2012
DOI: 10.1371/journal.pone.0044476
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Cilostazol Prevents Endothelin-Induced Smooth Muscle Constriction and Proliferation

Abstract: Cilostazol is a phosphodiesterase inhibitor that has been shown to inhibit platelet activation. Endothelin is known to be the most potent endogenous growth promoting and vasoactive peptide. In patients and animal models with stroke, the level of circulating endothelin increases and complicates the recovery progress contributed by vascular constriction (an immediate pathology) and vascular proliferation (a long-term pathology). However, the effects of cilostazol on endothelin have not been explored. To demonstr… Show more

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Cited by 25 publications
(20 citation statements)
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“…). Cilostazol is a specific inhibitor for phosphodiesterase‐3, an enzyme that metabolizes cAMP to AMP, and it also regulates intracellular calcium (Kawanabe et al, ). It has been known that cAMP and calcium could regulate cilia beating frequency (Nguyen et al, ; Monkkonen et al, ; Genzen et al, ), but the differential effect of cilostazol and many other pharmacological agents requires further in‐depth study to advance our understanding of the molecular and cellular biology of different ependymal cell types.…”
Section: Discussionmentioning
confidence: 99%
“…). Cilostazol is a specific inhibitor for phosphodiesterase‐3, an enzyme that metabolizes cAMP to AMP, and it also regulates intracellular calcium (Kawanabe et al, ). It has been known that cAMP and calcium could regulate cilia beating frequency (Nguyen et al, ; Monkkonen et al, ; Genzen et al, ), but the differential effect of cilostazol and many other pharmacological agents requires further in‐depth study to advance our understanding of the molecular and cellular biology of different ependymal cell types.…”
Section: Discussionmentioning
confidence: 99%
“…In our experiments, we used isolated primary VSMCs and endothelial cells from mouse femoral and mesenteric arteries in vitro. The isolation of primary cells is routinely performed in our laboratory for both endothelial cells (1) and VSMCs (17). Because the arteries were composed of only a single layer of endothelial cells, we regularly confirmed the presence of an endothelial marker (ICAM-2) using flow cytometry, as previously described (1).…”
Section: Methodsmentioning
confidence: 99%
“…These images were captured through a fura-2 filter kit that contains 25-mm 340/380-nm exciter filters, a dichroic mirror, and a wide-band 510-nm emission filter. A more detailed protocol has been previously described (17). To examine intracellular NO, cells were loaded for 30 min at 37°C with 20 M 4-amino-5-methylamino-2=,7=-difluorofluorescein (Invitrogen), as previously described (17).…”
Section: Methodsmentioning
confidence: 99%
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“…Notably, ET-1 is synthesized by arterial myocytes, 35 a cell that expresses GPR81. Further, a reduction in cAMP stimulates the production of ET-1 by myocytes, [36][37][38] as does vascular disease and injury. 39,40 The hemodynamic response to AZ′5538 is also consistent with this sequence: ET-1, via endothelin-A receptors, induces a stronger constriction of the afferent than efferent arteriole 41 and also causes pericyte contraction, reducing vasa recta blood flow, 42 both of which were found in our study.…”
Section: Discussionmentioning
confidence: 99%