Targeting Hydrogen Sulfide Modulates Dexamethasone-Induced Muscle Atrophy and Microvascular Rarefaction, through Inhibition of NOX4 and Induction of MGF, M2 Macrophages and Endothelial Progenitors
Long-term use of Glucocorticoids produces skeletal muscle atrophy and microvascular rarefaction. Hydrogen sulfide (H2S) has a potential role in skeletal muscle regeneration. However, the mechanisms still need to be elucidated. This is the first study to explore the effect of Sodium hydrosulfide (NaH...
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MDPI AG
2022-08-01
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| Online Access: | https://www.mdpi.com/2073-4409/11/16/2500 |
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| author | Mohamed Adel Hassan Reda Hassan Elsayed Mohammad El-Nablaway Shereen Hamed Amira Eladl Samah Fouad Eman Mohamad El Nashar Mohammed Lafi Al-Otaibi Mohammed R. Rabei |
| author_facet | Mohamed Adel Hassan Reda Hassan Elsayed Mohammad El-Nablaway Shereen Hamed Amira Eladl Samah Fouad Eman Mohamad El Nashar Mohammed Lafi Al-Otaibi Mohammed R. Rabei |
| author_sort | Mohamed Adel |
| collection | DOAJ |
| description | Long-term use of Glucocorticoids produces skeletal muscle atrophy and microvascular rarefaction. Hydrogen sulfide (H2S) has a potential role in skeletal muscle regeneration. However, the mechanisms still need to be elucidated. This is the first study to explore the effect of Sodium hydrosulfide (NaHS) H2S donor, against Dexamethasone (Dex)-induced soleus muscle atrophy and microvascular rarefaction and on muscle endothelial progenitors and M2 macrophages. Rats received either; saline, Dex (0.6 mg/Kg/day), Dex + NaHS (5 mg/Kg/day), or Dex + Aminooxyacetic acid (AOAA), a blocker of H2S (10 mg/Kg/day) for two weeks. The soleus muscle was examined for contractile properties. mRNA expression for Myostatin, Mechano-growth factor (MGF) and NADPH oxidase (NOX4), HE staining, and immunohistochemical staining for caspase-3, CD34 (Endothelial progenitor marker), vascular endothelial growth factor (VEGF), CD31 (endothelial marker), and CD163 (M2 macrophage marker) was performed. NaHS could improve the contractile properties and decrease oxidative stress, muscle atrophy, and the expression of NOX4, caspase-3, Myostatin, VEGF, and CD31 and could increase the capillary density and expression of MGF with a significant increase in expression of CD34 and CD163 as compared to Dex group. However, AOAA worsened the studied parameters. Therefore, H2S can be a promising target to attenuate muscle atrophy and microvascular rarefaction. |
| first_indexed | 2024-03-09T13:41:47Z |
| format | Article |
| id | doaj.art-d9dfbdecf9bb4a89988bb5091256dbc6 |
| institution | Directory Open Access Journal |
| issn | 2073-4409 |
| language | English |
| last_indexed | 2024-03-09T13:41:47Z |
| publishDate | 2022-08-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Cells |
| spelling | doaj.art-d9dfbdecf9bb4a89988bb5091256dbc62023-11-30T21:06:29ZengMDPI AGCells2073-44092022-08-011116250010.3390/cells11162500Targeting Hydrogen Sulfide Modulates Dexamethasone-Induced Muscle Atrophy and Microvascular Rarefaction, through Inhibition of NOX4 and Induction of MGF, M2 Macrophages and Endothelial ProgenitorsMohamed Adel0Hassan Reda Hassan Elsayed1Mohammad El-Nablaway2Shereen Hamed3Amira Eladl4Samah Fouad5Eman Mohamad El Nashar6Mohammed Lafi Al-Otaibi7Mohammed R. Rabei8Department of Medical Physiology, Faculty of Medicine, Mansoura University, Mansoura 35516, EgyptDepartment of Anatomy and Embryology, Faculty of Medicine, Mansoura University, Mansoura 35516, EgyptDepartment of Medical Biochemistry and Molecular Biology, Faculty of Medicine, Mansoura University, Mansoura 35516, EgyptDepartment of Medical Histology and Cell Biology, Faculty of Medicine, Mansoura University, Mansoura 35516, EgyptDepartment