Activation of K<sub>ATP</sub> channels by H<sub>2</sub>S in rat insulin‐secreting cells and the underlying mechanisms

Yang, Wei; Yang, Guangdong; Jia, Xuming; Wu, Lingyun; Wang, Rui

doi:10.1113/jphysiol.2005.097642

Cited by 448 publications

(338 citation statements)

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“…H 2 S can open K ATP channels in the cell membrane of aortic vascular smooth muscle, causing cytomembrane hyperpolarization. The K ATP channel is very important in the cardiovascular system [35][36][37][38][39][40][41] and H 2 S acts as an endogenous K ATP channel opener. K ATP channels are recognized for their cardioprotective role in ischemia [35] .…”

Section: Discussionmentioning

confidence: 99%

The vasorelaxing effect of hydrogen sulfide on isolated rat aortic rings versus pulmonary artery rings

et al. 2011

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Aim:To compare the vasorelaxing effects of hydrogen sulfide (H 2 S) on isolated aortic and pulmonary artery rings and to determine their action mechanisms. Methods: H 2 S-induced vasorelaxation of isolated rat aortic versus pulmonary artery rings under 95% O 2 and 5% CO 2 was analyzed. The expression of cystathinonine gamma-lyase (CSE), cystathionine beta synthase (CBS), 3-mercaptopyruvate sulfurtransferase (3MST), SUR2B and Kir6.1 was examined. Results: NaHS caused vasorelaxation of rat aortic and pulmonary artery rings in a dose-dependent manner. NaHS dilated aortic rings to a greater extent (16.4%, 38.4%, 64.1%, 84.3%, and 95.9% at concentrations of 50, 100, 200, 500, and 1000 μmol/L, respectively) than pulmonary artery rings (10.1%, 22.2%, 50.6%, 73.6%, and 84.6% at concentrations of 50, 100, 200, 500 and 1000 μmol/L, respec tively). The EC 50 of the vasorelaxant effect for aortic rings was 152.17 μmol/L, whereas the EC 50 for pulmonary artery rings was 233.65 μmol/L. The vasorelaxing effect of H 2 S was markedly blocked b y cellular and mitochondrial membrane K ATP channel blockers in aortic rings (P<0.01). In contrast, only the cellular membrane K ATP channel blocker inhibited H 2 S-induced vasorelaxation in pulmonary artery rings. SUR2B mRNA and protein expression was higher in aortic rings than in pulmonary artery rings. Cystathinonine gamma-lyase (CSE) but not cystathionine beta synthase (CBS) expression in aortic rings was higher than in pulmonary artery rings. 3-Mercapto pyruvate sulfurtransferase (3MST) mRNA was lower in aortic rings than in pulmonary artery rings. Conclusion: The vasorelaxing effect of H 2 S on isolated aortic rings was more pronounced than the effect on pulmonary artery rings at specific concentrations, which might be associated with increased expression of the K ATP channel subunit SUR2B.

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Section: Discussionmentioning

confidence: 99%

The vasorelaxing effect of hydrogen sulfide on isolated rat aortic rings versus pulmonary artery rings

et al. 2011

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“…16,17 It is reasoned that H 2 S would also affect other excitable cells that have functional K ATP channels. Pancreatic b-cells are among these cells and our earlier study in fact demonstrated the activation of K ATP channels in an insulin-secreting cell line, INS-1E, by H 2 S. 11 The K ATP channel-dependent effect of H 2 S on insulin release has also been shown in another insulin-secreting cell line, HIT-T15. 14 Insulin release from pancreatic islets is a critical event in homeostatic control of glucose metabolism and in pathogenic process of insulin resistance development, including diabetes.…”

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confidence: 95%

“…Only those cells of which K ATP channel activity was significantly decreased by high glucose (16 mM) and inhibited by K ATP channel blocker, gliclazide, were used in this study. 11 The cells in the recording chamber were superfused continuously with the bath solution at a rate of about 2 ml/min. A complete solution change in the recording chamber was accomplished within 30 s. All electrophysiological experiments were conducted at room temperature (20-221C).…”

Section: Glucose Tolerance Test and Insulin Tolerance Testmentioning

confidence: 99%

“…We have shown that CSE is the major H 2 S-generating enzyme in pancreatic islet, demonstrated by significant CSE protein expression, 11 and by our published data that PPG abolished the most H 2 S production from cultured INS-1E cells. 11 Among demonstrated cellular and molecular mechanisms for physiological effects of H 2 S are the activation of K ATP channels by H 2 S. In vascular smooth muscle cells, exogenous and endogenous H 2 S activated K ATP channels at whole-cell and single channel levels. 16,17 It is reasoned that H 2 S would also affect other excitable cells that have functional K ATP channels.…”

mentioning

confidence: 99%

“…[6][7][8][9][10] Endogenous production and physiological function of H 2 S in pancreas have been studied with identification of both CBS and CSE in rat pancreatic tissues or cloned rat pancreatic b-cell line. 11,12 In recent years, pathophysiological implications of the CSE/H 2 S system in diabetes have been reported. 12 CSE mRNA expression and H 2 S formation in rat pancreas was significantly increased after diabetes induction by streptozotocin injection.…”

