Curcumin Modulates SDF-1α/CXCR4–Induced Migration of Human Retinal Endothelial Cells (HRECs)

Sameermahmood, Zaheer; Balasubramanyam, Muthuswamy; Thangavel, Saravanan; Rema, M.

doi:10.1167/iovs.07-0456

Cited by 43 publications

(27 citation statements)

References 38 publications

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“…It was found that angiogenesis and the migration of human retinal endothelial cells induced by SDF-1a were inhibited by curcumin. 42 Caveolin-1 has been shown to play an important role in regulating the activity of eNOS through a direct interaction. 18 Therefore, inhibiting the protein expression of caveolin-1 may contribute to the activation of eNOS.…”

Section: Discussionmentioning

confidence: 99%

Curcumin Attenuates Rapamycin-induced Cell Injury of Vascular Endothelial Cells

Guo

Chen

Zhou

et al. 2015

Journal of Cardiovascular Pharmacology

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Although drug-eluting stents (DES) effectively improve the clinical efficacy of percutaneous coronary intervention, a high risk of late stent thrombosis and in-stent restenosis also exists after DES implantation. Anti-smooth muscle proliferation drugs, such as rapamycin, coating stents, not only inhibit the growth of vascular smooth muscle cells but also inhibit vascular endothelial cells and delay the reendothelialization. Therefore, the development of an ideal agent that protects vascular endothelial cells from rapamycin-eluting stents is of great importance for the next generation of DES. In this study, we demonstrated that rapamycin significantly inhibited the growth of rat aortic endothelial cells in both dose- and time-dependent manner in vitro. Cell apoptosis was increased and migration was decreased by rapamycin treatments in rat aortic endothelial cells in vitro. Surprisingly, treatment with curcumin, an active ingredient of turmeric, significantly reversed these detrimental effects of rapamycin. Moreover, curcumin increased the expression of vascular nitric oxide synthases (eNOS), which was decreased by rapamycin. Furthermore, caveolin-1, the inhibitor of eNOS, was decreased by curcumin. Knockdown of eNOS by small interfering RNA significantly abrogated the protective effects of curcumin. Taken together, our results suggest that curcumin antagonizes the detrimental effect of rapamycin on aortic endothelial cells in vitro through upregulating eNOS. Therefore, curcumin is a promising combined agent for the rescue of DES-induced reendothelialization delay.

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Section: Discussionmentioning

confidence: 99%

Curcumin Attenuates Rapamycin-induced Cell Injury of Vascular Endothelial Cells

Guo

Chen

Zhou

et al. 2015

Journal of Cardiovascular Pharmacology

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“…[28][29][30] SDF-1 also promotes endothelial tube formation. [31][32][33] We examined the effects of SDF-1 on capillary formation and outgrowth in vitro.…”

Section: Sdf-1 Promotes Capillary Formation In Vitromentioning

confidence: 99%

Microarray analysis of retinal endothelial tip cells identifies CXCR4 as a mediator of tip cell morphology and branching

