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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

Normal cardiac morphology and the expression of AQP1 in AQP1−/− and AQP1+/+ mice.((a) top) Heart images from the AQP1−/− and AQP1+/+ mice. ((a) bottom) The heart weight/body weight ratio was representative of adult mice at 8–10 weeks age. The values are expressed as the mean ± SEM. (n = 6, differences not significant). (b) Heart sections from the AQP1−/− and AQP1+/+ mice stained with H&E. Scale bar: 50 μm. (c) The RT-PCR (top) and Western blot (bottom) analyses demonstrate the relative expression levels of AQP1 in the AQP1−/− and AQP1+/+ mice hearts. Kidney tissue was used as positive control. (d) The AQP1 expression pattern in the normal hearts of both humans (left) and mice (right) as demonstrated via immunohistochemistry. Scale bar: 50 μm.
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f1: Normal cardiac morphology and the expression of AQP1 in AQP1−/− and AQP1+/+ mice.((a) top) Heart images from the AQP1−/− and AQP1+/+ mice. ((a) bottom) The heart weight/body weight ratio was representative of adult mice at 8–10 weeks age. The values are expressed as the mean ± SEM. (n = 6, differences not significant). (b) Heart sections from the AQP1−/− and AQP1+/+ mice stained with H&E. Scale bar: 50 μm. (c) The RT-PCR (top) and Western blot (bottom) analyses demonstrate the relative expression levels of AQP1 in the AQP1−/− and AQP1+/+ mice hearts. Kidney tissue was used as positive control. (d) The AQP1 expression pattern in the normal hearts of both humans (left) and mice (right) as demonstrated via immunohistochemistry. Scale bar: 50 μm.

Mentions: Figure 1a, top, depicts the normal hearts of the AQP1+/+ and AQP1−/− mice. The hearts of the AQP1+/+ and AQP1−/− mice exhibited similar sizes, gross anatomical features and weights [Fig. 1(a), bottom]. H&E staining demonstrated that the hearts of the AQP1+/+ and AQP1−/− mice exhibited similar histological features, as well as comparable myocardium thicknesses and myocyte densities [Fig. 1(b)]. AQP1 immunohistochemistry staining demonstrated that the endothelial cells exhibited expression patterns consistent with those of normal human hearts and AQP1+/+ mouse hearts [Fig. 1(d)], as brown staining was visible across the membranes of the endothelial cells and limited staining of the myocytes was visible. No specific staining was observed in the hearts of the control slices. The expression of AQP1 in human heart exhibits a pattern similar to that observed in the mouse heart.


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)

Normal cardiac morphology and the expression of AQP1 in AQP1−/− and AQP1+/+ mice.((a) top) Heart images from the AQP1−/− and AQP1+/+ mice. ((a) bottom) The heart weight/body weight ratio was representative of adult mice at 8–10 weeks age. The values are expressed as the mean ± SEM. (n = 6, differences not significant). (b) Heart sections from the AQP1−/− and AQP1+/+ mice stained with H&E. Scale bar: 50 μm. (c) The RT-PCR (top) and Western blot (bottom) analyses demonstrate the relative expression levels of AQP1 in the AQP1−/− and AQP1+/+ mice hearts. Kidney tissue was used as positive control. (d) The AQP1 expression pattern in the normal hearts of both humans (left) and mice (right) as demonstrated via immunohistochemistry. Scale bar: 50 μm.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f1: Normal cardiac morphology and the expression of AQP1 in AQP1−/− and AQP1+/+ mice.((a) top) Heart images from the AQP1−/− and AQP1+/+ mice. ((a) bottom) The heart weight/body weight ratio was representative of adult mice at 8–10 weeks age. The values are expressed as the mean ± SEM. (n = 6, differences not significant). (b) Heart sections from the AQP1−/− and AQP1+/+ mice stained with H&E. Scale bar: 50 μm. (c) The RT-PCR (top) and Western blot (bottom) analyses demonstrate the relative expression levels of AQP1 in the AQP1−/− and AQP1+/+ mice hearts. Kidney tissue was used as positive control. (d) The AQP1 expression pattern in the normal hearts of both humans (left) and mice (right) as demonstrated via immunohistochemistry. Scale bar: 50 μm.
Mentions: Figure 1a, top, depicts the normal hearts of the AQP1+/+ and AQP1−/− mice. The hearts of the AQP1+/+ and AQP1−/− mice exhibited similar sizes, gross anatomical features and weights [Fig. 1(a), bottom]. H&E staining demonstrated that the hearts of the AQP1+/+ and AQP1−/− mice exhibited similar histological features, as well as comparable myocardium thicknesses and myocyte densities [Fig. 1(b)]. AQP1 immunohistochemistry staining demonstrated that the endothelial cells exhibited expression patterns consistent with those of normal human hearts and AQP1+/+ mouse hearts [Fig. 1(d)], as brown staining was visible across the membranes of the endothelial cells and limited staining of the myocytes was visible. No specific staining was observed in the hearts of the control slices. The expression of AQP1 in human heart exhibits a pattern similar to that observed in the mouse heart.

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