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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 cardiomyocyte apoptosis following MI.(a) A quantitative analysis of apoptotic cells in the hearts of mice via a TUNEL assay (n = 6, *P < 0.001 vs sham. ##P < 0.01 vs AQP1+/+ MI mice). TUNEL quantification was based on 6 fields per heart and 6 hearts per group. (b) The heart tissues from the AQP1+/+ and AQP1−/− mice at 48 h following MI were lysed and subjected to Western blotting in order to analyze the expression of caspase-3, bcl-2 and bax. (c) Band densities were measured using Image J software and normalized to β-actin. The data are expressed as the mean ± SEM (n = 6, *P < 0.01 vs sham; #P < 0.05, ##P < 0.01 vs AQP1+/+ MI mice).
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f6: The effects of AQP1 deficiency on cardiomyocyte apoptosis following MI.(a) A quantitative analysis of apoptotic cells in the hearts of mice via a TUNEL assay (n = 6, *P < 0.001 vs sham. ##P < 0.01 vs AQP1+/+ MI mice). TUNEL quantification was based on 6 fields per heart and 6 hearts per group. (b) The heart tissues from the AQP1+/+ and AQP1−/− mice at 48 h following MI were lysed and subjected to Western blotting in order to analyze the expression of caspase-3, bcl-2 and bax. (c) Band densities were measured using Image J software and normalized to β-actin. The data are expressed as the mean ± SEM (n = 6, *P < 0.01 vs sham; #P < 0.05, ##P < 0.01 vs AQP1+/+ MI mice).

Mentions: In order to determine whether AQP1-dependent myocardial edema mediates cardiac myocyte injury, an apoptosis analysis was undertaken using terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining, and revealed that in non-ischemic heart tissue, the number of apoptotic cells were similar in both the AQP1+/+ MI mice and the AQP1−/− MI mice. However, the number of apoptotic cells in the ischemic heart tissue of the AQP1+/+ mice was significantly increased compared with the AQP1−/− mice following MI [Fig. 6(a)]. In order to confirm the above results, we analyzed the expression of the apoptosis proteins caspase3, bax and bcl-2 via immunoblotting. As expected, the expression levels of caspase3 and bcl-2 were significantly increased in the AQP1+/+ mice compared with the AQP1−/− mice following MI, whereas bax expression was significantly decreased in the AQP1+/+ mice compared with the AQP1−/− mice [Fig. 6(b)]. These results indicated that AQP1 deficiency protected against the development of cardiac dysfunction by attenuating cardiac apoptosis.


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 cardiomyocyte apoptosis following MI.(a) A quantitative analysis of apoptotic cells in the hearts of mice via a TUNEL assay (n = 6, *P < 0.001 vs sham. ##P < 0.01 vs AQP1+/+ MI mice). TUNEL quantification was based on 6 fields per heart and 6 hearts per group. (b) The heart tissues from the AQP1+/+ and AQP1−/− mice at 48 h following MI were lysed and subjected to Western blotting in order to analyze the expression of caspase-3, bcl-2 and bax. (c) Band densities were measured using Image J software and normalized to β-actin. The data are expressed as the mean ± SEM (n = 6, *P < 0.01 vs sham; #P < 0.05, ##P < 0.01 vs AQP1+/+ MI mice).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f6: The effects of AQP1 deficiency on cardiomyocyte apoptosis following MI.(a) A quantitative analysis of apoptotic cells in the hearts of mice via a TUNEL assay (n = 6, *P < 0.001 vs sham. ##P < 0.01 vs AQP1+/+ MI mice). TUNEL quantification was based on 6 fields per heart and 6 hearts per group. (b) The heart tissues from the AQP1+/+ and AQP1−/− mice at 48 h following MI were lysed and subjected to Western blotting in order to analyze the expression of caspase-3, bcl-2 and bax. (c) Band densities were measured using Image J software and normalized to β-actin. The data are expressed as the mean ± SEM (n = 6, *P < 0.01 vs sham; #P < 0.05, ##P < 0.01 vs AQP1+/+ MI mice).
Mentions: In order to determine whether AQP1-dependent myocardial edema mediates cardiac myocyte injury, an apoptosis analysis was undertaken using terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining, and revealed that in non-ischemic heart tissue, the number of apoptotic cells were similar in both the AQP1+/+ MI mice and the AQP1−/− MI mice. However, the number of apoptotic cells in the ischemic heart tissue of the AQP1+/+ mice was significantly increased compared with the AQP1−/− mice following MI [Fig. 6(a)]. In order to confirm the above results, we analyzed the expression of the apoptosis proteins caspase3, bax and bcl-2 via immunoblotting. As expected, the expression levels of caspase3 and bcl-2 were significantly increased in the AQP1+/+ mice compared with the AQP1−/− mice following MI, whereas bax expression was significantly decreased in the AQP1+/+ mice compared with the AQP1−/− mice [Fig. 6(b)]. These results indicated that AQP1 deficiency protected against the development of cardiac dysfunction by attenuating cardiac apoptosis.

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