MicroRNA regulation of stem cell differentiation and diseases of the bone and adipose tissue: Perspectives on miRNA biogenesis and cellular transcriptome

Martin, Elizabeth C.; Qureshi, Ammar T.; Dasa, Vinod; Freitas, Michael A.; Gimble, Jeffrey M.; Davis, Thomas A.

doi:10.1016/j.biochi.2015.02.012

Cited by 64 publications

(46 citation statements)

References 181 publications

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“…In some pathological conditions, there has a dysregulation of this miRNA processing machinery components, such as the expression levels of Drosha and Dicer are down-regulated in ovarian cancer and neuroblastomas, while Exportin-5 is also down-regulated in bladder cancer [7]. When these matured miRNAs are processed and expressed, they bind to partially complementary sites in target mRNAs, leading to mRNA degradation or protein translation interference causing translational repression, mRNA destabilization, and/or mRNA cleavage for post-transcriptional regulation of protein synthesis [8,9]. Furthermore, this interaction between the miRNA and target mRNA resulted in decreased target protein levels without affecting the stability of the mRNA.…”

Section: Mirnas: Treatment and Main Problemsmentioning

confidence: 99%

Cross-talk of MicroRNA and hydrogen sulfide: A novel therapeutic approach for bone diseases

Zhai

Tyagi

2017

Biomedicine & Pharmacotherapy

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Bone homeostasis requires a balance between the bone formation of osteoblasts and bone resorption of osteoclasts to maintain ideal bone mass and bone quality. An imbalance in bone remodeling processes results in bone metabolic disorders such as osteoporosis. Hydrogen sulfide (H2S), a gasotransmitter, has attracted the focus of many researchers due to its multiple physiological functions. It has been implicated in anti-inflammatory, vasodilatory, angiogenic, cytoprotective, anti-oxidative and anti-apoptotic mechanisms. H2S has also been shown to exert osteoprotective activity through its anti-inflammatory and anti-oxidative effects. However, the underlying molecular mechanisms by which H2S mitigates bone diseases are not completely understood. Experimental evidence suggests that H2S may regulate signaling pathways by directly influencing a gene in the cascade or interacting with some other gasotransmitter (carbon monoxide or nitric oxide) or both. MicroRNAs (miRNAs) are short non-coding RNAs which regulate gene expression by targeting, binding and suppressing mRNAs; thus controlling cell fate. Certainly, bone remodeling is also regulated by miRNAs expression and has been reported in many studies. MicroRNAs also regulate H2S biosynthesis. The inter-regulation of microRNAs and H2S opens a new possibility for exploring the H2S-microRNA crosstalk in bone diseases. However, the relationship between miRNAs, bone development, and H2S is still not well explained. This review focuses on miRNAs and their roles in regulating bone remodeling and possible mechanisms behind H2S mediated bone loss inhibition, H2S-miRNAs crosstalk in relation to the pathophysiology of bone remodeling, and future perspectives for miRNA-H2S as a therapeutic agent for bone diseases.

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Section: Mirnas: Treatment and Main Problemsmentioning

confidence: 99%

Cross-talk of MicroRNA and hydrogen sulfide: A novel therapeutic approach for bone diseases

Zhai

Tyagi

2017

Biomedicine & Pharmacotherapy

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“…Additionally, it has been known that microRNAs function as key regulators in stem cells (3, 4). MicroRNAs that are single stranded, small (~22 nucleotides) and non-coding RNAs generated from endogenous transcripts regulate gene expressions (5) and have important roles in cellular functions, such as cell proliferation or survival (6), fat metabolism regulation (7), mesenchymal stem cell differentiation (8), epithelial to mesenchymal transition (9), and even in antiviral defense (10). Additionally, recent studies have revealed that microRNAs are critical regulators for the differentiation of hESCs and cell fate determination during development (11–14).…”

Section: Introductionmentioning

confidence: 99%

Lineage-specific Expression of miR-200 Family in Human Embryonic Stem Cells during In Vitro Differentiation

