The interaction of IGF-1/IGF-1R and hydrogen sulfide on the proliferation of mouse primary vascular smooth muscle cells

Shuang, Tian; Fu, Ming; Yang, Guangdong; Wu, Lingyun; Wang, Rui

doi:10.1016/j.bcp.2017.12.009

Cited by 41 publications

(26 citation statements)

References 68 publications

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“…A previous study showed that H 2 S acting as a gasotransmitter can inhibit the proliferation of vascular smooth muscle cells [38][39][40]. Some research reported that SO 2 could inhibit the proliferation and migration of myocardial fibroblasts [41].…”

Section: Discussionmentioning

confidence: 99%

Endothelin-1 Downregulates Sulfur Dioxide/Aspartate Aminotransferase Pathway via Reactive Oxygen Species to Promote the Proliferation and Migration of Vascular Smooth Muscle Cells

Tian

Zhang

Huang

et al. 2020

Oxidative Medicine and Cellular Longevity

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The regulatory mechanisms for proliferation and migration of vascular smooth muscle cells have not yet been clear. The present study was designed to investigate whether and how endothelin-1 (ET-1) impacted the generation of endogenous sulfur dioxide (SO2) in rat vascular smooth muscle cell (VSMC) proliferation and migration. Primary VSMCs and purified aspartate aminotransferase (AAT) protein were used in this study. We found that in the presence of ET-1, the expression of PCNA and Ki-67 was upregulated and the migration of VSMCs was promoted, while the AAT activity and SO2 levels in VSMCs were reduced without any changes in AAT1 and AAT2 expression. SO2 supplementation successfully prevented the ET-1-facilitated expression of PCNA and Ki-67 and the migration of VSMCs. Interestingly, ET-1 significantly increased reactive oxygen species (ROS) production in association with SO2/AAT pathway downregulation in VSMCs compared with controls, while the ROS scavenger N-acetyl-L-cysteine (NAC) and the antioxidant glutathione (GSH) significantly abolished the ET-1-stimulated downregulation of the SO2/AAT pathway. Moreover, the AAT activity was reduced in purified protein after the treatment for 2 h. However, NAC and GSH blocked the hydrogen peroxide-induced AAT activity reduction. In conclusion, our results suggest that ET-1 results in the downregulation of the endogenous SO2/AAT pathway via ROS generation to enhance the proliferation and migration of VSMCs.

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Section: Discussionmentioning

confidence: 99%

Endothelin-1 Downregulates Sulfur Dioxide/Aspartate Aminotransferase Pathway via Reactive Oxygen Species to Promote the Proliferation and Migration of Vascular Smooth Muscle Cells

Tian

Zhang

Huang

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…Supplement of H 2 S inhibited angiotensin II‐induced neonatal rat cardiac fibroblast proliferation, attenuated skin and lung fibrosis in systemic sclerosis, and alleviated insulin‐like growth factor‐1 (IGF‐1)–induced mouse primary vascular smooth muscle cell proliferation . However, there is a paradoxical finding that no mater H 2 S inhibitors or H 2 S donors suppressed HCT116 colon cancer cell proliferation .…”

Section: Discussionmentioning

confidence: 99%

Exogenous hydrogen sulphide supplement accelerates skin wound healing via oxidative stress inhibition and vascular endothelial growth factor enhancement

Hua

et al. 2019

Experimental Dermatology

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Hydrogen sulphide (H2S) is an important gasotransmitter with several physiological functions. However, the roles and the detailed mechanisms of H2S on skin wound healing are not known well. In the present study, 129S1/SvImJ mice were intraperitoneally injected with NaHS (50 μmol/kg/d) for 2 weeks. Then, a round wound of 6 mm diameter with depth into the dermis was made. The skin wound area, blood perfusion, superoxide production, malondialdehyde (MDA) levels, total antioxidant capacity (T‐AOC), expression of vascular endothelial growth factor (VEGF), dynamin‐related protein 1 (DRP1) and optic atrophy 1 (OPA1) were measured. After NaHS (50 μmol/L) pre‐administration for 4 hours, cell migration rate, DRP1, OPA1 and α–smooth muscle actin (α‐SMA) expression, superoxide production and mitochondrial membrane potential in primary skin fibroblasts were measured. Tube formation in human umbilical vein endothelial cells (HUVECs) and cell migration in human keratinocytes were also measured. The results showed that NaHS pretreatment significantly accelerated wound healing and improved blood flow in the wound after operation. NaHS increased VEGF expression in the wound and promoted tube formation in HUVECs. Meanwhile, NaHS attenuated reactive oxygen species (ROS) production, suppressed MDA level but restored T‐AOC in the wound. NaHS also promoted skin fibroblasts migration and α‐SMA expression after scratch. Moreover, NaHS alleviated ROS, increased mitochondrial membrane potential, decreased DRP1 but enhanced OPA1 expression in skin fibroblasts after scratch. NaHS also accelerated human keratinocytes migration after scratch. Taken together, exogenous H2S supplementary accelerated the skin wound healing, which might be related to oxidative stress inhibition and VEGF enhancement.

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“…In addition, H 2 S dramatically inhibited the transcription and expression of Brg1 gene, reduced the recruitment of Brg1 in the promoter region of proliferating genes (pcna, ntf3 and PDGFα) and consequently inhibited the proliferation of VSMCs [59] . On the other hand, H 2 S not only decreased the expression of insulin-like growth factor-1 receptor (IGF-1R), but also modified IGF-1R through sulfhydration to prevent IGF-1 binding, ultimately inhibiting VSMC proliferation [60] . Recently, Wang et al [61] demonstrated that calcium-sensing receptor (CaSR) increased endogenous generation of H 2 S via calcium-CaM signal pathways, ultimately inhibiting the proliferation of VSMCs.…”

Section: Physiological Regulation Of Blood Vessels By H 2 mentioning

confidence: 99%

Hydrogen sulfide and vascular regulation – An update

Chen

Tang

et al. 2021

Journal of Advanced Research

103

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The interaction of IGF-1/IGF-1R and hydrogen sulfide on the proliferation of mouse primary vascular smooth muscle cells

Cited by 41 publications

References 68 publications

Endothelin-1 Downregulates Sulfur Dioxide/Aspartate Aminotransferase Pathway via Reactive Oxygen Species to Promote the Proliferation and Migration of Vascular Smooth Muscle Cells

Endothelin-1 Downregulates Sulfur Dioxide/Aspartate Aminotransferase Pathway via Reactive Oxygen Species to Promote the Proliferation and Migration of Vascular Smooth Muscle Cells

Exogenous hydrogen sulphide supplement accelerates skin wound healing via oxidative stress inhibition and vascular endothelial growth factor enhancement

Hydrogen sulfide and vascular regulation – An update

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