Sulfide Enhancement of Pmn Apoptosis

Mariggiò, Maria Addolorata; Minunno, V.; Riccardi, S.; Santacroce, Rosa; Rinaldis, P. De; Fumarulo, Ruggiero

doi:10.3109/08923979809034822

Cited by 65 publications

(45 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…H 2 S inhibits IL-2 production by and proliferation of T cell lymphocytes (283). Similar effects were also reported for polymorphonuclear cells, wherein 1 mM H 2 S induced PMN apoptosis (153).…”

Section: A Role Of H 2 S In T Cell Activationsupporting

confidence: 67%

Regulation of Cellular Redox Signaling by Matricellular Proteins in Vascular Biology, Immunology, and Cancer

Roberts

Kaur

Isenberg

2017

Antioxidants & Redox Signaling

View full text Add to dashboard Cite

Significance: In contrast to structural elements of the extracellular matrix, matricellular proteins appear transiently during development and injury responses, but their sustained expression can contribute to chronic disease. Through interactions with other matrix components and specific cell surface receptors, matricellular proteins regulate multiple signaling pathways, including those mediated by reactive oxygen and nitrogen species and H 2 S. Dysregulation of matricellular proteins contributes to the pathogenesis of vascular diseases and cancer. Defining the molecular mechanisms and receptors involved is revealing new therapeutic opportunities. Recent Advances: Thrombospondin-1 (TSP1) regulates NO, H 2 S, and superoxide production and signaling in several cell types. The TSP1 receptor CD47 plays a central role in inhibition of NO signaling, but other TSP1 receptors also modulate redox signaling. The matricellular protein CCN1 engages some of the same receptors to regulate redox signaling, and ADAMTS1 regulates NO signaling in Marfan syndrome. In addition to mediating matricellular protein signaling, redox signaling is emerging as an important pathway that controls the expression of several matricellular proteins. Critical Issues: Redox signaling remains unexplored for many matricellular proteins. Their interactions with multiple cellular receptors remains an obstacle to defining signaling mechanisms, but improved transgenic models could overcome this barrier. Future Directions: Therapeutics targeting the TSP1 receptor CD47 may have beneficial effects for treating cardiovascular disease and cancer and have recently entered clinical trials. Biomarkers are needed to assess their effects on redox signaling in patients and to evaluate how these contribute to their therapeutic efficacy and potential side effects. Antioxid. Redox Signal. 27, 874-911.

show abstract

Section: A Role Of H 2 S In T Cell Activationsupporting

confidence: 67%

Regulation of Cellular Redox Signaling by Matricellular Proteins in Vascular Biology, Immunology, and Cancer

Roberts

Kaur

Isenberg

2017

Antioxidants & Redox Signaling

View full text Add to dashboard Cite

show abstract

“…The former hypothesis has been confirmed (14), but the latter had only been deduced from the reported effects of H 2 S on proliferation or apoptosis of other types of cells. H 2 S possesses an anti-proliferative effect on T-lymphocytes and induces apoptotic death of polymorphonuclear cells (24,25). Our laboratory also has shown that overproduction of H 2 S via up-regulation of the expression of CSE inhibits HEK-293 cell proliferation and induces human aorta smooth muscle cell (HASMC) apoptosis, and that exogenously applied H 2 S at physiologically relevant concentrations induces apoptosis of HASMCs (15,18,19).…”

