Altered Balance Between Extracellular Proteolysis and Antiproteolysis is Associated with Adaptive Coronary Arteriogenesis

Cai, Wei; Vosschulte, Regina; Afsah-Hedjri, Abdollah; Koltai, Sophie; Kocsis, Elisabeth; Scholz, Dimitri; Kostin, Sawa; Schäper, Wolfgang; Schaper, Jutta

doi:10.1006/jmcc.2000.1137

Cited by 94 publications

(76 citation statements)

References 52 publications

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“…28 Yu and Stamenkovic 29 reported that CD44 can facilitate the activation of TGF-␤ 1 by localizing matrix metalloproteinase-9 to the plasma membrane. Because the expression of this metalloproteinase is increased during collateral artery growth, 13 it is possible that the pathway of TGF-␤ 1 activation is also disturbed in the present CD44-deficient model. Further studies are needed to test this hypothesis.…”

Section: Discussionmentioning

confidence: 95%

“…10 -12 Monocytes/macrophages accumulate around proliferating arteries, where they produce matrix metalloproteinases, proinflammatory cytokines, and growth factors, which orchestrate the remodeling of collateral vessels to high-capacity arteries. 13,14 CD44 also regulates the biological activity of several growth factors, such as fibroblast growth factor (FGF)-2, platelet-derived growth factor (PDGF)-B, and hepatocyte growth factor (HGF). CD44 binds and presents these factors to their high-affinity receptors and promotes signaling and stability by protecting them from degradation.…”

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confidence: 99%

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CD44 Regulates Arteriogenesis in Mice and Is Differentially Expressed in Patients With Poor and Good Collateralization

et al. 2004

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Background-Arteriogenesis refers to the development of collateral conductance arteries and is orchestrated by circulating monocytes, which invade growing collateral arteries and act as suppliers of cytokines and growth factors. CD44 glycoproteins are involved in leukocyte extravasation but also in the regulation of growth factor activation, stability, and signaling. Here, we explored the role of CD44 during arteriogenesis. Methods and Results-CD44 expression increases strongly during collateral artery growth in a murine hind-limb model of arteriogenesis. This CD44 expression is of great functional importance, because arteriogenesis is severely impaired in CD44 Ϫ/Ϫ mice (wild-type, 54.5Ϯ14.9% versus CD44 Ϫ/Ϫ , 24.1Ϯ9.2%, PϽ0.001). The defective arteriogenesis is accompanied by reduced leukocyte trafficking to sites of collateral artery growth (wild-type, 29Ϯ12% versus CD44 Ϫ/Ϫ , 18Ϯ7% CD11b-positive cells/square, PϽ0.01) and reduced expression of fibroblast growth factor-2 and platelet-derived growth factor-B protein. Finally, in patients with single-vessel coronary artery disease, the maximal expression of CD44 on activated monocytes is reduced in case of impaired collateral artery formation (poor collateralization, 1764Ϯ572 versus good collateralization, 2817Ϯ1029 AU, PϽ0.05). Conclusions-For the first time, the pivotal role of CD44 during arteriogenesis is shown. The expression of CD44 increases during arteriogenesis, and the deficiency of CD44 severely impedes arteriogenesis. Maximal CD44 expression on isolated monocytes is decreased in patients with a poor collateralization compared with patients with a good collateralization.

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Section: Discussionmentioning

confidence: 95%

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confidence: 99%

CD44 Regulates Arteriogenesis in Mice and Is Differentially Expressed in Patients With Poor and Good Collateralization

et al. 2004

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“…MMP-2 and its active proenzyme pro-MMP-2 have important intracellular functions, particularly in angiogenesis (10). Proteolytic degradation of the basement membrane of the parent vessel and ECFC immigration requires proteolytic enzymes including MMPs.…”

