Calphostin C as a rapid and strong inducer of apoptosis in human coronary artery smooth muscle cells

Krueger, Kristopher; Hunter, William J.; DelCore, Michael; Agrawal, Devendra K.

doi:10.1016/s1567-5769(03)00206-6

Cited by 8 publications

(4 citation statements)

References 27 publications

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“…16 We have recently reported that TNF-a was expressed by VSMC in atheromatous plaques and TNF-a alone or in combination with other cytokines stimulated apoptosis of VSMC. 17 In this study, we show for the first time that TNF-a can induce the autophagy in plaque VSMC. During autophagy part of the cytoplasm or entire organelles were sequestered into double-membraned vesicles, called autophagic vacuoles or autophagosomes.…”

Section: Discussionmentioning

confidence: 55%

“…In the atherosclerotic lesion, inflammatory processes change the structural integrity of the coronary plaque and activated macrophages are known to produce cytokines, proteolytic enzymes and growth factors that alter growth and survival of VSMC and modify the extracellular matrix 16 . We have recently reported that TNF‐α was expressed by VSMC in atheromatous plaques and TNF‐α alone or in combination with other cytokines stimulated apoptosis of VSMC 17 . In this study, we show for the first time that TNF‐α can induce the autophagy in plaque VSMC.…”

Section: Discussionmentioning

confidence: 99%

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Insulin‐like growth factor‐1 and TNF‐α regulate autophagy through c‐jun N‐terminal kinase and Akt pathways in human atherosclerotic vascular smooth cells

et al. 2006

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Summary A balance between programmed cell death and survival of vascular smooth muscle cells (VSMC) in the fibrous cap, which is primarily composed of VSMC and extracellular matrix, appears to best correlate with plaque instability or stability and is controlled by growth factors and cytokines. Autophagy is also involved in programmed cell death. We assessed the effect of TNF-a and insulin-like growth factor-1 (IGF-1) on the expression of autophagic genes, microtubule-associated protein 1 light chain 3 (MAPLC-3) and Beclin-1 in VSMC isolated from atherosclerotic plaques. Transmission electron microscopy showed a significantly higher number of vacuolated cells in the TNF-atreated VSMC and a markedly lower number in the IGF-1-treated VSMC when compared with the untreated control group. TNF-a-induced MAPLC-3 mRNA expression through c-jun N-terminal kinase and protein kinase B pathways and induced Beclin-1 protein expression through the c-jun N-terminal kinase pathway. Expression of MAPLC-3 and Beclin-1 correlated with autophagic cell death of plaque VSMC. IGF-1 inhibited MAPLC-3 mRNA transcripts through the Akt pathway. These findings suggest that the expression of autophagy genes can be influenced by IGF-1 and TNF-a through c-jun N-terminal kinase or Akt pathways and autophagy might be involved in the regulation of plaque stability.

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Section: Discussionmentioning

confidence: 55%

Section: Discussionmentioning

confidence: 99%

Insulin‐like growth factor‐1 and TNF‐α regulate autophagy through c‐jun N‐terminal kinase and Akt pathways in human atherosclerotic vascular smooth cells

et al. 2006

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“…4 Insulin-like growth factor-1 (IGF-1) is a 70-amino-acid peptide that mediates most of its biological effects through the IGF-1 receptor (IGF-1R), which has intrinsic tyrosine-kinase activity. 5 IGF-1 can cause many cellular effects, including embryonic viability, growth, differentiation, cell-cycle regulation, cell proliferation and apoptosis inhibition/cell survival through the activation of PI3-K-Akt-protein kinase B and rasraf-MAPK/ERK kinase-mitogen-activated protein kinase pathways. 6 The balance between proliferation and apoptosis of VSMC plays a crucial role in the progression of the atheroma plaque.…”

Section: Introductionmentioning

confidence: 99%

Differential effects of insulin‐like growth factor‐1 and atheroma‐associated cytokines on cell proliferation and apoptosis in plaque smooth muscle cells of symptomatic and asymptomatic patients with carotid stenosis

