Expression of monocarboxylate transporter (MCT) 1 and MCT4 in overloaded mice plantaris muscle

Kitaoka, Yu; Machida, Masanao; Takemasa, Tohru; Hatta, Hideo

doi:10.1007/s12576-011-0167-6

Cited by 16 publications

(17 citation statements)

References 38 publications

(48 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It protects the heart from I/R injury by sustaining energy supply during ischemic stress and reducing the likelihood of cardiomyocyte cell death. Furthermore, in other studies, AMPK activation induced increases in MCT1 and MCT4 protein content in rat skeletal muscle [11,12,13]. In the current study, we also found that MCT1 and MCT4 protein expression was increased with increases in AMPK phosphorylation status during the I/R period.…”

Section: Discussionsupporting

confidence: 86%

“…Considering lactate may be a major energy resource for the failing heart, and may preserve or even improve myocardial performance [30,33], this possibly indicates that the hearts are failing and have a greater reliance on carbohydrates. It is suggested that regulation of MCT expression seems to be translational [13]. We did not find increased MCT expression, which may be due to the time frame of observation.…”

Section: Discussioncontrasting

confidence: 61%

“…Recent reports have shown that AMP-activated protein kinase (AMPK) activation increases MCT1 and MCT4 protein expression in skeletal muscle [11,12,13]. Furthermore, the current view is that AMPK protects the heart from I-R injury by sustaining an energy supply [2,14].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

MCT1 and MCT4 Expression During Myocardial Ischemic-Reperfusion Injury in the Isolated Rat Heart

Zhu

Su³

2013

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Myocardium ischemia-reperfusion (I/R) injury can be caused by imbalances in cellular metabolism. Lactate, transported by monocarboxylate transporters (MCTs), has been implicated as a mechanism in this process. The present study was designed to investigate the expression and functional role of MCTs in rat hearts during ischemia and reperfusion. Methods: Langendorff-perfused rat hearts were subjected to 20 minutes stabilization, 30 minutes of global ischemia and 60 minutes reperfusion. Hearts were collected serially for detecting expression changes in MCT1, MCT4 during myocardial I/R injury and lactate concentration was measured. Post-ischemic left ventricular function and infract size were determined at end-point, followed by the pretreatment of D-lactate, a competitive inhibitor of MCTs. Results: MCT4 was significantly increased following global ischemia and MCT1 expression was increased during the early stages of reperfusion in isolated rat hearts, while the expression of the ancillary protein CD147 was increased during I/R injury. We determined increases in AMPK phosphorylation status, which was significantly elevated following ischemia and early reperfusion. Blocking monocarboxylate transport by competitive inhibition with D-lactate caused decreased left ventricular performance and increased infarct size. Conclusion: Increased MCT4 expression facilitates lactate extrusion during the ischemic period, while increased MCT1 may facilitate lactate transport into and out of cells simultaneously during early reperfusion, with increases in AMPK phosphorylation status during the myocardial I/R period. Lactate transport by MCTs has a profound protective effect during myocardial ischemia reperfusion injury.

show abstract

Section: Discussionsupporting

confidence: 86%

Section: Discussioncontrasting

confidence: 61%

See 1 more Smart Citation

MCT1 and MCT4 Expression During Myocardial Ischemic-Reperfusion Injury in the Isolated Rat Heart

Zhu

Su³

2013

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…Red and white tibialis anterior (TA) muscle samples were homogenized as previously described (19,20) using lysis buffer (1% Triton X-100, 50 mm Tris-HCl, 1 mm EDTA, 1 mm EGTA, 50 mm sodium fluoride, 10 mm sodium beta-glycerol phosphate, 5 mm sodium pyrophosphate, and 2 mm dithiothreitol, pH 7.5) containing 10 mg/mL of pepstatin A, aprotinin, and leupeptin; 1 mm of Na orthovanadate, and 0.177 mg/mL of phenylmethylsulfonyl fluoride. Protein concentrations were measured by the Bradford method.…”

Section: Animalsmentioning

confidence: 99%

Chronic Post-Exercise Lactate Administration with Endurance Training Increases Glycogen Concentration and Monocarboxylate Transporter 1 Protein in Mouse White Muscle

Hoshino

Hanawa

Takahashi

et al. 2014

J Nutr Sci Vitaminol

Self Cite

View full text Add to dashboard Cite

“…Intact, isolated single muscle fibres from mouse EDL and peroneus muscles were used [5], [26], [27]. These hindlimb skeletal muscles express NKCC1 [23], MCT1 and MCT4 [14], [24].…”

Section: Methodsmentioning

confidence: 99%

Inward Flux of Lactate- through Monocarboxylate Transporters Contributes to Regulatory Volume Increase in Mouse Muscle Fibres

Lindinger

Leung²,

Hawke³

2013

PLoS ONE

View full text Add to dashboard Cite

Mouse and rat skeletal muscles are capable of a regulatory volume increase (RVI) after they shrink (volume loss resultant from exposure to solutions of increased osmolarity) and that this RVI occurs mainly by a Na-K-Cl-Cotransporter (NKCC) - dependent mechanism. With high-intensity exercise, increased extracellular osmolarity is accompanied by large increases in extracellular [lactate-]. We hypothesized that large increases in [lactate-] and osmolarity augment the NKCC-dependent RVI response observed with a NaCl (or sucrose) - induced increase in osmolarity alone; a response that is dependent on lactate- influx through monocarboxylate transporters (MCTs). Single mouse muscle fibres were isolated and visualized under light microscopy under varying osmolar conditions. When solution osmolarity was increased by adding NaLac by 30 or 60 mM, fibres lost significantly less volume and regained volume sooner compared to when NaCl was used. Phloretin (MCT1 inhibitor) accentuated the volume loss compared to both NaLac controls, supporting a role for MCT1 in the RVI response in the presence of elevated [lactate-]. Inhibition of MCT4 (with pCMBS) resulted in a volume loss, intermediate to that seen with phloretin and NaLac controls. Bumetanide (NKCC inhibitor), in combination with pCMBS, reduced the magnitude of volume loss, but volume recovery was complete. While combined phloretin-bumetanide also reduced the magnitude of the volume loss, it also largely abolished the cell volume recovery. In conclusion, RVI in skeletal muscle exposed to raised tonicity and [lactate-] is facilitated by inward flux of solute by NKCC- and MCT1-dependent mechanisms. This work demonstrates evidence of a RVI response in skeletal muscle that is facilitated by inward flux of solute by MCT-dependent mechanisms. These findings further expand our understanding of the capacities for skeletal muscle to volume regulate, particularly in instances of raised tonicity and lactate- concentrations, as occurs with high intensity exercise.

show abstract

Expression of monocarboxylate transporter (MCT) 1 and MCT4 in overloaded mice plantaris muscle

Cited by 16 publications

References 38 publications

MCT1 and MCT4 Expression During Myocardial Ischemic-Reperfusion Injury in the Isolated Rat Heart

MCT1 and MCT4 Expression During Myocardial Ischemic-Reperfusion Injury in the Isolated Rat Heart

Chronic Post-Exercise Lactate Administration with Endurance Training Increases Glycogen Concentration and Monocarboxylate Transporter 1 Protein in Mouse White Muscle

Inward Flux of Lactate- through Monocarboxylate Transporters Contributes to Regulatory Volume Increase in Mouse Muscle Fibres

Contact Info

Product

Resources

About