Limits...
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 cardiac contractile function following MI.(a) A representative tracing of LV hemodynamic recordings obtained in vivo using a conductance catheter in both the sham-operated mice and both the AQP1−/− and AQP1+/+ mice at 18 hours following MI. (b) The LV systolic pressures (LVSPs) (n = 12), heart rates (HRs) (n = 12) (c), LV end-diastolic pressures (LVEDPs) (n = 12) (d) and maximal positive (e) and minimal negative (f) first derivatives of LV pressure (+dP/dtmax and –dP/dtmin) (n = 12). The values are expressed as the mean ± SEM. *P < 0.01 vs sham; #P < 0.05, ##P < 0.01 vs AQP1+/+ MI mice.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4562302&req=5

f3: The effects of AQP1 deficiency on cardiac contractile function following MI.(a) A representative tracing of LV hemodynamic recordings obtained in vivo using a conductance catheter in both the sham-operated mice and both the AQP1−/− and AQP1+/+ mice at 18 hours following MI. (b) The LV systolic pressures (LVSPs) (n = 12), heart rates (HRs) (n = 12) (c), LV end-diastolic pressures (LVEDPs) (n = 12) (d) and maximal positive (e) and minimal negative (f) first derivatives of LV pressure (+dP/dtmax and –dP/dtmin) (n = 12). The values are expressed as the mean ± SEM. *P < 0.01 vs sham; #P < 0.05, ##P < 0.01 vs AQP1+/+ MI mice.

Mentions: In order to determine the role of AQP1 in cardiac function following MI, we assessed HR, LVSP, LVEDP, +dP/dtmax and −dP/dtminin vivo at 18 hours following MI using an LV catheter that simultaneously measures pressure, as depicted in Fig. 3(a). LVSP (b), HR (c), and +dP/dtmax (e), as well as −dP/dtmin (f), were significantly decreased in the AQP1+/+ and AQP1−/− MI mice, whereas LVEDP (d) was increased compared with the control mice. However, LV +dP/dtmax and −dP/dtmin were greater, and LVEDP was smaller in the AQP1−/− mice compared with the AQP1+/+ mice. These results suggest that AQP1 deficiency protected against cardiac functional impairment following 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 cardiac contractile function following MI.(a) A representative tracing of LV hemodynamic recordings obtained in vivo using a conductance catheter in both the sham-operated mice and both the AQP1−/− and AQP1+/+ mice at 18 hours following MI. (b) The LV systolic pressures (LVSPs) (n = 12), heart rates (HRs) (n = 12) (c), LV end-diastolic pressures (LVEDPs) (n = 12) (d) and maximal positive (e) and minimal negative (f) first derivatives of LV pressure (+dP/dtmax and –dP/dtmin) (n = 12). The values are expressed as the mean ± SEM. *P < 0.01 vs sham; #P < 0.05, ##P < 0.01 vs AQP1+/+ MI mice.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f3: The effects of AQP1 deficiency on cardiac contractile function following MI.(a) A representative tracing of LV hemodynamic recordings obtained in vivo using a conductance catheter in both the sham-operated mice and both the AQP1−/− and AQP1+/+ mice at 18 hours following MI. (b) The LV systolic pressures (LVSPs) (n = 12), heart rates (HRs) (n = 12) (c), LV end-diastolic pressures (LVEDPs) (n = 12) (d) and maximal positive (e) and minimal negative (f) first derivatives of LV pressure (+dP/dtmax and –dP/dtmin) (n = 12). The values are expressed as the mean ± SEM. *P < 0.01 vs sham; #P < 0.05, ##P < 0.01 vs AQP1+/+ MI mice.
Mentions: In order to determine the role of AQP1 in cardiac function following MI, we assessed HR, LVSP, LVEDP, +dP/dtmax and −dP/dtminin vivo at 18 hours following MI using an LV catheter that simultaneously measures pressure, as depicted in Fig. 3(a). LVSP (b), HR (c), and +dP/dtmax (e), as well as −dP/dtmin (f), were significantly decreased in the AQP1+/+ and AQP1−/− MI mice, whereas LVEDP (d) was increased compared with the control mice. However, LV +dP/dtmax and −dP/dtmin were greater, and LVEDP was smaller in the AQP1−/− mice compared with the AQP1+/+ mice. These results suggest that AQP1 deficiency protected against cardiac functional impairment following 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