Section: Discussionmentioning

confidence: 99%

Vitamin D improves the angiogenic properties of endothelial progenitor cells

Grundmann

Haidar

Placzko

et al. 2012

American Journal of Physiology-Cell Physiology

137

113

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The main pathogenic feature of preeclampsia is maternal endothelial dysfunction that results from impaired angiogenesis and reduced endothelial repair capacity. In addition, preeclampsia risk is associated with vitamin D deficiency. We hypothesized that vitamin D3 stimulates proangiogenic properties of endothelial colony-forming cells (ECFCs). ECFCs were obtained and cultured from cord blood and characterized by immunocytochemistry and flow cytometry. Proliferation, total length of tubule formation on Matrigel, expression of VEGF mRNA, and pro-matrix metalloproteinases (MMP)-2 activity were assessed after treatment of ECFCs with vitamin D 3. Specificity of the observed effects was tested by blocking the vitamin D receptor (VDR) or the VEGF signaling pathway. ECFCs treated with 10 nM vitamin D3 showed a 1.27 times higher tubule formation compared with vehicle-treated controls (1.27 Ϯ 0.19) as well as a 1.36 times higher proliferation rate (1.36 Ϯ 0.06). Vitamin D3 induced pro-MMP-2 activity (1.29 Ϯ 0.17) and VEGF mRNA levels (1.74 Ϯ 0.73) in ECFCs. VDR blocking by pyridoxal-5-phosphate (0.73 Ϯ 0.19) or small interfering RNA (0.75 Ϯ 0.17) and VEGF inhibition by Su5416 (0.56 Ϯ 0.16) or soluble fms-like tyrosine kinase-1 (0.7 Ϯ 0.14) reduced tubule formation and pro-MMP-2 activity (pyridoxal-5-phosphate: 0.84 Ϯ 0.09; Su5416: 0.79 Ϯ 0.11; or sFlt: 0.88 Ϯ 0.13). This effect was neutralized by vitamin D3. Consequently, vitamin D3 significantly promoted angiogenesis in ECFCs in vitro possibly due to an increase in VEGF expression and pro-MMP-2 activity. Since angiogenesis is a crucial feature in the pathophysiology of preeclampsia these findings could explain the positive influence of vitamin D3 in reducing preeclampsia risk. vitamin D; preeclampsia; ECFC; angiogenesis; VEGF VITAMIN D, PRIMARILY KNOWN for its important role in calcium homeostasis and bone metabolism, influences the cardiovascular system through unclear mechanisms (33). Vitamin D deficiency is associated with increased all-cause and cardiovascular disease mortality, coronary heart disease, and various cardiovascular risk factors (33).Preeclampsia, a pregnancy-specific disorder that affects 3-7% of all pregnancies, is a major cause of maternal and fetal morbidity and mortality (43) and is associated with an increased risk for cardiovascular events later in life (6). Endothelial dysfunction underlies the hypertension, proteinuria, and multiorgan damage that occur during preeclampsia. The mechanisms that contribute to the disturbed endothelial homeostasis in the pathophysiology of preeclampsia remain unclear (41,46). Compared with normal pregnancies, preeclampsia is characterized by marked changes in vitamin D and calcium metabolism (3). Epidemiological studies have demonstrated an association between low maternal vitamin D levels and the incidence of preeclampsia (23, 27) and suggest vitamin D deficiency to be an independent risk factor for the development of preeclampsia (7). Moreover, vitamin D supplementation studies also showed protective effects on pr...

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“…Infiltrating monocytes/macrophages, in particular, have been shown to exhibit an important mediation function in arteriogenesis: Collateral artery growth is directly correlated to peripheral blood monocyte concentration (17), and chemoattraction or activation of monocytes via MCP-1 or transforming growth factor-␤1 results in a significant increase in conductance of the developing collateral vasculature (18,22,41). Little is known about the mechanisms of action by which macrophages stimulate arterial growth, but the production of inflammatory cytokines (6), growth factors, and enzymes such as matrix metalloproteinases seems to be of functional importance (8). Furthermore, previous studies showed a strong immunohistochemical staining of monocytes for TNF-␣ (1).…”

Section: Discussionmentioning

confidence: 99%

Anti-tumor necrosis factor-α therapies attenuate adaptive arteriogenesis in the rabbit

Grundmann¹,

Hoefer²,

Ulusans³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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Altered Balance Between Extracellular Proteolysis and Antiproteolysis is Associated with Adaptive Coronary Arteriogenesis

Cited by 94 publications

References 52 publications

CD44 Regulates Arteriogenesis in Mice and Is Differentially Expressed in Patients With Poor and Good Collateralization

CD44 Regulates Arteriogenesis in Mice and Is Differentially Expressed in Patients With Poor and Good Collateralization

Vitamin D improves the angiogenic properties of endothelial progenitor cells

Anti-tumor necrosis factor-α therapies attenuate adaptive arteriogenesis in the rabbit

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