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The Effect of Sera from Children with Obstructive Sleep Apnea Syndrome (OSAS) on Human Cardiomyocytes Differentiated
Hen Haddad1, Sharon Etzion2, Tatiana Rabinski2
1Shraga Segal Department of Microbiology, Immunology and Genetics, Faculty of Health Sciences, Ben Gurion University of the Negev, Beer-Sheva 8410501, Israel.
Insights
Pediatric obstructive sleep apnea syndrome (OSAS) sera negatively impacts human heart cells, reducing their function and viability via inflammatory pathways. This study introduces a novel human stem cell model for investigating OSAS cardiovascular risks.
Area of Science:
- Cardiovascular Science
- Sleep Medicine
- Stem Cell Biology
Background:
- Obstructive sleep apnea syndrome (OSAS) is linked to significant cardiovascular morbidity and mortality.
- Previous studies indicated sera from pediatric OSAS patients induce adverse effects in rat cardiomyocytes.
- Systemic inflammation is a proposed mechanism connecting OSAS to cardiovascular disease.
Purpose of the Study:
- To investigate the effects of sera from pediatric OSAS patients on human cardiomyocytes derived from embryonic stem cells (hES-CMs).
- To explore the role of NF-κB inflammatory pathways in OSAS-related cardiovascular pathology using a novel in vitro model.
Main Methods:
- Differentiation of human embryonic stem cells (hES) into beating human cardiomyocytes (CMs).
- Incubation of hES-CMs with sera from pediatric OSAS patients and healthy children.
- Assessment of cellular morphology, NF-κB pathway activation (p50 and p65 subunits), cardiomyocyte beating rate, contraction amplitude, and intracellular calcium signaling.
Main Results:
- OSAS sera significantly increased NF-κB p50 and p65 subunit expression in hES-CMs.
- Incubation with OSAS sera led to a marked reduction in cardiomyocyte beating rate and contraction amplitude.
- A significant decrease in intracellular calcium signals was observed in hES-CMs exposed to OSAS sera.
Conclusions:
- The study confirms and expands previous findings using a novel human stem cell-derived cardiomyocyte model.
- Results support the hypothesis that NF-κB-dependent inflammation is a key factor in the cardiovascular complications of OSAS.
- This hES-CM model provides a new platform for studying the molecular mechanisms of cardiovascular pathology in OSAS.
Abstract:
Obstructive sleep apnea syndrome (OSAS) patients suffer from cardiovascular morbidity, which is the leading cause of death in this disease. Based on our previous work with transformed cell lines and primary rat cardiomyocytes, we determined that upon incubation with sera from pediatric OSAS patients, the cell's morphology changes, NF-κB pathway is activated, and their beating rate and viability decreases. These results suggest an important link between OSAS, systemic inflammatory signals and end-organ cardiovascular diseases. In this work, we confirmed and expanded these observations on a new in vitro system of beating human cardiomyocytes (CM) differentiated from human embryonic stem cells (hES). Our results show that incubation with pediatric OSAS sera, in contrast to sera from healthy children, induces over-expression of NF-κB p50 and p65 subunits, marked reduction in CMs beating rate, contraction amplitude and a strong reduction in intracellular calcium signal. The use of human CM cells derived from embryonic stem cells has not been previously reported in OSAS research. The results further support the hypothesis that NF-κB dependent inflammatory pathways play an important role in the evolution of cardiovascular morbidity in OSAS. This study uncovers a new model to investigate molecular and functional aspects of cardiovascular pathology in OSAS.
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