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Aquaporin-1 Deficiency Protects Against Myocardial Infarction by Reducing Both Edema and Apoptosis in Mice.

Li L, Weng Z, Yao C, Song Y, Ma T - Sci Rep (2015)

Bottom Line: Under physiological conditions, AQP1-/- mice develop normally; however, in the setting of MI, they exhibit cardioprotective properties, as shown by reduced cardiac infarct size determined via NBT staining, improved cardiac function determined via left ventricular catheter measurements, decreased AQP1-dependent myocardial edema determined via water content assays, and decreased apoptosis determined via TUNEL analysis.AQP1 deficiency protected cardiac function from ischemic injury following MI.Furthermore, AQP1 deficiency reduced microvascular permeability via the stabilization of HIF-1α levels in endothelial cells and decreased cellular apoptosis following MI.

View Article: PubMed Central - PubMed

Affiliation: Liaoning Medical University, Department of Cell Biology, Jinzhou, PR China.

ABSTRACT
Many studies have determined that AQP1 plays an important role in edema formation and resolution in various tissues via water transport across the cell membrane. The aim of this research was to determine both if and how AQP1 is associated with cardiac ischemic injury, particularly the development of edema following myocardial infarction (MI). AQP1+/+ and AQP1-/- mice were used to create the MI model. Under physiological conditions, AQP1-/- mice develop normally; however, in the setting of MI, they exhibit cardioprotective properties, as shown by reduced cardiac infarct size determined via NBT staining, improved cardiac function determined via left ventricular catheter measurements, decreased AQP1-dependent myocardial edema determined via water content assays, and decreased apoptosis determined via TUNEL analysis. Cardiac ischemia caused by hypoxia secondary to AQP1 deficiency stabilized the expression of HIF-1α in endothelial cells and subsequently decreased microvascular permeability, resulting in the development of edema. The AQP1-dependent myocardial edema and apoptosis contributed to the development of MI. AQP1 deficiency protected cardiac function from ischemic injury following MI. Furthermore, AQP1 deficiency reduced microvascular permeability via the stabilization of HIF-1α levels in endothelial cells and decreased cellular apoptosis following MI.

No MeSH data available.


Related in: MedlinePlus

The effects of AQP1 deficiency on the expression of HIF-1α and AQP1 at 24 hours after MI.(a) Photographs and a quantitative analysis of the expression of HIF-1α via Western blotting in the AQP1−/− and AQP1+/+ mice. The HIF-1α expression level was significantly increased following MI in the AQP1+/+ mice compared with the AQP1−/− mice (n = 6, *P < 0.01 vs sham. ##P < 0.01 vs AQP1+/+ MI mice). (b) Photographs and a quantitative analysis of the expression of AQP1 via Western blotting in the AQP1+/+ MI mice compared with the sham-operated AQP1+/+ mice (n = 6, *P < 0.01).
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f5: The effects of AQP1 deficiency on the expression of HIF-1α and AQP1 at 24 hours after MI.(a) Photographs and a quantitative analysis of the expression of HIF-1α via Western blotting in the AQP1−/− and AQP1+/+ mice. The HIF-1α expression level was significantly increased following MI in the AQP1+/+ mice compared with the AQP1−/− mice (n = 6, *P < 0.01 vs sham. ##P < 0.01 vs AQP1+/+ MI mice). (b) Photographs and a quantitative analysis of the expression of AQP1 via Western blotting in the AQP1+/+ MI mice compared with the sham-operated AQP1+/+ mice (n = 6, *P < 0.01).

Mentions: In order to determine the cellular mechanisms underlying AQP1-dependent myocardial edema, we examined HIF-1α levels in cardiac tissue following MI. Increases in the HIF-1α levels of vascular endothelial cells represent one of the earliest responses to myocardial ischemia and infarction16. Our previous in vitro studies have demonstrated that AQPs facilitate the secretion of specific cytokines17. Therefore, the HIF-1α level during the early phase of MI was assayed via immunoblotting. Figure 5(a) demonstrates that the expression of HIF-1α in the AQP1+/+ MI mice was significantly increased compared with the AQP1−/− MI mice. Moreover, the level of AQP1 expression in the MI mice was also increased compared with the control mice [Fig. 5(b)]. The level of HIF-1α expression correlated with AQP1 expression and reinforced its involvement in MI.


