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Hypoxia augments the calcium-activated chloride current carried by anoctamin-1 in cardiac vascular endothelial cells of neonatal mice.

Wu MM, Lou J, Song BL, Gong YF, Li YC, Yu CJ, Wang QS, Ma TX, Ma K, Hartzell HC, Duan DD, Zhao D, Zhang ZR - Br. J. Pharmacol. (2014)

Bottom Line: The density of ICl ( C a) detected in CVECs was significantly inhibited by T16Ainh -A01, an Ano1 inhibitor, and a pore-targeting, specific anti-Ano1 antibody, and was markedly decreased in Ano1 gene knockdown CVECs.Ano1 formed CaCC in CVECs of neonatal mice.Ano1 may play a role in the pathophysiological processes during ischaemia in heart, and therefore, Ano1 might be a potential therapeutic target to prevent ischaemic damage.

View Article: PubMed Central - PubMed

Affiliation: Departments of Clinical Pharmacy and Cardiology, Institute of Clinical Pharmacy, The 2nd Affiliated Hospital, Key Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, Harbin Medical University, Harbin, China.

No MeSH data available.


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qRT-PCR demonstrating hypoxia induces an altered expression ratio of Ano1 splicing variants in CVECs. (A and B) The relative mRNA expression levels of exons 6b and 13 excluded Ano1 were significantly up-regulated by hypoxia (n = 7). (C) Hypoxia did not affect the expression levels of exon 15 excluded Ano1 (n = 7). *P < 0.05, significantly different from control.
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fig07: qRT-PCR demonstrating hypoxia induces an altered expression ratio of Ano1 splicing variants in CVECs. (A and B) The relative mRNA expression levels of exons 6b and 13 excluded Ano1 were significantly up-regulated by hypoxia (n = 7). (C) Hypoxia did not affect the expression levels of exon 15 excluded Ano1 (n = 7). *P < 0.05, significantly different from control.

Mentions: The human Ano1 splicing variants (deletion of exons 6b, 13 and 15) are known to generate the currents with distinct biophysical properties to wild-type Ano1 (Ferrera et al., 2009; Mazzone et al., 2011). Furthermore, there are a variety of Ano1 splicing variants in mouse heart and these splicing events are highly conserved between human and mouse (O'Driscoll et al., 2011). Therefore, we examined whether hypoxia may cause the changes in the ratio of Ano1 splicing variants, which, in turn, alter the biophysical properties of Ano1-mediated ICa(Cl). Our qRT-PCR data showed that under hypoxic condition, the mRNA expression levels of Ano1 splicing variants lacking of exons 6b and 13 (Fig. 7A and B), but not lacking exon 15 (Fig. 7C), were significantly higher than those of control (the primers used are listed in Supporting Information Table 2). These results suggest that changes in the ratio of Ano1 splicing variants may involve in the altered biophysical properties of Ano1-mediated ICa(Cl) under hypoxic condition.


Hypoxia augments the calcium-activated chloride current carried by anoctamin-1 in cardiac vascular endothelial cells of neonatal mice.

Wu MM, Lou J, Song BL, Gong YF, Li YC, Yu CJ, Wang QS, Ma TX, Ma K, Hartzell HC, Duan DD, Zhao D, Zhang ZR - Br. J. Pharmacol. (2014)

qRT-PCR demonstrating hypoxia induces an altered expression ratio of Ano1 splicing variants in CVECs. (A and B) The relative mRNA expression levels of exons 6b and 13 excluded Ano1 were significantly up-regulated by hypoxia (n = 7). (C) Hypoxia did not affect the expression levels of exon 15 excluded Ano1 (n = 7). *P < 0.05, significantly different from control.
© Copyright Policy - open-access
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4128065&req=5

fig07: qRT-PCR demonstrating hypoxia induces an altered expression ratio of Ano1 splicing variants in CVECs. (A and B) The relative mRNA expression levels of exons 6b and 13 excluded Ano1 were significantly up-regulated by hypoxia (n = 7). (C) Hypoxia did not affect the expression levels of exon 15 excluded Ano1 (n = 7). *P < 0.05, significantly different from control.
Mentions: The human Ano1 splicing variants (deletion of exons 6b, 13 and 15) are known to generate the currents with distinct biophysical properties to wild-type Ano1 (Ferrera et al., 2009; Mazzone et al., 2011). Furthermore, there are a variety of Ano1 splicing variants in mouse heart and these splicing events are highly conserved between human and mouse (O'Driscoll et al., 2011). Therefore, we examined whether hypoxia may cause the changes in the ratio of Ano1 splicing variants, which, in turn, alter the biophysical properties of Ano1-mediated ICa(Cl). Our qRT-PCR data showed that under hypoxic condition, the mRNA expression levels of Ano1 splicing variants lacking of exons 6b and 13 (Fig. 7A and B), but not lacking exon 15 (Fig. 7C), were significantly higher than those of control (the primers used are listed in Supporting Information Table 2). These results suggest that changes in the ratio of Ano1 splicing variants may involve in the altered biophysical properties of Ano1-mediated ICa(Cl) under hypoxic condition.

Bottom Line: The density of ICl ( C a) detected in CVECs was significantly inhibited by T16Ainh -A01, an Ano1 inhibitor, and a pore-targeting, specific anti-Ano1 antibody, and was markedly decreased in Ano1 gene knockdown CVECs.Ano1 formed CaCC in CVECs of neonatal mice.Ano1 may play a role in the pathophysiological processes during ischaemia in heart, and therefore, Ano1 might be a potential therapeutic target to prevent ischaemic damage.

View Article: PubMed Central - PubMed

Affiliation: Departments of Clinical Pharmacy and Cardiology, Institute of Clinical Pharmacy, The 2nd Affiliated Hospital, Key Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, Harbin Medical University, Harbin, China.

No MeSH data available.


Related in: MedlinePlus