2013
DOI: 10.1161/circresaha.112.300695
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Cortistatin Inhibits Migration and Proliferation of Human Vascular Smooth Muscle Cells and Decreases Neointimal Formation on Carotid Artery Ligation

Abstract: Rationale: Proliferation and migration of smooth muscle cells (SMCs) are key steps for the progression of atherosclerosis and restenosis. Cortistatin is a multifunctional neuropeptide belonging to the somatostatin family that exerts unique functions in the nervous and immune systems. Cortistatin is elevated in plasma of patients experiencing coronary heart disease and attenuates vascular calcification. Objective: … Show more

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Cited by 54 publications
(75 citation statements)
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“…In many vascular pathological conditions including atherosclerosis and restenosis after angioplasty treatment, the abnormal proliferation and migration of VSMCs are crucial events in regulating the formation of neointimal hyperplasia, thickening of the inner layer of blood vessels (Duran-Prado et al, 2013;Miyake et al, 2011). Our previous study showed that recombinant WISP1 treatment induces proliferation and migration of rat VSMCs .…”
Section: Discussionmentioning
confidence: 99%
“…In many vascular pathological conditions including atherosclerosis and restenosis after angioplasty treatment, the abnormal proliferation and migration of VSMCs are crucial events in regulating the formation of neointimal hyperplasia, thickening of the inner layer of blood vessels (Duran-Prado et al, 2013;Miyake et al, 2011). Our previous study showed that recombinant WISP1 treatment induces proliferation and migration of rat VSMCs .…”
Section: Discussionmentioning
confidence: 99%
“…Inhibition of the Akt/mTOR signaling cascade by phosphatase and tensin homolog deleted on chromosome 10 (PTEN) (a phosphatase that converts phosphatidylinositol 4,5-trisphosphate to phosphatidylinositol 4,5-bisphosphate, inhibiting Akt phosphorylation), rapamycin (which blocks mTOR), or Akt inhibition (specific inhibitors that bind to Akt to prevent its phosphorylation), has been well demonstrated to attenuate cell proliferation in cancer cells (64), embryonic stem cells (2,61), vascular progenitor cells (25,27), coronary arterial smooth muscle cells (9,14), and PASMC (19,20,29,49). Our previous work has also demonstrated the importance of the Akt/mTOR pathway in both thrombin-and PDGF-induced enhancement of store-operated Ca 2ϩ entry (SOCE) and cell proliferation in PASMC (44,45), whereas downregulation of transient receptor potential canonical (TRPC) channels reduced SOCE and significantly inhibit PASMC proliferation and migration (59,72).…”
mentioning
confidence: 99%
“…The proliferation of VSMCs is the main phase for the progression of atherosclerosis and restenosis (Duran-Prado et al ., 2013). Herein, the effects of KR-36676 on the proliferation of UII (50 nM)-stimulated hAoSMCs were assessed through analysis of DNA synthesis using the incorporation of BrdU.…”
Section: Resultsmentioning
confidence: 99%
“…The activation of MAPK is known to have critical role in the UII-induced proliferation of VSMCs (Djordjevic et al ., 2005; Duran-Prado et al ., 2013). Therefore, the effects of inhibitors of p38 MAPK, JNK, and ERK1/ on VSMC proliferation were examined.…”
Section: Resultsmentioning
confidence: 99%