Aquaporin-1 Deficiency Protects Against Myocardial Infarction by Reducing Both Edema and Apoptosis in Mice.

Li L, Weng Z, Yao C, Song Y, Ma T - Sci Rep (2015)

The effects of AQP1 deficiency on the expression of HIF-1α and AQP1 at 24 hours after MI.(a) Photographs and a quantitative analysis of the expression of HIF-1α via Western blotting in the AQP1−/− and AQP1+/+ mice. The HIF-1α expression level was significantly increased following MI in the AQP1+/+ mice compared with the AQP1−/− mice (n = 6, *P < 0.01 vs sham. ##P < 0.01 vs AQP1+/+ MI mice). (b) Photographs and a quantitative analysis of the expression of AQP1 via Western blotting in the AQP1+/+ MI mice compared with the sham-operated AQP1+/+ mice (n = 6, *P < 0.01).
© Copyright Policy - open-access
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4562302&req=5

f5: The effects of AQP1 deficiency on the expression of HIF-1α and AQP1 at 24 hours after MI.(a) Photographs and a quantitative analysis of the expression of HIF-1α via Western blotting in the AQP1−/− and AQP1+/+ mice. The HIF-1α expression level was significantly increased following MI in the AQP1+/+ mice compared with the AQP1−/− mice (n = 6, *P < 0.01 vs sham. ##P < 0.01 vs AQP1+/+ MI mice). (b) Photographs and a quantitative analysis of the expression of AQP1 via Western blotting in the AQP1+/+ MI mice compared with the sham-operated AQP1+/+ mice (n = 6, *P < 0.01).
Mentions: In order to determine the cellular mechanisms underlying AQP1-dependent myocardial edema, we examined HIF-1α levels in cardiac tissue following MI. Increases in the HIF-1α levels of vascular endothelial cells represent one of the earliest responses to myocardial ischemia and infarction16. Our previous in vitro studies have demonstrated that AQPs facilitate the secretion of specific cytokines17. Therefore, the HIF-1α level during the early phase of MI was assayed via immunoblotting. Figure 5(a) demonstrates that the expression of HIF-1α in the AQP1+/+ MI mice was significantly increased compared with the AQP1−/− MI mice. Moreover, the level of AQP1 expression in the MI mice was also increased compared with the control mice [Fig. 5(b)]. The level of HIF-1α expression correlated with AQP1 expression and reinforced its involvement in MI.

Bottom Line: Under physiological conditions, AQP1-/- mice develop normally; however, in the setting of MI, they exhibit cardioprotective properties, as shown by reduced cardiac infarct size determined via NBT staining, improved cardiac function determined via left ventricular catheter measurements, decreased AQP1-dependent myocardial edema determined via water content assays, and decreased apoptosis determined via TUNEL analysis.AQP1 deficiency protected cardiac function from ischemic injury following MI.Furthermore, AQP1 deficiency reduced microvascular permeability via the stabilization of HIF-1α levels in endothelial cells and decreased cellular apoptosis following MI.

View Article: PubMed Central - PubMed

Affiliation: Liaoning Medical University, Department of Cell Biology, Jinzhou, PR China.

ABSTRACT
Many studies have determined that AQP1 plays an important role in edema formation and resolution in various tissues via water transport across the cell membrane. The aim of this research was to determine both if and how AQP1 is associated with cardiac ischemic injury, particularly the development of edema following myocardial infarction (MI). AQP1+/+ and AQP1-/- mice were used to create the MI model. Under physiological conditions, AQP1-/- mice develop normally; however, in the setting of MI, they exhibit cardioprotective properties, as shown by reduced cardiac infarct size determined via NBT staining, improved cardiac function determined via left ventricular catheter measurements, decreased AQP1-dependent myocardial edema determined via water content assays, and decreased apoptosis determined via TUNEL analysis. Cardiac ischemia caused by hypoxia secondary to AQP1 deficiency stabilized the expression of HIF-1α in endothelial cells and subsequently decreased microvascular permeability, resulting in the development of edema. The AQP1-dependent myocardial edema and apoptosis contributed to the development of MI. AQP1 deficiency protected cardiac function from ischemic injury following MI. Furthermore, AQP1 deficiency reduced microvascular permeability via the stabilization of HIF-1α levels in endothelial cells and decreased cellular apoptosis following MI.

No MeSH data available.


Related in: MedlinePlus