of Pharmacology, Faculty of Medicine, Mansoura University, Mansoura 35516, EgyptMedical Experimental Research Center (MERC), Faculty of Medicine, Mansoura University, Mansoura 35516, EgyptDepartment of Anatomy, College of Medicine, King Khalid University, Abha 61421, Saudi ArabiaDepartment of Orthopedics, College Medicine, King Khalid University, Abha 61421, Saudi ArabiaDepartment of Medical Physiology, Faculty of Medicine, Mansoura University, Mansoura 35516, EgyptLong-term use of Glucocorticoids produces skeletal muscle atrophy and microvascular rarefaction. Hydrogen sulfide (H2S) has a potential role in skeletal muscle regeneration. However, the mechanisms still need to be elucidated. This is the first study to explore the effect of Sodium hydrosulfide (NaHS) H2S donor, against Dexamethasone (Dex)-induced soleus muscle atrophy and microvascular rarefaction and on muscle endothelial progenitors and M2 macrophages. Rats received either; saline, Dex (0.6 mg/Kg/day), Dex + NaHS (5 mg/Kg/day), or Dex + Aminooxyacetic acid (AOAA), a blocker of H2S (10 mg/Kg/day) for two weeks. The soleus muscle was examined for contractile properties. mRNA expression for Myostatin, Mechano-growth factor (MGF) and NADPH oxidase (NOX4), HE staining, and immunohistochemical staining for caspase-3, CD34 (Endothelial progenitor marker), vascular endothelial growth factor (VEGF), CD31 (endothelial marker), and CD163 (M2 macrophage marker) was performed. NaHS could improve the contractile properties and decrease oxidative stress, muscle atrophy, and the expression of NOX4, caspase-3, Myostatin, VEGF, and CD31 and could increase the capillary density and expression of MGF with a significant increase in expression of CD34 and CD163 as compared to Dex group. However, AOAA worsened the studied parameters. Therefore, H2S can be a promising target to attenuate muscle atrophy and microvascular rarefaction.https://www.mdpi.com/2073-4409/11/16/2500muscle atrophyH2SNaHSMGFNOX-4Myostatin |
| spellingShingle | Mohamed Adel Hassan Reda Hassan Elsayed Mohammad El-Nablaway Shereen Hamed Amira Eladl Samah Fouad Eman Mohamad El Nashar Mohammed Lafi Al-Otaibi Mohammed R. Rabei Targeting Hydrogen Sulfide Modulates Dexamethasone-Induced Muscle Atrophy and Microvascular Rarefaction, through Inhibition of NOX4 and Induction of MGF, M2 Macrophages and Endothelial Progenitors Cells muscle atrophy H2S NaHS MGF NOX-4 Myostatin |
| title | Targeting Hydrogen Sulfide Modulates Dexamethasone-Induced Muscle Atrophy and Microvascular Rarefaction, through Inhibition of NOX4 and Induction of MGF, M2 Macrophages and Endothelial Progenitors |
| title_full | Targeting Hydrogen Sulfide Modulates Dexamethasone-Induced Muscle Atrophy and Microvascular Rarefaction, through Inhibition of NOX4 and Induction of MGF, M2 Macrophages and Endothelial Progenitors |
| title_fullStr | Targeting Hydrogen Sulfide Modulates Dexamethasone-Induced Muscle Atrophy and Microvascular Rarefaction, through Inhibition of NOX4 and Induction of MGF, M2 Macrophages and Endothelial Progenitors |
| title_full_unstemmed | Targeting Hydrogen Sulfide Modulates Dexamethasone-Induced Muscle Atrophy and Microvascular Rarefaction, through Inhibition of NOX4 and Induction of MGF, M2 Macrophages and Endothelial Progenitors |
| title_short | Targeting Hydrogen Sulfide Modulates Dexamethasone-Induced Muscle Atrophy and Microvascular Rarefaction, through Inhibition of NOX4 and Induction of MGF, M2 Macrophages and Endothelial Progenitors |
| title_sort | targeting hydrogen sulfide modulates dexamethasone induced muscle atrophy and microvascular rarefaction through inhibition of nox4 and induction of mgf m2 macrophages and endothelial progenitors |
| topic | muscle atrophy H2S NaHS MGF NOX-4 Myostatin |
| url | https://www.mdpi.com/2073-4409/11/16/2500 |
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