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CTRP12 Ameliorated Lipopolysaccharide-Induced Cardiomyocyte Injury
Meng-Qiao Zhou1, E Jin1, Jing Wu2
1Cardiology Function Examination Room, The First People's Hospital of Jingmen.
Insights
C1q/tumor necrosis factor (TNF)-related protein 12 (CTRP12) protects heart cells from sepsis-induced injury. CTRP12 reduces inflammation and oxidative stress by activating the NRF2 pathway, preserving cardiomyocyte viability.
Area of Science:
- Cardiovascular Biology
- Metabolic Regulation
- Cellular Injury Mechanisms
Background:
- C1q/tumor necrosis factor (TNF)-related protein 12 (CTRP12) is known to regulate glucose and lipid metabolism.
- The role of CTRP12 in cardiovascular disease, especially sepsis-induced cardiac injury, remains largely unexplored.
- Sepsis can lead to significant cardiac dysfunction, necessitating research into protective mechanisms.
Purpose of the Study:
- To investigate the protective role of CTRP12 in an in vitro model of sepsis-induced cardiomyocyte injury.
- To elucidate the molecular mechanisms underlying CTRP12's effects on inflammatory and oxidative stress pathways in cardiomyocytes.
- To determine the involvement of the Nuclear factor E2-related factor 2 (NRF2) pathway in CTRP12-mediated cardioprotection.
Main Methods:
- Establishment of an in vitro cardiomyocyte injury model using lipopolysaccharide (LPS) stimulation.
- Overexpression of CTRP12 in cardiomyocytes via an adenovirus delivery system.
- Assessment of inflammatory cytokine release (TNFα, IL-1, IL-6), reactive oxygen species (ROS) levels, oxidative/redox balance markers (superoxide dismutase, NADPH oxidase, malondialdehyde), apoptosis (TUNEL, Bcl-1/Bax ratio), and NRF2 expression.
Main Results:
- CTRP12 overexpression significantly reduced the release of pro-inflammatory cytokines (TNFα, IL-1, IL-6) from LPS-stimulated cardiomyocytes.
- CTRP12 attenuated the LPS-induced increase in ROS levels and restored the oxidative/redox balance.
- CTRP12 overexpression decreased cardiomyocyte apoptosis and improved the Bcl-1/Bax ratio, while increasing NRF2 expression.
- Silencing NRF2 abolished the protective effects of CTRP12, confirming its crucial role.
Conclusions:
- CTRP12 exerts significant protective effects against LPS-induced cardiomyocyte injury.
- CTRP12 mitigates inflammation and oxidative stress in cardiomyocytes.
- The cardioprotective effects of CTRP12 are mediated through the activation of the NRF2 signaling pathway.
Abstract:
C1q/tumor necrosis factor (TNF)-related protein 12 (CTRP12) is a secretory protein that participates in the regulation of glucose and lipid metabolism in obesity and diabetes. Its role in cardiovascular disease, particularly sepsis-induced cardiac injury, is unclear. Here, we stimulated cardiomyocytes with lipopolysaccharide (LPS) to establish an in vitro cardiomyocyte injury model and CTRP12 was overexpressed with an adenovirus delivery system. Overexpression of CTRP12 reduced the transcription and release of pro-inflammatory cytokines from LPS-stimulated cardiomyocytes, including TNFα, interleukin-1 (IL-1), and IL-6. Reactive oxygen species (ROS) level increased and the oxidation/redox system was disturbed in LPS-stimulated cardiomyocytes, as evident from the decrease in superoxide dismutase activity and an increase in reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity and malondialdehyde level. CTRP12 overexpression decreased the increasing level of ROS and ameliorated the unbalance in the oxidation/redox system in LPS-stimulated cardiomyocytes. The viability of cardiomyocytes decreased after LPS stimulation, and the cells underwent apoptosis. CTRP12-overexpressing cardiomyocytes showed a decrease in the number of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL)-positive cells, and the ratio of B cell lymphoma (Bcl)-1/Bax in these cells was recovered. In comparison with the control group, LPS-stimulated cardiomyocytes showed reduced expression of nuclear factor E2-related factor 2 (NRF2), while CTRP12-overexpressing cardiomyocytes showed elevated NRF2 expression. Small-interfering RNA-mediated silencing of NRF2 expression in cardiomyocytes resulted in the inhibition of the protective effects of CTRP12. Thus, CTRP12 ameliorated injury in LPS-stimulated cardiomyocytes in an NRF2-dependent manner.
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