Hypertrophic Stimulus Application in Sirt3 Mice
Objective: To evaluate the cardiac hypertrophic response in Sirt3-deficient and Sirt3-transgenic mice when subjected to hypertrophic stimuli, and to determine the protective mechanisms of Sirt3 against cardiac hypertrophy
This is a Hypertrophic Stimulus Application in Sirt3 Mice protocol using mouse as the model organism. The procedure involves 6 procedural steps, 1 materials. Extracted from a 2009 paper published in Journal of Clinical Investigation.
Model and subjects
mouse • Not explicitly specified in provided text • unknown • 8 weeks and older • Not specified in provided text
Study window
~8 week study window
Core workflow
Baseline assessment of Sirt3-deficient mice • Application of hypertrophic stimuli to Sirt3-deficient mice • Application of hypertrophic stimuli to Sirt3-transgenic mice
Primary readouts
- Presence and severity of cardiac hypertrophy
- Interstitial fibrosis in cardiac tissue
- Cellular ROS levels
- Expression of antioxidant genes (MnSOD and catalase)
Key equipment and reagents
Verified items
0
Direct vendor links
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Protocol Steps
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Baseline assessment of Sirt3-deficient mice
Sirt3-deficient mice were observed for normal activity and examined for signs of cardiac pathology at 8 weeks of age
Note: Sirt3-deficient mice appeared to have normal activity but showed signs of cardiac hypertrophy and interstitial fibrosis
View evidence from paper
“Although Sirt3-deficient mice appeared to have normal activity, they showed signs of cardiac hypertrophy and interstitial fibrosis at 8 weeks of age”
Application of hypertrophic stimuli to Sirt3-deficient mice
Hypertrophic stimuli were applied to Sirt3-deficient mice to evaluate their cardiac hypertrophic response
Note: Application of hypertrophic stimuli produced a severe cardiac hypertrophic response in these mice
View evidence from paper
“Application of hypertrophic stimuli to these mice produced a severe cardiac hypertrophic response”
Application of hypertrophic stimuli to Sirt3-transgenic mice
The same hypertrophic stimuli were applied to Sirt3-expressing transgenic mice to compare protective effects
Note: Sirt3-expressing Tg mice were protected from the hypertrophic stimuli that affected deficient mice
View evidence from paper
“Sirt3-expressing Tg mice were protected from similar stimuli”
In vitro cardiomyocyte culture experiments
Primary cultures of cardiomyocytes were used to investigate the molecular mechanisms by which Sirt3 blocks cardiac hypertrophy
Note: Sirt3 activated Foxo3a-dependent antioxidant-encoding genes (MnSOD and catalase) to decrease ROS levels
View evidence from paper
“In primary cultures of cardiomyocytes, Sirt3 blocked cardiac hypertrophy by activating the forkhead box O3a–dependent, antioxidant–encoding genes manganese superoxide dismutase (MnSOD) and catalase (Cat)”
Assessment of ROS-dependent signaling pathways
Evaluation of how reduced ROS levels suppressed downstream signaling cascades involved in cardiac hypertrophy
Note: Reduced ROS suppressed Ras activation and MAPK/ERK and PI3K/Akt pathway signaling
View evidence from paper
“Reduced ROS levels suppressed Ras activation and downstream signaling through the MAPK/ERK and PI3K/Akt pathways”
Assessment of transcription and translation factor activity
Evaluation of repressed activity of hypertrophy-related transcription factors (GATA4, NFAT) and translation factors (eIF4E, S6P)
Note: Suppression of these factors resulted from reduced ROS-mediated signaling
View evidence from paper
“This resulted in repressed activity of transcription factors, specifically GATA4 and NFAT, and translation factors, specifically eukaryotic initiation factor 4E (elf4E) and S6 ribosomal protein (S6P)”