Strasser¹,

Kaminker²,

Tessier‐Lavigne³

2010

Blood

247

226

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The development of the vertebrate vascular system is mediated by both genetic patterning of vessels and by angiogenic sprouting in response to hypoxia. Both of these processes depend on the detection of environmental guidance cues by endothelial cells. A specialized subtype of endothelial cell known as the tip cell is thought to be involved in the detection and response to these cues, but the molecular signaling pathways used by tip cells to mediate tissue vascularization remain largely uncharacterized. To identify genes critical to tip cell function, we have developed a method to isolate them using laser capture microdissection, permitting comparison of RNA extracted from endothelial tip cells with that of endothelial stalk cells using microarray analysis. Genes enriched in tip cells include ESM-1, angiopoietin-2, and SLP-76. CXCR4, a receptor for the chemokine stromal-cell derived factor-1, was also identified as a tip cell-enriched gene, and we provide evidence for a novel role for this receptor in mediating tip cell morphology and vascular patterning in the neonatal retina. IntroductionDuring embryogenesis, the vertebrate circulatory system develops through the overlapping processes of vasculogenesis and angiogenesis. Vasculogenesis is the migration and differentiation of endothelial cells from hematopoietic precursors. Angiogenesis involves the sprouting of blood vessel networks and their maturation into an organized, functional circulatory system. 1,2 Many aspects of angiogenesis are also recapitulated in the adult during normal conditions, such as pregnancy, and pathologic situations, such as inflammation and cancer. 3 An understanding of the molecular mechanisms that govern this process is critical for the development of novel proangiogenic and antiangiogenic therapeutics.A specialized subset of endothelial cells known as tip cells is thought to mediate vessel growth and patterning. Tip cells are found at the growing end of a nascent vascular sprout and are characterized by abundant and dynamic filopodia. These filopodia are thought to detect cues in the local environment and translate them into directed motility. 4,5 Tip cells are responsive to angiogenic factors, such as vascular endothelial growth factor-A (VEGF-A), 6 as well as classic axon guidance factors, such as netrin-1. 7 The generation of new tip cells is limited by the activity of Delta-like 4 (Dll4), [8][9][10][11] which is specifically up-regulated in tip cells. 12 Signaling of Dll4 through Notch receptors on adjacent cells has been proposed to inhibit their development into tip cells. 13 Despite these advances, the mechanisms that may promote or mediate the generation of new tip cells remain incompletely understood.Recently, endothelial tip cells have become a topic of intense scrutiny, 3 but many critical questions remain about their function and how they may differ from neighboring stalk cells. Expression of several genes, including VEGF receptor 2 (VEGFR2), 6 Dll4, PDGF-B, 6 and VEGFR3, 14 has been shown to be higher in retinal tip cel...

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“…In earlier findings of Fujiwara et al (2008), they demonstrated that curcumin increased the phosphorylation of AMPK and its downstream (Premanand et al 2006). In another study conducted by Sameermahmood et al (2008), they demonstrated that curcumin has an inhibitory effect on stromal cell-derived factor-1 (SDF-1) α-induced HREC migration by reducing downstream PI3K/Akt signals and blocking the upstream Ca 2+ influx (Sameermahmood et al 2008). In the retina of STZinduced diabetic rats, curcumin modulated the oxidatively modified DNA (8-OHdG), glutathione, SODC, and inflammatory parameters, including IL-1β, TNF-α, VEGF, and NF-кB, and may also inhibit the activation of nucleotide excision repair enzymes ).…”

Section: Antidiabetic Role Of Curcuminmentioning

confidence: 87%

Curcumin and its allied analogues: epigenetic and health perspectives - a review

Imran¹,

Nadeem²,

Khan³

et al. 2017

Czech J. Food Sci.

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Curcumin (diferuoyl methane) is a yellow active ingredient present in turmeric. It is a homodimer of feruloylmethane that comprises a hydroxyl and methoxy group (heptadiene with two Michael acceptors), and α-, β-diketone. It contains various metabolites, i.e. hexahydrocurcumin (HHC), tetrahydrocurcumin (THC), octahydrocurcumin (OHC), dihydrocurcumin (DHC), curcumin sulphate, and curcumin glucuronide. Curcumin has been proven the most effective histone deacetylase (HDAC) inhibitor in HeLa nuclear extracts. It has the ability to affect the Akt, growth factors, NF-kB, and metastatic and angiogenic pathways. Curcumin has a strong therapeutic or preventive potential against several major human ailments, i.e. suppression of inflammation, cardiovascular, diabetes, tumorigenesis, chronic fatigue, antidepressant and neurological activities, depression, loss of muscle and bone, and neuropathic pain. In future, higher utilisation of curcumin as an active agent in food based products is required to curtail the human health disorders.

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Curcumin Modulates SDF-1α/CXCR4–Induced Migration of Human Retinal Endothelial Cells (HRECs)

Abstract: This study indicates that curcumin has an inhibitory effect on SDF-1alpha-induced HREC migration. The plausible mechanism of action could be upstream blockage of Ca(2+) influx and the downstream reduction of PI3-K/AKT signals.

Cited by 43 publications

References 38 publications

Curcumin Attenuates Rapamycin-induced Cell Injury of Vascular Endothelial Cells

Curcumin Attenuates Rapamycin-induced Cell Injury of Vascular Endothelial Cells

Microarray analysis of retinal endothelial tip cells identifies CXCR4 as a mediator of tip cell morphology and branching

Curcumin and its allied analogues: epigenetic and health perspectives - a review

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