Potential role of microRNA-503 in Icariin-mediated prevention of high glucose-induced endoplasmic reticulum stress

Su, Baolin; Wang, Liangliang; L, Zhang; Zhang, Shu; Li, Qiang; Chen, Gang-Yi

doi:10.4239/wjd.v14.i8.1234

Cited by 3 publications

(1 citation statement)

References 43 publications

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“…In conclusion, it is evident that HG conditions have detrimental effects on different cell types, including cancer cells, and may also change their normal functions, i.e. migration potential and invasiveness[ 1 , 2 , 48 - 50 ]. Hence, understanding the mechanism of apoptosis by chronic exposure to HG, both in vitro and in vivo , will help efforts to combine preconditioning strategies, especially the subcellular preconditioning approach.…”

Section: Discussionmentioning

confidence: 99%

High glucose microenvironment and human mesenchymal stem cell behavior

Mateen,

Alaagib,

Haider

2024

World J Stem Cells

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High glucose (HG) culture conditions in vitro and persistent exposure to hyperglycemia in diabetes patients are detrimental to stem cells, analogous to any other cell type in our body. It interferes with diverse signaling pathways, i.e. mammalian target of rapamycin (mTOR)-phosphoinositide 3-kinase (PI3K)-Akt signaling, to impact physiological cellular functions, leading to low cell survival and higher cell apoptosis rates. While elucidating the underlying mechanism responsible for the apoptosis of adipose tissue-derived mesenchymal stem cells (MSCs), a recent study has shown that HG culture conditions dysregulate mTOR-PI3K-Akt signaling in addition to mitochondrial malfunctioning due to defective mitochondrial membrane potential (MtMP) that lowers ATP production. This organelle-level dysfunction energy-starves the cells and increases oxidative stress and ultrastructural abnormalities. Disruption of the mitochondrial electron transport chain produces an altered mitochondrial NAD+/NADH redox state as evidenced by a low NAD+/NADH ratio that primarily contributes to the reduced cell survival in HG. Some previous studies have also reported altered mitochondrial membrane polarity (causing hyperpolarization) and reduced mitochondrial cell mass, leading to perturbed mitochondrial homeostasis. The hostile microenvironment created by HG exposure creates structural and functional changes in the mitochondria, altering their bioenergetics and reducing their capacity to produce ATP. These are significant data, as MSCs are extensively studied for tissue regeneration and restoring their normal functioning in cell-based therapy. Therefore, MSCs from hyperglycemic donors should be cautiously used in clinical settings for cell-based therapy due to concerns of their poor survival rates and increased rates of post engraftment proliferation. As hyperglycemia alters the bioenergetics of donor MSCs, rectifying the loss of MtMP may be an excellent target for future research to restore the normal functioning of MSCs in hyperglycemic patients.

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Section: Discussionmentioning

confidence: 99%

High glucose microenvironment and human mesenchymal stem cell behavior

Mateen,

Alaagib,

Haider

2024

World J Stem Cells

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Effect of icariin on ovarian cancer: a combined network pharmacology and meta-analysis of in vitro studies approach

Cao,

Chen,

Zou

et al. 2024

Front. Pharmacol.

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IntroductionAn abundance of experimental evidence indicates that icariin (ICA) could potentially exert an anti-tumor effect on ovarian cancer (OC). Nevertheless, the reliability of this evidence remains ambiguous. This study aimed to explore the impact of ICA on OC and the underlying mechanisms.MethodsBioinformatics analysis was employed to pinpoint ICA-targeted genes and signaling pathways implicated in OC, utilizing network pharmacology. Subsequently, PubMed, EMBASE, and Web of Science databases were systematically searched from 2001 through June 2023 for in vitro trials evaluating the anti-tumor efficacy of conventional ICA versus placebo in OC. The pathways and genes identified in the literature were recorded, and the therapeutic targets were statistically analyzed and compared with the predicted targets from network pharmacology to confirm the precision of the targets.Results and DiscussionFourteen target genes were validated with success. The pathways corresponding to the remaining genes—excluding these 14—were analyzed and found to be primarily associated with cell apoptosis, anti-tumor, and other related pathways. Out of the 76 studies retrieved, eight fulfilled the inclusion criteria. The subsequent meta-analysis suggested that ICA treatment was significantly correlated with reduced cell growth and induced apoptosis. This study demonstrated a certain efficacy of ICA compared to placebo in enhancing anti-tumor outcomes, characterized by increased abilities in reducing cell growth and inducing apoptosis. The pathways involved in the therapeutic effect may be linked to cell apoptosis and anti-tumor mechanisms.

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Icariin accelerates bone regeneration by inducing osteogenesis-angiogenesis coupling in rats with type 1 diabetes mellitus

Zheng,

Hu,

et al. 2024

World J Diabetes

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BACKGROUND Icariin (ICA), a natural flavonoid compound monomer, has multiple pharmacological activities. However, its effect on bone defect in the context of type 1 diabetes mellitus (T1DM) has not yet been examined. AIM To explore the role and potential mechanism of ICA on bone defect in the context of T1DM. METHODS The effects of ICA on osteogenesis and angiogenesis were evaluated by alkaline phosphatase staining, alizarin red S staining, quantitative real-time polymerase chain reaction, Western blot, and immunofluorescence. Angiogenesis-related assays were conducted to investigate the relationship between osteogenesis and angiogenesis. A bone defect model was established in T1DM rats. The model rats were then treated with ICA or placebo and micron-scale computed tomography, histomorphometry, histology, and sequential fluorescent labeling were used to evaluate the effect of ICA on bone formation in the defect area. RESULTS ICA promoted bone marrow mesenchymal stem cell (BMSC) proliferation and osteogenic differentiation. The ICA treated-BMSCs showed higher expression levels of osteogenesis-related markers (alkaline phosphatase and osteocalcin) and angiogenesis-related markers (vascular endothelial growth factor A and platelet endothelial cell adhesion molecule 1) compared to the untreated group. ICA was also found to induce osteogenesis-angiogenesis coupling of BMSCs. In the bone defect model T1DM rats, ICA facilitated bone formation and CD31hiEMCNhi type H-positive capillary formation. Lastly, ICA effectively accelerated the rate of bone formation in the defect area. CONCLUSION ICA was able to accelerate bone regeneration in a T1DM rat model by inducing osteogenesis-angiogenesis coupling of BMSCs.

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Potential role of microRNA-503 in Icariin-mediated prevention of high glucose-induced endoplasmic reticulum stress

Cited by 3 publications

References 43 publications

High glucose microenvironment and human mesenchymal stem cell behavior

High glucose microenvironment and human mesenchymal stem cell behavior

Effect of icariin on ovarian cancer: a combined network pharmacology and meta-analysis of in vitro studies approach

Icariin accelerates bone regeneration by inducing osteogenesis-angiogenesis coupling in rats with type 1 diabetes mellitus

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