Kim

Park

et al. 2017

IJSC

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Although microRNAs have emerged as key regulators in diverse cellular processes, the roles of microRNAs are poorly understood in human embryonic stem cells (hESCs) during differentiation into specialized cell types. In this study, we used a microRNA array with 799 human microRNA probes to examine the expression profiles of microRNAs in hESCs during differentiation into endodermal and mesodermal lineages in vitro. Among the microRNAs analyzed, 7 and 20 microRNAs were enriched in the developmental process of hESCs into mesodermal and endodermal lineages, respectively. In particular, the expression levels of miR-200 family, which is known to regulate the epithelial to mesenchymal transition (EMT), gradually increased in hESCs during differentiation into hepatocytes while they gradually decreased during differentiation into vascular endothelial cells. Downregulation of ZEB1, a direct target of miR-200 family, and E-CADHERIN, a target protein of ZEB1, was observed in hESCs during differentiation into endodermal and mesodermal lineages, respectively. These results indicate that miR-200 family has an important role in determining the cell fate between endodermal and mesodermal lineages from the pluripotent state.

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“…Then miRNA suppresses transcription of genes through binding to 3′ untranslated region (3′UTR) of the complementary mRNA sequence . The miRNAs influence diverse cellular events such as development, proliferation, differentiation, and apoptosis . It is also suggested that the miRNA acts as a tumor suppressor or an oncogene depending their target in cancer cells .…”

Section: Introductionmentioning

confidence: 99%

Suberoylanilide hydroxamic acid induces thioredoxin1‐mediated apoptosis in lung cancer cells via up‐regulation of miR‐129‐5p

You

Park

2017

Molecular Carcinogenesis

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Histone deacetylase (HDAC) inhibitors, especially suberoylanilide hydroxamic acid (SAHA) induce apoptosis in various cancer cells. Here, we investigated the effect of SAHA on apoptosis in lung cancer cells and addressed the role of reactive oxygen species (ROS), glutathione (GSH), and thioredoxin1 (Trx1) levels in this process. We also identified the miRNAs that down-regulate Trx1 expression at RNA level and thereby influence apoptotic cell death of SAHA increased intracellular ROS levels and promoted apoptotic cell death in cancerous cells but not in non-cancerous normal lung cells. Likewise, SAHA induced GSH depletion specifically in cancerous cells. While N-acetyl cysteine (NAC) reduced ROS level and reversed the effect of SAHA on cell death, L-buthionine sulfoximine (BSO) further enhanced GSH depletion, and promoted cell death. SAHA decreased the mRNA and protein levels of Trx1 in lung cancer cells. Knockdown/suppression of Trx1 intensified apoptosis in SAHA-treated lung cancer cells whereas overexpression of Trx1 prevented the cell death in these cells. SAHA up-regulated the level of miR-129-5p, which binds to 3' untranslated region (3'UTR) of Trx1 and down-regulates Trx1 expression. Down-regulation of Trx1 led to activation of apoptosis-signal regulating kinase (ASK), which induced apoptotic cell death by triggering ASK-JNK or ASK-p38 kinase pathway. In conclusion, changes in ROS and GSH levels in SAHA-treated lung cancer cells partially co-related with cell death. SAHA induced apoptosis via the down-regulation of Trx1, which was regulated by miR-129-5p.

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MicroRNA regulation of stem cell differentiation and diseases of the bone and adipose tissue: Perspectives on miRNA biogenesis and cellular transcriptome

Cited by 64 publications

References 181 publications

Cross-talk of MicroRNA and hydrogen sulfide: A novel therapeutic approach for bone diseases

Cross-talk of MicroRNA and hydrogen sulfide: A novel therapeutic approach for bone diseases

Lineage-specific Expression of miR-200 Family in Human Embryonic Stem Cells during In Vitro Differentiation

Suberoylanilide hydroxamic acid induces thioredoxin1‐mediated apoptosis in lung cancer cells via up‐regulation of miR‐129‐5p

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