Long-term zinc deprivation accelerates rat vascular smooth muscle cell proliferation involving the down-regulation of JNK1/2 expression in MAPK signaling

Alcantara, Ethel H.; Shin, Mee-Young; Feldmann, Jörg; Nixon, Graeme F.; Beattie, John; Kwun, In Sook

doi:10.1016/j.atherosclerosis.2013.01.030

Cited by 36 publications

(27 citation statements)

References 30 publications

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“…25 Furthermore, in a Swedish cohort, a highly dietary intake of Zn 2þ was associated with a reduced risk of PCaspecific mortality providing medical impact regarding Zn 2þ and prostate pathogenesis. 26 Interestingly, in proliferative studies using rat vascular SMCs, a long-term Zn 2þ deprivation generates accelerated proliferation, 27 whereas Zn 2þ supplement increased human airway SMC apoptosis, 28 which supports our results.…”

Section: Commentsupporting

confidence: 82%

Zinc Induces a Bell-shaped Proliferative Dose-response Effect in Cultured Smooth Muscle Cells From Benign Prostatic Hyperplasia

Adolfsson

Bloth

Hägg

et al. 2015

Urology

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Section: Commentsupporting

confidence: 82%

Zinc Induces a Bell-shaped Proliferative Dose-response Effect in Cultured Smooth Muscle Cells From Benign Prostatic Hyperplasia

Adolfsson

Bloth

Hägg

et al. 2015

Urology

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“…In vitro , vSMCs replicated slower when cultured at 80∼120 μM zinc ion concentration . Even when Zn 2+ was low to 50 m M , the proliferative damage still occurred in a long‐term exposure experiment . In addition, the free Zn 2+ also hindered the cell movement of human aortic SMCs .…”

Section: Discussionmentioning

confidence: 98%

Magnesium ion leachables induce a conversion of contractile vascular smooth muscle cells to an inflammatory phenotype

et al. 2018

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Phenotype switching is a characteristic response of vascular smooth muscle cells (vSMCs) to the dynamic microenvironment and contributes to all stages of atherosclerotic plaque. Here, we immersed pure magnesium and AZ31 alloy in the completed medium under cell culture condition, applied the resultant leaching extracts to the isolated contractile rat aortic vSMCs and investigated how vSMCs phenotypically responded to the degradation of the magnesium-based stent materials. vSMCs became more proliferative and migratory but underwent more apoptosis when exposed to the degradation products of pure magnesium; while the AZ31 extracts caused less cell division but more apoptosis, thus slowing cell moving and growing. Noticeably, both leaching extracts dramatically downregulated the contractile phenotypic genes at mRNA and protein levels while significantly induced the inflammatory adhesive molecules and cytokines. Exogenously added Mg ions excited similar transformations of vSMCs. With the liberation or supplementation of Mg 2+ , the expression patterns of the pro-contractile transactivator myocardin and the pro-inflammatory transcriptional factor kruppel-like factor 4 (KLF4) were reversed. Overall, the degradation of the Mg-based materials would evoke a shift of the contractile vSMCs to an inflammatory phenotype via releasing Mg ions to induce a transition from the phenotypic control of vSMCs by the myocardin to that by the KLF4.How to cite this article: Zhou Y, Liu X, Huang N, Chen Y. 2019. Magnesium ion leachables induce a conversion of contractile vascular smooth muscle cells to an inflammatory phenotype. J Biomed Mater Res Part B 2019:107B:988-1001.

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“…Cells were also cultured with zinc level (0, 1, 15 μM ZnCl 2 ) by adding zinc back to culture media with the chelexed FBS. Chelexed FBS provided zinc-depleted serum for the cell culture for cellular zinc depletion (8). …”

Section: Methodsmentioning

confidence: 99%

Phosphate-Induced Rat Vascular Smooth Muscle Cell Calcification and the Implication of Zinc Deficiency in A7r5 Cell Viability

Shin

Kwun

2013

JFN

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The calcification of vascular smooth muscle cells (VSMCs) is considered one of the major contributors for vascular disease. Phosphate is known as the inducer for VSMC calcification. In this study, we assessed whether phosphate affected cell viability and fetuin-A, a calcification inhibitor protein, both which are related to VSMC calcification. Also, VSMC viability by zinc level was assessed. The results showed that phosphate increased Ca and P deposition in VSMCs (A7r5 cell line, rat aorta origin). This phosphate-induced Ca and P deposition was consistent with the decreased A7r5 cell viability (P<0.05), which implies phosphate-induced calcification in A7r5 cells might be due to the decreased VSMC cell viability. As phosphate increased, the protein expression of fetuin-A protein was up-regulated. A7r5 cell viability decreased as the addition of cellular zinc level was decreased (P<0.05). The results suggested that zinc deficiency causes the decreased cell viability and it would be the future study to clarify how zinc does act for VSMC cell viability. The results suggest that the decreased VSMC viability by high P or low Zn in VSMCs may be the risk factor for vascular disease.

show abstract

Long-term zinc deprivation accelerates rat vascular smooth muscle cell proliferation involving the down-regulation of JNK1/2 expression in MAPK signaling

Cited by 36 publications

References 30 publications

Zinc Induces a Bell-shaped Proliferative Dose-response Effect in Cultured Smooth Muscle Cells From Benign Prostatic Hyperplasia

Zinc Induces a Bell-shaped Proliferative Dose-response Effect in Cultured Smooth Muscle Cells From Benign Prostatic Hyperplasia

Magnesium ion leachables induce a conversion of contractile vascular smooth muscle cells to an inflammatory phenotype

Phosphate-Induced Rat Vascular Smooth Muscle Cell Calcification and the Implication of Zinc Deficiency in A7r5 Cell Viability

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