Presenter Type

UNO Graduate Student (Masters)

Major/Field of Study

Health and Kinesiology

Other

Health and Kinesiology

Advisor Information

Song-Young Park

Location

MBSC304 - G (Masters)

Presentation Type

Oral Presentation

Start Date

24-3-2023 9:00 AM

End Date

24-3-2023 10:15 AM

Abstract

INTRODUCTION: Hydrogen sulfide (H2S) is a gaseous signaling molecule that serves various roles in the vasculature, such as upregulating angiogenesis, vascular smooth muscle relaxation, protecting endothelial function, and regulating redox balance. Despite H2S’s positive impacts on vascular homeostasis, it is important to note that its actions depend on its concentrations. At high concentrations, H2S has been reported to increase oxidative stress damage, such as oxidation of cysteine residues and lipid peroxidation. This may indicate that H2S may act as a ‘double-edged sword’ in the field of vascular physiology. Peripheral artery disease (PAD) is an atherosclerotic disease which manifested by claudication (leg pain during walking). Growing evidence suggests that abnormal H2S level may present with vascular diseases, however, only a few animal studies investigated the H2S and H2S -mediated oxidative stress damage in vascular disease models, and there are currently no available studies for human vascular disease patients, such as patients with PAD. Therefore, the purpose of this study was to examine the H2S and oxidative stress damage in peripheral blood mononuclear cells (PBMCs) and skeletal muscle tissues from patients with PAD. METHODS: Western blot was performed using skeletal muscle tissues and PBMCs to examine protein expression of cystathionase (CTH), which catalyzes production of H2S, and glutathione peroxidase-4 (GPx-4) and catalase (CAT), which are antioxidant markers, from healthy adults (CON) and patients with PAD (PAD). RESULTS: Patients with PAD show a lower expression of CTH compared to CON (P < 0.01, PAD: 1.61 ± 0.44, CON: 8.53 ± 0.46). However, CAT expression was not different between groups (P = 0.429, PAD: 0.03 ± 0.02, CON: 0.01 ± 0.01). In addition, CAT and GPx-4 expression was assessed in CON PBMCs (CAT: 5.07 ± 1.14, GPx-4: 0.63 ± 0.3). CONCLUSION: CTH protein expression in the skeletal muscle is attenuated in PAD compared to CON. However, CAT protein expression in the skeletal muscle is not different between groups. These data suggest an impairment is present in the H2S signaling system in the skeletal muscle of patients with PAD.

Scheduling

9:15-10:30 a.m., 10:45 a.m.-Noon

COinS
 
Mar 24th, 9:00 AM Mar 24th, 10:15 AM

Impaired hydrogen sulfide protein expression in patients with peripheral artery disease

MBSC304 - G (Masters)

INTRODUCTION: Hydrogen sulfide (H2S) is a gaseous signaling molecule that serves various roles in the vasculature, such as upregulating angiogenesis, vascular smooth muscle relaxation, protecting endothelial function, and regulating redox balance. Despite H2S’s positive impacts on vascular homeostasis, it is important to note that its actions depend on its concentrations. At high concentrations, H2S has been reported to increase oxidative stress damage, such as oxidation of cysteine residues and lipid peroxidation. This may indicate that H2S may act as a ‘double-edged sword’ in the field of vascular physiology. Peripheral artery disease (PAD) is an atherosclerotic disease which manifested by claudication (leg pain during walking). Growing evidence suggests that abnormal H2S level may present with vascular diseases, however, only a few animal studies investigated the H2S and H2S -mediated oxidative stress damage in vascular disease models, and there are currently no available studies for human vascular disease patients, such as patients with PAD. Therefore, the purpose of this study was to examine the H2S and oxidative stress damage in peripheral blood mononuclear cells (PBMCs) and skeletal muscle tissues from patients with PAD. METHODS: Western blot was performed using skeletal muscle tissues and PBMCs to examine protein expression of cystathionase (CTH), which catalyzes production of H2S, and glutathione peroxidase-4 (GPx-4) and catalase (CAT), which are antioxidant markers, from healthy adults (CON) and patients with PAD (PAD). RESULTS: Patients with PAD show a lower expression of CTH compared to CON (P < 0.01, PAD: 1.61 ± 0.44, CON: 8.53 ± 0.46). However, CAT expression was not different between groups (P = 0.429, PAD: 0.03 ± 0.02, CON: 0.01 ± 0.01). In addition, CAT and GPx-4 expression was assessed in CON PBMCs (CAT: 5.07 ± 1.14, GPx-4: 0.63 ± 0.3). CONCLUSION: CTH protein expression in the skeletal muscle is attenuated in PAD compared to CON. However, CAT protein expression in the skeletal muscle is not different between groups. These data suggest an impairment is present in the H2S signaling system in the skeletal muscle of patients with PAD.