2006

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Summary Morbidity and mortality from atherosclerosis are associated with complicated atherosclerotic lesions due to plaque rupture, which is regulated by a balance between proliferation and apoptosis of vascular smooth muscle cells (VSMC). We examined insulin-like growth factor-1 (IGF-1)-induced survival of plaque VSMC from carotid endarterectomy specimens and investigated the underlying cellular mechanisms in the presence and absence of IL-12 and IFN-g. Both IL-12 and IFN-g were strongly expressed in symptomatic atherosclerotic plaques as compared with asymptomatic plaques. In asymptomatic plaque VSMC, IGF-1 induced the survival and proliferation of VSMC and accelerated VSMC into S-phase. IL-12 or IFN-g inhibited proliferation and VSMC were arrested in the G 0 -G 1 phase. IGF-1 markedly inhibited the expression of p27 kip and p21 cip and significantly induced cyclin E and cyclin D. Both cytokines by themselves increased the expression of p27 kip and p21 cip and inhibited cyclin E and cyclin D. On the contrary, in symptomatic VSMC there was already increased apoptosis of VSMC and there was no significant effect of IGF-1 or inflammatory cytokines on proliferation, apoptosis or the expression of p27 kip and p21 cip and cyclin D and E. These data suggest that IGF-1 is more potent in inducing the survival of VSMC from the endarterectomy specimens of asymptomatic patients as compared to that of symptomatic subjects and cytokines associated with atheroma lesions decrease the activity of IGF-1-induced survival in the VSMC of asymptomatic plaques. The different expression and activity of cell cycle regulatory proteins could be responsible for apoptosis of VSMC and destabilization of atherosclerotic plaques.

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“…These studies suggest that excessive autophagy is one of the mechanisms in histiocyte injury. Studies have shown that under certain conditions, the activation of autophagy may cause VSMC necrosis and apoptosis (Krueger et al, 2003 ), suggesting that autophagy plays an important role in vascular diseases by regulating VSMC function. To further explore the role of autophagy homeostasis in the improvement of vascular reactivity after hemorrhagic shock by SGB, autophagy-related drugs were used in rats with hemorrhagic shock in vivo and VSMCs in vitro .…”

Section: Discussionmentioning

confidence: 99%

Autophagy Is Involved in Stellate Ganglion Block Reversing Posthemorrhagic Shock Mesenteric Lymph-Mediated Vascular Hyporeactivity

Wang

Zhao

et al. 2021

Front. Physiol.

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Objective: The aim of this study was to clarify the role of autophagy in stellate ganglion block (SGB) reversing posthemorrhagic shock mesenteric lymph (PHSML)-mediated vascular hyporeactivity.Methods: Hemorrhagic shock model in conscious rats was employed to observe the effects of SGB (0.2 ml of 0.25% ropivacaine hydrochloride hydrate) and autophagy inhibitor 3-methyladenine (3-MA; 30 mg/kg) on the vascular reactivity of second-order rat mesenteric arteries in vitro, while the effects of PHSML (1 ml/kg) and autophagy agonist rapamycin (Rapa, 10 mg/kg) on the beneficial effect of SGB were investigated. The cellular viability, contractility, and autophagy-related protein expressions in vascular smooth muscle cells (VSMCs) were detected following treatments of PHSML, PHSML obtained from the rats that underwent hemorrhagic shock plus SGB (PHSML-SGB), and PHSML plus 3-MA (5 mM), respectively.Results: Hemorrhagic shock significantly decreased the vascular reactivity to gradient norepinephrine (NE), which is reversed by the SGB treatment and 3-MA administration. On the contrary, PHSML intravenous infusion and Rapa administration inhibited the vascular contractile responses in rats that underwent hemorrhagic shock plus SGB treatment. PHSML treatment significantly inhibited the cellular viability and contractility in VSMCs, increased the expressions of LC3-II and Beclin 1, and decreased the expression of p62, along with opposite appearances in these indices following PHSML-SGB treatment. In addition, 3-MA counteracted the adverse roles of PHSML in these indices in VSMCs.Conclusion: SGB inhibits PHSML-mediated vascular hyporeactivity by reducing the excessive autophagy in VSMCs.

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Calphostin C as a rapid and strong inducer of apoptosis in human coronary artery smooth muscle cells

Cited by 8 publications

References 27 publications

Insulin‐like growth factor‐1 and TNF‐α regulate autophagy through c‐jun N‐terminal kinase and Akt pathways in human atherosclerotic vascular smooth cells

Insulin‐like growth factor‐1 and TNF‐α regulate autophagy through c‐jun N‐terminal kinase and Akt pathways in human atherosclerotic vascular smooth cells

Differential effects of insulin‐like growth factor‐1 and atheroma‐associated cytokines on cell proliferation and apoptosis in plaque smooth muscle cells of symptomatic and asymptomatic patients with carotid stenosis

Autophagy Is Involved in Stellate Ganglion Block Reversing Posthemorrhagic Shock Mesenteric Lymph-Mediated Vascular Hyporeactivity

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