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Isolation, Characterization, and Differentiation of Cardiac Stem Cells from the Adult Mouse Heart
Published on: January 7, 2019
Modulation of cardiac stem cell characteristics by metoprolol in hypertensive heart disease
Sherin Saheera1, Ajay Godwin Potnuri1, Renuka R Nair2
1Division of Cellular and Molecular Cardiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Thiruvananthapuram, Kerala, 695011, India.
Insights
Metoprolol treatment improved cardiac stem cell (CSC) function in spontaneously hypertensive rats (SHRs). The drug enhanced CSC migration, proliferation, and survival, while reducing oxidative stress and senescence, potentially preventing hypertension-induced heart damage.
Area of Science:
- Cardiovascular Biology
- Stem Cell Research
- Pharmacology
Background:
- Hypertension causes cardiac hypertrophy and failure, linked to oxidative stress and reduced cardiac stem cell (CSC) efficiency.
- Maintaining CSC function is crucial for preventing progressive cardiac remodeling in heart disease.
- The impact of cardioprotective antihypertensive drugs on CSCs remains largely unexplored.
Purpose of the Study:
- To investigate the effects of metoprolol, a cardioprotective antihypertensive agent, on CSC function in spontaneously hypertensive rats (SHRs).
- To determine if metoprolol can prevent the deterioration of CSC efficiency caused by hypertension.
Main Methods:
- Spontaneously hypertensive rats (SHRs) were treated with metoprolol (50 mg/kg/day) for 2 months.
- Cardiac stem cells (CSCs) were isolated from treated SHRs, untreated SHRs, and normotensive Wistar rats.
- CSC migration, proliferation, differentiation, survival, oxidative stress, and senescence were evaluated.
Main Results:
- SHRs exhibited decreased CSC migration and proliferation, and increased oxidative stress and senescence compared to Wistar rats.
- Metoprolol treatment in SHRs significantly enhanced CSC migration and proliferation, and improved stemness retention.
- Metoprolol-treated SHRs showed reduced cellular senescence and oxidative stress, with CSC attributes comparable to Wistar rats.
Conclusions:
- Metoprolol treatment restores cardiac stem cell efficiency in hypertensive rats.
- Improved CSC function is expected to mitigate hypertension-induced cardiac remodeling.
- This study highlights a potential therapeutic mechanism for metoprolol in managing hypertensive heart disease.
Abstract:
Cardiac stem cells (CSCs) play a vital role in cardiac remodeling. Uncontrolled hypertension leads to cardiac hypertrophy, followed by cardiac failure. Pathological remodeling is associated with enhanced oxidative stress. Decreased cardiac stem cell efficiency is speculated in heart diseases. Maintaining a healthy stem cell population is essential for preventing progressive cardiac remodeling. Some anti-hypertensive drugs are cardioprotective. However, the effect of these drugs on CSCs has not been investigated. Metoprolol is a cardioprotective anti-hypertensive agent. To examine whether metoprolol can prevent the deterioration of CSC efficiency, spontaneously hypertensive rats (SHRs) were treated with this drug, and the effects on stem cell function were evaluated. Six-month-old male SHRs were treated with metoprolol (50 mg × kg-1per day) for 2 months. The effectiveness of the treatment at reducing blood pressure and reducing hypertrophy was ensured, and the animals were killed. Cardiac stem cells were isolated from the atrial tissue, and the effect of metoprolol on stem cell migration, proliferation, differentiation, and survival was evaluated by comparing the treated SHRs with untreated SHRs and normotensive Wistar rats. Compared to the Wistar rats, the SHR rats presented with a decrease in stem cell migration and proliferation and an increase in intracellular oxidative stress and senescence. Treating SHRs with metoprolol increased CSC migration and proliferation potential and stemness retention. Cellular senescence and oxidative stress were reduced. The attributes of stem cells from the metoprolol-treated SHRs were comparable to those of the Wistar rats. The restoration of stem cell efficiency is expected to prevent hypertension-induced progressive cardiac remodeling.
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