Influence of Intracellular Zinc on Cultures of Rat Cardiac Neural Crest Cells

Yang, Hsunhui; Keen, Carl L.; Lanoue, Louise

doi:10.1002/bdrb.21135

Cited by 7 publications

(2 citation statements)

References 86 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…TPEN [K d =2.6×10 −16 M (34)], another Zn chelator, exhibited an increased affinity for Zn 2+ compared with CQ [K d =~1×10 −7 M (34)]. Previous studies (35,36) indicated TPEN was an effective tool for inhibiting Zn in cell models, so it was selected for the in vitro experiments.…”

Section: Discussionmentioning

confidence: 99%

Zinc supplementation inhibits the high glucose‑induced EMT of peritoneal mesothelial cells by activating the Nrf2 antioxidant pathway

et al. 2019

View full text Add to dashboard Cite

The high glucose (HG)-induced epithelial-mesenchymal transition (EMT) of peritoneal mesothelial cells (PMCs) serves an important role in peritoneal fibrosis (PF) during peritoneal dialysis. Our previous study reported that zinc (Zn) supplementation prevented the HG-induced EMT of rat PMCs in vitro . In the present study, the role of Zn in HG-induced EMT was investigated in vivo using a rat model of PF. Additionally, the molecular mechanisms underlying HG-induced EMT were studied in human PMCs (HPMCs). In the rat model of PF, HG treatment increased the glucose transfer capacity and decreased the ultrafiltration volume. Histopathological analysis revealed peritoneal thickening, increased expression of vimentin and decreased expression of E-cadherin. ZnSO 4 significantly ameliorated the aforementioned changes, whereas Zn inhibition by clioquinol significantly aggravated the effects of HG on rats. The effects of Zn on HPMCs was assessed using western blot analysis, Transwell assays and flow cytometry. It was revealed that Zn also significantly suppressed the extent of the EMT, and reduced reactive oxygen species production and the migratory ability of HG-induced HPMCs, whereas Zn inhibition by N',N',N',N'-tetrakis (2-pyridylmethyl) ethylenediamine significantly potentiated the HG-induced EMT of HPMCs. HG-stimulated HPMCs exhibited increased expression of nuclear factor-like 2 (Nrf2) in the nucleus, and total cellular NAD(P)H quinone dehydrogenase 1 (NQO1) and heme oxygenase-1 (HO-1), the target proteins of the Nrf2 antioxidant pathway. Zn supplementation further promoted nuclear Nrf2 expression, and increased the expression of target proteins of the Nrf2 antioxidant pathway, whereas Zn depletion decreased nuclear Nrf2, NQO1 and HO-1 expression compared with the HG group. In conclusion, Zn supplementation was proposed to suppress the effects of HG on the EMT by stimulating the Nrf2 antioxidant pathway and subsequently reducing oxidative stress in PMCs.

show abstract

Section: Discussionmentioning

confidence: 99%

Zinc supplementation inhibits the high glucose‑induced EMT of peritoneal mesothelial cells by activating the Nrf2 antioxidant pathway

et al. 2019

View full text Add to dashboard Cite

show abstract

“…Further studies have illustrated that cardiac malformations induced by Zn deficiency were mainly involved in the great vessels, the outflow tract and the development of the atrium and ventricle, which may possibly due to the anomalous distribution, amount, and function of cardiac neural crest cells (cNCC) during embryonic development ( 55 , 56 ). Indeed, rat cNCC cells cultured in Zn-deficient media exhibited decreased cell viability, and elevated oxidative stress levels and active caspase-3 expressions ( 57 ). Another study used connexin-43 (Cx43) and HNK-1 as biomarkers of cNCC and found abnormal amount and distribution of Cx43 and HNK-1 in the embryonic hearts of Zn-deficient rats ( 56 ).…”

Section: Essential Trace Elements and Congenital Heart Diseasesmentioning

confidence: 99%

Exposure to essential and non-essential trace elements and risks of congenital heart defects: A narrative review

et al. 2023

View full text Add to dashboard Cite

Congenital heart defects (CHDs) are congenital abnormalities involving the gross structures of the heart and large blood vessels. Environmental factors, genetic factors and their interactions may contribute to the pathogenesis of CHDs. Generally, trace elements can be classified into essential trace elements and non-essential trace elements. Essential trace elements such as copper (Cu), zinc (Zn), iron (Fe), selenium (Se), and manganese (Mn) play important roles in human biological functions such as metabolic function, oxidative stress regulation, and embryonic development. Non-essential trace elements such as cadmium (Cd), arsenic (As), lead (Pb), nickle (Ni), barium (Ba), chromium (Cr) and mercury (Hg) are harmful to health even at low concentrations. Recent studies have revealed the potential involvement of these trace elements in the pathogenesis of CHDs. In this review, we summarized current studies exploring exposure to essential and non-essential trace elements and risks of CHDs, in order to provide further insights for the pathogenesis and prevention of CHDs.

show abstract

Does roundup affect zinc functions in a bivalve mollusk in ex vivo exposure?

et al. 2022

View full text Add to dashboard Cite

Influence of Intracellular Zinc on Cultures of Rat Cardiac Neural Crest Cells

Abstract: Zn deficiency can result in oxidative stress in cNCC, and subsequent decreases in their population and metabolic activity. These data support the concept that Zn deficiency associated developmental heart defects may arise in part as a consequence of altered cNCC metabolism.

Cited by 7 publications

References 86 publications

Zinc supplementation inhibits the high glucose‑induced EMT of peritoneal mesothelial cells by activating the Nrf2 antioxidant pathway

Zinc supplementation inhibits the high glucose‑induced EMT of peritoneal mesothelial cells by activating the Nrf2 antioxidant pathway

Exposure to essential and non-essential trace elements and risks of congenital heart defects: A narrative review

Does roundup affect zinc functions in a bivalve mollusk in ex vivo exposure?

Contact Info

Product

Resources

About