early invasion of monocytes/ macrophages, reexpression of fetal proteins, extracellular proteolysis, migration of smooth muscle (SM) cells, and involvement of gap junction proteins (3,4,29). The notion that apoptosis of SM cells, fibroblasts, or myocytes creates space for the enlargement of collateral vessels has also been proposed (23).…”

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confidence: 99%

Remodeling of the adventitia during coronary arteriogenesis

Cai

Koltai

Kocsis

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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We studied the role of the adventitia in adaptive arteriogenesis during the phase of active growth of coronary collateral vessels (CV) induced by chronic occlusion of the left circumflex coronary artery in canine hearts. We used electron microscopy and immunoconfocal (IF) labeling for bFGF, matrix metalloproteinase (MMP)-2, MMP-9, tissue-type plasminogen activator (tPA), its inhibitor (PAI-1), fibronectin (FN), and Ki-67. Proliferation of smooth muscle cells and adventitial fibroblasts was evident. Quantitative IF showed that adventitial MMP-2, MMP-9, and FN were 9.2-, 7.5-, and 8.6-fold, bFGF was 5.1-fold, and PAI-1 was 3.4-fold higher in CV than in normal vessels (NV). The number of fibroblasts was 5-fold elevated in CV, but the elastic fiber content was 25-fold greater in NV than in CV. Perivascular myocyte damage and induction of endothelial nitric oxide synthase in peri-CV capillaries indicate expansion of CV. It was concluded that adventitial activation is associated with the development of CV through cell proliferation, production of growth factors, and induction of extracellular proteolysis thereby contributing to remodeling during adaptive arteriogenesis. collateral vessel growth; metalloproteinases; extracellular proteolysis; dog CORONARY COLLATERAL VESSEL GROWTH in the dog heart, induced by chronic occlusion of a major coronary artery, results in a 20-50 times increase in diameter (21). The mechanism of collateral vessel growth is only partially understood. Many factors or events have been indicated to make contributions to this process, e.g., increased shear stress, early invasion of monocytes/ macrophages, reexpression of fetal proteins, extracellular proteolysis, migration of smooth muscle (SM) cells, and involvement of gap junction proteins (3,4,29). The notion that apoptosis of SM cells, fibroblasts, or myocytes creates space for the enlargement of collateral vessels has also been proposed (23). These studies addressed the crucial role of endothelium and of SM cells in the development of coronary collateral vessels.However, the importance of the tunica adventitia in vascular remodeling was largely neglected, although enlargement of collateral vessels without participation of the adventitia seems not conceivable. We hypothesize that the adventitia is activated and might be an important contributor to the development of coronary collaterals.The development of coronary collateral vessels has been classified into three phases: early growth (2-3 wk postsurgery), active growth (4-6 wk postsurgery), and maturation (8-12 wk postsurgery) (4). An early study showed that an acute inflammatory reaction was present in the adventitia of collateral vessels in the phase of early growth (2). However, in the phases of active growth and maturation, inflammatory cells have not been observed in the adventitia, and fibroblasts are the predominant cells residing in the adventitia. Fibroblasts have been demonstrated to be active participants in vascular remodeling (20,25,26). Here, we studied the question whether typica...

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“…10,11 Furthermore, Ang-1 and Ang-2 exert their biological effects by binding to the same tyrosine kinase receptor Tie-2. Ang-2 can act as a partial antagonist of Ang-1, especially in hypoxic conditions; 15,19,20 however, the regulatory mechanisms for the expression of both Ang-1 and Ang- 2 have not yet been completely elucidated.…”

Section: Dynamics Of Ang/tie-2 System In the Coronary Circulationmentioning

confidence: 99%

Angiopoietin-1, Angiopoietin-2 and Tie-2 in the Coronary Circulation of Patients With and Without Coronary Collateral Vessels

Mitsuma

Kodama

Hirono

et al. 2007

Circ J

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Vascular Remodeling and Altered Protein Expression During Growth of Coronary Collateral Arteries

Cited by 126 publications

References 0 publications

Migration of Mononuclear Cells Expressing β-Actin Through the Adventitia into Media and Intima in Coronary Arteriogenesis and Venogenesis in Ischemic Myocardium

Migration of Mononuclear Cells Expressing β-Actin Through the Adventitia into Media and Intima in Coronary Arteriogenesis and Venogenesis in Ischemic Myocardium

Remodeling of the adventitia during coronary arteriogenesis

Angiopoietin-1, Angiopoietin-2 and Tie-2 in the Coronary Circulation of Patients With and Without Coronary Collateral Vessels

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