Hydrogen Sulfide Promotes Bone Homeostasis by Balancing Inflammatory Cytokine Signaling in CBS-Deficient Mice through an Epigenetic Mechanism

Behera, Jyotirmaya; Kimberly, K.; Voor, Michael J.; Metreveli, Naira; Tyagi, Suresh C.; Tyagi, Neetu

doi:10.1038/s41598-018-33149-9

Cited by 44 publications

(46 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Indeed, H 2 S deficiency in BMSC attenuates both osteogenesis and proliferation. In keeping with this, CBS-deficient mice have decreased serum and intracellular levels of H 2 S and a severe osteoporotic phenotype [158,159]. The H 2 S administration to CBS deficient mice of can restore normal bone homeostasis [158].…”

Section: Cortisol Secretion Peripheral Activation and Sensitivitymentioning

confidence: 70%

“…In keeping with this, CBS-deficient mice have decreased serum and intracellular levels of H 2 S and a severe osteoporotic phenotype [158,159]. The H 2 S administration to CBS deficient mice of can restore normal bone homeostasis [158]. One of the supposed mechanisms is the increase of Journal of Diabetes Research Hcy that leads to and oxidative damage and dysfunction of the BMMSCs.…”

Section: Cortisol Secretion Peripheral Activation and Sensitivitymentioning

confidence: 87%

“…In BMSC, H 2 S has a fundamental role for maintaining cell proliferation and differentiation [158]. Indeed, H 2 S deficiency in BMSC attenuates both osteogenesis and proliferation.…”

Section: Cortisol Secretion Peripheral Activation and Sensitivitymentioning

confidence: 99%

See 2 more Smart Citations

Pathophysiology and Management of Type 2 Diabetes Mellitus Bone Fragility

Eller-Vainicher

Cairoli

Grassi

et al. 2020

Journal of Diabetes Research

View full text Add to dashboard Cite

Individuals with type 2 diabetes mellitus (T2DM) have an increased risk of bone fragility fractures compared to nondiabetic subjects. This increased fracture risk may occur despite normal or even increased values of bone mineral density (BMD), and poor bone quality is suggested to contribute to skeletal fragility in this population. These concepts explain why the only evaluation of BMD could not be considered an adequate tool for evaluating the risk of fracture in the individual T2DM patient. Unfortunately, nowadays, the bone quality could not be reliably evaluated in the routine clinical practice. On the other hand, getting further insight on the pathogenesis of T2DM-related bone fragility could consent to ameliorate both the detection of the patients at risk for fracture and their appropriate treatment. The pathophysiological mechanisms underlying the increased risk of fragility fractures in a T2DM population are complex. Indeed, in T2DM, bone health is negatively affected by several factors, such as inflammatory cytokines, muscle-derived hormones, incretins, hydrogen sulfide (H2S) production and cortisol secretion, peripheral activation, and sensitivity. All these factors may alter bone formation and resorption, collagen formation, and bone marrow adiposity, ultimately leading to reduced bone strength. Additional factors such as hypoglycemia and the consequent increased propensity for falls and the direct effects on bone and mineral metabolism of certain antidiabetic medications may contribute to the increased fracture risk in this population. The purpose of this review is to summarize the literature evidence that faces the pathophysiological mechanisms underlying bone fragility in T2DM patients.

show abstract

Section: Cortisol Secretion Peripheral Activation and Sensitivitymentioning

confidence: 70%

Section: Cortisol Secretion Peripheral Activation and Sensitivitymentioning

confidence: 87%

See 1 more Smart Citation

Pathophysiology and Management of Type 2 Diabetes Mellitus Bone Fragility

Eller-Vainicher

Cairoli

Grassi

et al. 2020

Journal of Diabetes Research

View full text Add to dashboard Cite

show abstract

“…Deficiency in CBS or CSE causes marked hyperhomocysteinemia and hypertension in mice [15,16]. Disruption of CBS in mice causes metabolic osteoporosis that is prevented by supplementation of H 2 S [31]. Deficiency in CSE promotes neurodegeneration in Huntington's disease [18].…”

Section: Endogenous H 2 S Productionmentioning

confidence: 99%

Emerging pharmacological tools to control hydrogen sulfide signaling in critical illness

Marutani

Ichinose

2020

ICMx

View full text Add to dashboard Cite

Hydrogen sulfide (H 2 S) has long been known as a toxic environmental hazard. Discovery of physiological roles of H 2 S as a neurotransmitter by Kimura and colleagues triggered an intensive research in the biological roles of H 2 S in the past decades. Manipulation of H 2 S levels by inhibiting H 2 S synthesis or administration of H 2 S-releasing molecules revealed beneficial as well as harmful effects of H 2 S. As a result, it is now established that H 2 S levels are tightly controlled and too much or too little H 2 S levels cause harm. Nonetheless, translation of sulfide-based therapy to clinical practice has been stymied due to the very low therapeutic index of sulfide and the incomplete understanding of endogenous sulfide metabolism. One potential strategy to circumvent this problem is to use a safe and stable sulfide metabolite that may mediate effects of H 2 S. Alternatively, endogenous sulfide levels may be controlled using specific sulfide scavengers. In this review article, the role of endogenous H 2 S production and catabolism will be briefly reviewed followed by an introduction of thiosulfate and H 2 S scavengers as novel pharmacological tools to control H 2 S-dependent signaling.

show abstract

“…HHcy has also been shown to significantly increase HDAC activity in human retinal endothelial cells (HRECs), human retinal pigmented epithelial cells (ARPE-19) , and Cbs-deficient mice retinas [65]. On the other hand, an animal study has shown that HHcy causes inhibition of HDAC3 activity [148].…”

Section: Histone Modifications In Hhcymentioning

confidence: 99%

Dysregulation of Epigenetic Mechanisms of Gene Expression in the Pathologies of Hyperhomocysteinemia

Perła-Kaján

Jakubowski

2019

IJMS

View full text Add to dashboard Cite

Hyperhomocysteinemia (HHcy) exerts a wide range of biological effects and is associated with a number of diseases, including cardiovascular disease, dementia, neural tube defects, and cancer. Although mechanisms of HHcy toxicity are not fully uncovered, there has been a significant progress in their understanding. The picture emerging from the studies of homocysteine (Hcy) metabolism and pathophysiology is a complex one, as Hcy and its metabolites affect biomolecules and processes in a tissue- and sex-specific manner. Because of their connection to one carbon metabolism and editing mechanisms in protein biosynthesis, Hcy and its metabolites impair epigenetic control of gene expression mediated by DNA methylation, histone modifications, and non-coding RNA, which underlies the pathology of human disease. In this review we summarize the recent evidence showing that epigenetic dysregulation of gene expression, mediated by changes in DNA methylation and histone N-homocysteinylation, is a pathogenic consequence of HHcy in many human diseases. These findings provide new insights into the mechanisms of human disease induced by Hcy and its metabolites, and suggest therapeutic targets for the prevention and/or treatment.

show abstract

Hydrogen Sulfide Promotes Bone Homeostasis by Balancing Inflammatory Cytokine Signaling in CBS-Deficient Mice through an Epigenetic Mechanism

Cited by 44 publications

References 57 publications

Pathophysiology and Management of Type 2 Diabetes Mellitus Bone Fragility

Pathophysiology and Management of Type 2 Diabetes Mellitus Bone Fragility

Emerging pharmacological tools to control hydrogen sulfide signaling in critical illness

Dysregulation of Epigenetic Mechanisms of Gene Expression in the Pathologies of Hyperhomocysteinemia

Contact Info

Product

Resources

About