Section: Discussionmentioning

confidence: 99%

H2S, Endoplasmic Reticulum Stress, and Apoptosis of Insulin-secreting Beta Cells

Yang

et al. 2007

Journal of Biological Chemistry

183

143

View full text Add to dashboard Cite

Cystathionine ␥-lyase (CSE) is a key enzyme in the transsulfuration pathway, which uses L-cysteine to produce hydrogen sulfide (H 2 S). Functional changes of pancreatic beta cells induced by endogenous H 2 S have been reported, but the effect of the CSE/H 2 S system on pancreatic beta cell survival has not been known. In this study, we demonstrate that H 2 S at physiologically relevant concentrations induced apoptosis of INS-1E cells, an insulin-secreting beta cell line. Transfection of INS-1E cells with a recombinant defective adenovirus containing the CSE gene (Ad-CSE) resulted in a significant increase in CSE expression and H 2 S production. Ad-CSE transfection also stimulated apoptosis. The other two end products of CSE-catalyzed enzymatic reaction, ammonium and pyruvate, had no effects on INS-1E cell apoptosis, indicating that overexpression of CSE may stimulate INS-1E cell apoptosis via increased endogenous production of H 2 S. Both exogenous H 2 S (100 M) and Ad-CSE transfection inhibited ERK1/2 but activated p38 MAPK. Interestingly, BiP and CHOP, two indicators of endoplasmic reticulum (ER) stress, were up-regulated in H 2 S-and CSE-mediated apoptosis in INS-1E cells. After suppressing CHOP mRNA expression, H 2 S-induced apoptosis of INS-1E cells was significantly decreased. Inhibition of p38 MAPK, but not of ERK1/2, inhibited the expression of BiP and CHOP and decreased H 2 S-stimulated apoptosis, suggesting that p38 MAPK activation functions upstream of ER stress to initiate H 2 S-induced apoptosis. It is concluded that H 2 S induces apoptosis of insulin-secreting beta cells by enhancing ER stress via p38 MAPK activation. Our findings may help unmask a novel role of CSE/H 2 S system in regulating pancreatic functions under physiological condition and in diabetes.Cystathionine ␥-lyase (CSE, 5 EC 4.4.1.1) is a key pyridoxal 5Ј-phosphate-dependent enzyme in the trans-sulfuration pathway, which uses L-cysteine to produce hydrogen sulfide (H 2 S), a novel and important gasotransmitter (1-3). Endogenous productions of H 2 S in different organs and tissues as well as the circulatory concentration of H 2 S have been elucidated, and the physiological importance of H 2 S has gained increasing recognition (2-5).Diabetes is a spectrum of clinical conditions arising from relative or absolute insulin deficiency with decreased functional beta cell mass (6). Any change in beta cell mass must reflect an imbalance between proliferation (neogenesis or replication) and cell death (necrosis or apoptosis) (7). Excessive loss of beta cells constitutes one of the causes of diabetes, and apoptosis is considered to be the main mode of beta cell death in type I and type II diabetes (8). In recent years, pathophysiological implications of the CSE/H 2 S system in diabetes have been reported (9, 10). Endogenous production of H 2 S together with the expression of CSE and cystathionine ␤-synthase (CBS), another H 2 S-producing enzyme, was identified in rat pancreatic tissues (9, 10). CSE mRNA expression and H 2 S formation in the rat...

show abstract

“…Little is known about the cellular consequences of an elevated CSE expression or about the associated increase in endogenously produced H 2 S. CSE-derived H 2 S inhibits cell proliferation (8,14) and induces cell death predominantly by an apoptotic mechanism in polymorphonuclear cells (11,13) . Deficiency of CSE activity in humans is presumed to cause cystathioninemia (cystathioninuria), an autosomal recessive inborn error probably with no consistent clinical consequence (12,14) .…”

Section: Discussionmentioning

confidence: 99%

IMMUNOHISTOCHEMICAL APPROACH REVEALS LOCALIZATION OF CYSTATHIONINE-?-LYASE AND CYSTATHIONINE-ß-SYNTHETASE IN ETHANOL-INDUCED GASTRIC MUCOSA DAMAGE IN MICE

Medeiros¹,

Soares

Brito

et al. 2013

Arq. Gastroenterol.

View full text Add to dashboard Cite

-Context -Hydrogen sulphide (H 2 S) has been proved to be a neuromodulator and contributes to the maintenance of gastric mucosal integrity in damage caused by anti-inflammatory nonsteroidal drugs. Previously, we demonstrated that H 2 S synthesis is essential to gastric protection against ethanol. Objective -To better understanding the role of H 2 S and the detailed localization of its production in both normal and injured stomach due to ethanol injection, we studied the expression of cystathionine-γ-lyase (CSE) and cystathionine-β-synthetase (CBS) isoforms in gastric mucosa of mice treated with saline or 50% ethanol. Methods -Mice were treated by gavage with saline or 50% ethanol (0.5 mL/25 g). After 1 hour, mice were sacrificed, and gastric tissue was evaluated by histological and immunohistochemical analysis specific for CSE and CBS. Results -We have demonstrated a non-specific expression of CBS in the normal gastric mucosa and expression of CSE occurring mainly in the parietal cells of the animals treated with ethanol.Conclusion -Thus, we demonstrated that the expression of CBS appears to be constitutive and diffuse across the gastric epithelium, while the expression of CSE appears to be induced in parietal cells by damage agents such as ethanol. HEADINGS -Gastric mucosa. Cystathionine-β-Synthase. Cystathionine-γ-Lyase. Ethanol. Immunohistochemistry. Mice.

show abstract

Sulfide Enhancement of Pmn Apoptosis

Cited by 65 publications

References 20 publications

Regulation of Cellular Redox Signaling by Matricellular Proteins in Vascular Biology, Immunology, and Cancer

Regulation of Cellular Redox Signaling by Matricellular Proteins in Vascular Biology, Immunology, and Cancer

H2S, Endoplasmic Reticulum Stress, and Apoptosis of Insulin-secreting Beta Cells

IMMUNOHISTOCHEMICAL APPROACH REVEALS LOCALIZATION OF CYSTATHIONINE-?-LYASE AND CYSTATHIONINE-ß-SYNTHETASE IN ETHANOL-INDUCED GASTRIC MUCOSA DAMAGE IN MICE

Contact Info

Product

Resources

About