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Lentiviral-mediated p38 MAPK RNAi attenuates aldosterone-induced myocyte apoptosis
Yan Zhou1, Yuanhong Liang, Jie Wei
1Department of Emergency, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
Abstract:
Aldosterone-induced myocyte apoptosis is an important component of cardiovascular disease. While the p38 mitogen-activated protein kinase (p38 MAPK) pathway has been shown to be crucial in myocyte apoptosis, whether aldosterone induces myocyte apoptosis through this pathway remains unclear. In the present study, three individual strands of p38 MAPK short hairpin RNA (ShRNA), delivered by lentiviral vectors (PGLV), were constructed and used to explore the role of p38 MAPK pathway activation in aldosterone-mediated myocyte apoptosis in cultured myocytes and normotensive rats. Aldosterone stimulation increased myocyte apoptosis, caspase-3 expression levels and p38 MAPK mRNA and protein expression levels in vitro and in vivo. PGLV-ShRNA3 transduction decreased aldosterone-mediated myocyte apoptosis and p38 MAPK mRNA and protein expression levels in vitro (all P<0.01). PGLV-ShRNA3 transduction significantly decreased aldosterone-mediated myocyte apoptosis, p38 MAPK mRNA and protein expression levels in normotensive rats (P<0.01, P<0.01 and P<0.05, respectively). Results from the present study suggest that aldosterone directly induces myocyte apoptosis through the p38 MAPK pathway and the gene silencing of p38 MAPK may protect cardiac myocytes from aldosterone-mediated apoptosis.
Insights
Aldosterone triggers heart cell death via the p38 mitogen-activated protein kinase (p38 MAPK) pathway. Gene silencing of p38 MAPK protected cardiac myocytes from this aldosterone-induced apoptosis, suggesting a therapeutic target.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Cellular Signaling
Background:
- Aldosterone-induced myocyte apoptosis contributes significantly to cardiovascular disease progression.
- The p38 mitogen-activated protein kinase (p38 MAPK) pathway is implicated in myocyte apoptosis, but its role in aldosterone-mediated apoptosis is not fully understood.
Purpose of the Study:
- To investigate the role of p38 MAPK pathway activation in aldosterone-induced myocyte apoptosis.
- To determine if silencing p38 MAPK can protect cardiac myocytes from aldosterone-induced cell death.
Main Methods:
- Constructed lentiviral vectors (PGLV) carrying three distinct p38 MAPK short hairpin RNA (ShRNA) sequences.
- Utilized cultured myocytes and normotensive rat models to assess aldosterone effects.
- Measured myocyte apoptosis, caspase-3 expression, and p38 MAPK mRNA/protein levels.
Main Results:
- Aldosterone stimulation increased myocyte apoptosis and p38 MAPK expression both in vitro and in vivo.
- Transduction with PGLV-ShRNA3 significantly reduced aldosterone-induced myocyte apoptosis and p38 MAPK levels in cultured myocytes (P<0.01).
- PGLV-ShRNA3 significantly decreased aldosterone-mediated myocyte apoptosis, p38 MAPK mRNA, and protein expression in normotensive rats (P<0.01, P<0.01, P<0.05).
Conclusions:
- Aldosterone directly induces cardiac myocyte apoptosis through the p38 MAPK pathway.
- Gene silencing of p38 MAPK demonstrates potential protective effects against aldosterone-mediated myocyte apoptosis, highlighting a therapeutic strategy for cardiovascular disease.
