Abstract:Hydrogen sulfide (H 2 S) has long been known as a toxic gas. However, recently accumulated evidence suggests that H 2 S contributes to a variety of physiologic and pathologic processes. Endogenous H 2 S production is regulated by multiple enzymes that are differentially expressed in the cardiovascular, neuronal, immune, renal, respiratory, gastrointestinal, reproductive, liver, and endocrine systems. Alteration of H 2 S metabolism may affect multiple signaling pathways and tissue homeostasis. The growing numbe… Show more
“…H 2 S is a gaseous transmitter that has recently been associated with the function of MSCs and bone metabolism [ 25 ]. It has been elucidated that the production of force-induced H 2 S in hPDLSCs modulated the accumulation of macrophage and osteoclastic and osteogenic activities in the alveolar bone through regulation of the secretion of monocyte chemoattractant protein-1 and the receptor activator of the nuclear factor- κ B ligand/osteoprotegerin (RANKL/OPG) system and then controlled the process of OTM [ 26 ].…”
Section: The Molecules Transmitting the Orthodontic Force To Pdlscmentioning
Periodontal ligament stem cells (PDLSCs) possess self-renewal, multilineage differentiation, and immunomodulatory properties. They play a crucial role in maintaining periodontal homeostasis and also participated in orthodontic tooth movement (OTM). Various studies have applied controlled mechanical stimulation to PDLSCs and investigated the effects of orthodontic force on PDLSCs. Physical stimuli can regulate the proliferation and differentiation of PDLSCs. During the past decade, a variety of studies has demonstrated that applied forces can activate different signaling pathways in PDLSCs, including MAPK, TGF-β/Smad, and Wnt/β-catenin pathways. Besides, recent advances have highlighted the critical role of orthodontic force in PDLSC fate through mediators, such as IL-11, CTHRC1, miR-21, and H2S. This perspective review critically discusses the PDLSC fate to physical force in vitro and orthodontic force in vivo, as well as the underlying molecular mechanism involved in OTM.
“…H 2 S is a gaseous transmitter that has recently been associated with the function of MSCs and bone metabolism [ 25 ]. It has been elucidated that the production of force-induced H 2 S in hPDLSCs modulated the accumulation of macrophage and osteoclastic and osteogenic activities in the alveolar bone through regulation of the secretion of monocyte chemoattractant protein-1 and the receptor activator of the nuclear factor- κ B ligand/osteoprotegerin (RANKL/OPG) system and then controlled the process of OTM [ 26 ].…”
Section: The Molecules Transmitting the Orthodontic Force To Pdlscmentioning
Periodontal ligament stem cells (PDLSCs) possess self-renewal, multilineage differentiation, and immunomodulatory properties. They play a crucial role in maintaining periodontal homeostasis and also participated in orthodontic tooth movement (OTM). Various studies have applied controlled mechanical stimulation to PDLSCs and investigated the effects of orthodontic force on PDLSCs. Physical stimuli can regulate the proliferation and differentiation of PDLSCs. During the past decade, a variety of studies has demonstrated that applied forces can activate different signaling pathways in PDLSCs, including MAPK, TGF-β/Smad, and Wnt/β-catenin pathways. Besides, recent advances have highlighted the critical role of orthodontic force in PDLSC fate through mediators, such as IL-11, CTHRC1, miR-21, and H2S. This perspective review critically discusses the PDLSC fate to physical force in vitro and orthodontic force in vivo, as well as the underlying molecular mechanism involved in OTM.