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Pancreatic islet overproduction of H2S and suppressed insulin release in Zucker diabetic rats

Yang

Jia

et al. 2009

Laboratory Investigation

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Hydrogen sulfide (H 2 S) has been traditionally known for its toxic effects on living organisms. The role of H 2 S in the homeostatic regulation of pancreatic insulin metabolism has been unclear. The present study is aimed at elucidating the effect of endogenously produced H 2 S on pancreatic insulin release and its role in diabetes development. Diabetes development in Zucker diabetic fatty (ZDF) rats was evaluated in comparison with Zucker fatty (ZF) and Zucker lean (ZL) rats. Pancreatic H 2 S production and insulin release were also assayed. It was found that H 2 S was generated in rat pancreas islets, catalyzed predominantly by cystathionine g-lyase (CSE). Pancreatic CSE expression and H 2 S production were greater in ZDF rats than in ZF or ZL rats. ZDF rats exhibited reduced serum insulin level, hyperglycemia, and insulin resistance. Inhibition of pancreatic H 2 S production in ZDF rats by intraperitoneal injection of DL-propargylglycine (PPG) for 4 weeks increased serum insulin level, lowered hyperglycemia, and reduced hemoglobin A1c level (Po0.05). Although in ZF rats it also reduced pancreatic H 2 S production and serum H 2 S level, PPG treatment did not alter serum insulin and glucose level. Finally, H 2 S significantly increased K ATP channel activity in freshly isolated rat pancreatic b-cells. It appears that insulin release is impaired in ZDF because of abnormally high pancreatic production of H 2 S. New therapeutic approach for diabetes management can be devised based on our observation by inhibiting endogenous H 2 S production from pancreas. KEYWORDS: diabetes; hydrogen sulfide; insulin release; K ATP channel; pancreas; type 2 diabetes mellitus Known as a swamp gas or 'rotten egg' gas, hydrogen sulfide (H 2 S) has yielded a public image of air pollutant for centuries. Physiological importance of H 2 S as a gasotransmitter has been realized for less than a decade. Endogenous production of H 2 S from L-cysteine is catalyzed by cystathionine b-synthase (CBS) and/or cystathionine g-lyase (CSE) with ammonium and pyruvate as co-products. 1 This process occurs in different organs and tissues, such as neuronal, vascular, and intestinal tissues. 2 Physiological concentrations of circulating H 2 S have been reported in the range of 45-300 mM. 1 At this physiological range, exogenous H 2 S has been shown to relax different vascular tissues, including isolated rat aortae and perfused mesenteric artery bed. 3-5 Altered cell proliferation or apoptosis induced by H 2 S has also been widely reported. [6][7][8][9][10] Endogenous production and physiological function of H 2 S in pancreas have been studied with identification of both CBS and CSE in rat pancreatic tissues or cloned rat pancreatic b-cell line. 11,12 In recent years, pathophysiological implications of the CSE/H 2 S system in diabetes have been reported. 12 CSE mRNA expression and H 2 S formation in rat pancreas was significantly increased after diabetes induction by streptozotocin injection. 12 CBS expression was reported in pancreatic acinar cells. 13 Y...

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Aggregation‐Induced Emission Polymers

Zhang

Wan

Wei

2017

Encyclopedia of Polymer Science and Technology

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Aggregation‐induced emission (AIE) is an unusual fluorescent phenomenon characterized by strong luminescence observed in the aggregated state or in high‐concentration solutions. AIE‐active polymers have been extensively explored for various applications. Owing to their unique AIE property, these polymers overcome the aggregation caused quenching effect observed in conventional organic dyes. This makes the AIE‐active polymers especially attractive for biomedical applications due to the aggregation of AIEgens in aqueous solution. AIE‐active polymers have shown great potential for chemical/biological sensors, biological imaging, multimodel imaging, drug delivery, nanotheranostics, and organic light emission diodes owing to their outstanding properties such as ultrabrightness, versatile design, and multifunctional potential. This article presents recent advances in the fabrication strategies and biomedical applications of AIE‐active polymers.

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Activation of K_ATP channels by H₂S in rat insulin‐secreting cells and the underlying mechanisms

Cited by 448 publications

References 44 publications

The vasorelaxing effect of hydrogen sulfide on isolated rat aortic rings versus pulmonary artery rings

The vasorelaxing effect of hydrogen sulfide on isolated rat aortic rings versus pulmonary artery rings

Pancreatic islet overproduction of H2S and suppressed insulin release in Zucker diabetic rats

Aggregation‐Induced Emission Polymers

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Activation of KATP channels by H2S in rat insulin‐secreting cells and the underlying mechanisms

Cited by 448 publications

References 44 publications

The vasorelaxing effect of hydrogen sulfide on isolated rat aortic rings versus pulmonary artery rings

The vasorelaxing effect of hydrogen sulfide on isolated rat aortic rings versus pulmonary artery rings

Pancreatic islet overproduction of H2S and suppressed insulin release in Zucker diabetic rats

Aggregation‐Induced Emission Polymers

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Activation of K_ATP channels by H₂S in rat insulin‐secreting cells and the underlying mechanisms