“…A relevant increase in brain tissue CBS relative expression was obtained in accordance with [74,[82][83] Where MSCs are vital progenitor cells owing the capability to differentiate into vital cells with maintaining tissue homeostasis and proliferation of neural stem cells. While a suppression in oxidative stress brain tissue level (MDA) with a simultaneous increase in (GSH) was observed following intracerebral MSCs transplantation.These obtained results are in accordance with [12], where oxidative stress markers in brain tissue were suggested to be suppressed by intracerebral transplantation of MSCs as a result of expressing antiinflammatory cytokines involved in brain tissue repair introduced by MSCs via Bcl2 activation with attenuating Bax expression preventing brain damage [12,84].An additional beneficial action of transplanting MSCs intracerebrally within LPS induced AD in rats was their ability to suppress ACAT brain tissue relative expression level, which can not only be related to the lipid engulfing macrophage polarization effect but also to its ability to suppress inflammatory cascades such as TNF-α expression and caspase-3 where they play a vital role in up regulating the brain cholesterol ACAT level [12,[85][86].…”
Background: Memory disorders have been characterized by being a devastating long term incurable diseases with a huge social impact in addition to a diminished efficient available medical treatments. Deep Brain stimulation via using neuroprotective inducers for treatment of brain structure degenerative diseases such as Alzheimer's disease (AD) can be considered as being a promising successful therapy due to its various targets and underlying mechanisms for improving brain dysfunction. Objectives: The main aim of this study is to suggest therapeutic protocol having the potentials for restoring normal neurons diverse population and modifying neuropathological deposited hallmarks including both positive and negative lesions. Materials and Methods: Rats were divided into nine groups: (G1) control ;(G2) rats received LPS as a method of inducing nongenetically manipulated AD;(G3)AD rats received NaHS;(G4) AD rats received MSCs intracerebrally;(G5) AD rats received MSCs+NaHS;(G6)AD rats received kefir+GB;(G7)AD rats received MSCs+kefir+GB;(G8)AD rats received NaHS+kefir+GB; (G9) AD rats received MSCs+NaHS+kefir+GB. Results: AD induction resulted in down-regulation of CBS expression and GSH brain tissue level accompanied with overexpression in amyloid-β protein, MAPK, tau protein, ACAT expression and MDA brain tissue level in addition to elevated caspase-3 serum level. Conclusion: The implantation of amyloid reliving therapy that do have a wide clinical impact if initiated at benign plaques stage before irreversible brain damage occurs. The following effects have been observed following the administration of suggested medical protocol where a decrease in AD pathological deposited hallmarks has been observed with maintaining inflammatory brain factors by functioning as a potent neuroregenerative.
“…Again, it is noteworthy another aspect regarding the importance of CSE/H 2 S system in the bone context, namely in bone tissue engineering. It has in fact been recently demonstrated that cells exposed to H 2 S have potential applications in regenerative medicine, since modulation of H 2 S metabolism may serve as a therapeutic approach to promote the viability of transplanted mesenchymal stem cells (MSCs) and facilitate MSC-based regeneration [ 40 , 41 ].…”
Hydrogen sulfide (H2S), generated in the osteoblasts predominantly via cystathionine-γ-lyase (CSE), is bone protective. Previous studies suggested that the onset of bone loss due to estrogen deficiency is associated to decreased levels of H2S and blunted gene expression of CSE. However, there are still a lot of unknowns on how H2S levels influence bone cells function. The present study aims to explore the mechanisms by which estrogen may regulate CSE expression, in particular the role of estrogen receptor alpha (ERα) in human osteoblasts (hOBs). Vertebral lamina derived hOBs were characterized and then assessed for CSE expression by western blot analysis in the presence or absence of ERα overexpression. Bioinformatic analysis, luciferase reporter assay and ChIP assay were performed to investigate ERα recruitment and activity on hCSE gene promoter.Three putative half Estrogen Responsive Elements (EREs) were identified in the hCSE core promoter and were found to participate in the ERα – mediated positive regulation of CSE expression. All osteoblast samples responded to ERα over-expression increasing the levels of CSE protein in a comparable manner. Notably, the ERα recruitment on the regulatory regions of the CSE promoter occurred predominantly in female hOBs than in male hOBs. The obtained results suggest that CSE/H2S system is in relation with estrogen signaling in bone in a gender specific manner.
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