Down-regulation of myocardial infarction associated transcript 1 improves myocardial ischemia-reperfusion injury in aged diabetic rats by inhibition of activation of NF-κB signaling pathway

Liu, Yaoxia; Wang, Tao; Zhang, Min; Chen, Ping; Yu, Yerong

doi:10.1016/j.cbi.2019.01.001

Cited by 30 publications

(25 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Its expression is aberrantly expressed in multiple diseases, like b-thalassemia [22], breast cancer [23] and schizophrenia [24], indicating MIAT as an important regulator of these diseases. MIAT was also found to participate in the injury of various human body part, such as diabetic optic nerve [25], myocardial tissue [26] and renal tubules [27]. Thereby, knockdown of MIAT may have clinical significance in preventing or treating human diseases [13].…”

Section: Discussionmentioning

confidence: 99%

Silence of lncRNA MIAT protects ATDC5 cells against lipopolysaccharides challenge via up-regulating miR-132

Song

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

View full text Add to dashboard Cite

The over-expanding role of lncRNA myocardial infarction associated transcript (MIAT) in various human diseases has been recently revealed. This study attempted to see the role of MIAT in a cell model of osteoarthritis (OA). ATDC5 cells were subjected to lipopolysaccharides (LPS) to mimic a cell model of OA. The effects of MIAT on the model were tested by performing CCK-8 assay, flow cytometry, qRT-PCR, western blot and ELISA. The downstream miRNA and signalling pathways were studied by utilizing qRT-PCR and western blot. Transfection of ATDC5 cells with the shRNA specific against MIAT significantly attenuated LPS-evoked apoptosis and cytokines release. At the meantime, the viability loss and the cleavage of caspases were ameliorated as well. MIAT overexpressed lead to the opposite result. Further, miR-132 was found to be negatively regulated by MIAT. The protective effects of MIAT silence were flattened when miR-132 expression was suppressed. Besides that the inhibitory effects of MIAT silence on LPS-evoked NF-jB and JNK activation were eliminated by miR-132 silence. This study illustrated that silence of MIAT protected ATDC5 cells against LPS challenge. The chondroprotective effects of MIAT silence may be via up-regulation of miR-132 and inhibition of NF-jB and JNK pathways.

show abstract

Section: Discussionmentioning

confidence: 99%

Silence of lncRNA MIAT protects ATDC5 cells against lipopolysaccharides challenge via up-regulating miR-132

Song

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

View full text Add to dashboard Cite

show abstract

“…Dynamic changes in lncRNA expression have been demonstrated upon activation of NF-kB signalling. These changes not only regulate NF-kB activity through direct interaction between lncRNA and NF-kB or its transcripts, but also regulate NF-kB signalling activity indirectly, through upstream components [26][27][28].…”

Section: Discussionmentioning

confidence: 99%

“…MIAT, also termed as Gomafu in human or Rncr2 in mouse [6][7][8], is a promising functional factor among all disease-associated lncRNAs, and exhibits deregulation in multiple diseases, including upregulation in ischemic stroke, myocardial infarction, neuroendocrine prostate cancer, non-small-cell lung cancer, diabetic cardiomyopathy, cataract, chronic chagas disease cardiomyopathy, chronic lymphocytic leukemia and down-regulation in schizophrenia, diabetic nephropathy, bone disease [9]. It has recently found that MIAT is upregulated in hearts of a mouse model of AMI, and knocking it down improves cardiac function by inhibition of activation of NF-κB signaling pathway [10]. Furthermore, knockdown of MIAT improved cardiac functions, decreased cardiomyocytes apoptosis and attenuated inflammatory cell infiltration in vivo [11].…”

Section: Introductionmentioning

confidence: 99%

Targeting MIAT reduces apoptosis of cardiomyocytes after ischemia/reperfusion injury

Chen¹,

Zhang²,

Yu³

et al. 2019

Bioengineered

View full text Add to dashboard Cite

This study aims to investigate the role of targeting lncRNA myocardial infarction-associated transcript (MIAT) in protection against hypoxia/reoxygenation (H/R) injury in H9c2 cells in vitro and myocardial ischemia/reperfusion (I/R) injury in vivo by regulating expression of NF-kB and p53 upregulated modulator of apoptosis (PUMA). H9C2 cells were infected with lentivirus expressing the short-hairpin RNA direct against human MIAT gene (Lv-MIAT shRNA) or lentivirus expressing scrambled control (Lv-NC shRNA) or PUMA siRNA or p65 siRNA or their control siRNA respectively. Then the H9c2 cells were infected with Lv-shRNA to 2 hours of hypoxia (H) and 24 hour of reoxygenation (R). 100 ul of Lv-MIAT shRNA (1 × 10 8 PFU) or Lv-NC shRNA was transfected into mouse hearts, then the hearts were subjected to I/R (1h/72 h). We discovered targeting MIAT remarkably enhanced H9c2 cell viability, decreased H/R-induced cell apoptosis and LDH leakage and significantly decreased I/R-induced myocardial infarct size, reduced myocardial apoptosis and enhanced the heart function. Targeting MIAT downregulated p65 nuclear translocation, NF-κB activity and anti-apoptotic protein cleaved-caspase-3, Bax, and upregulated anti-apoptotic protein Bcl-2 induced by H/R or I/R. Our study suggests that targeting MIAT may protect against H9c2 cardiomyoblasts H/R injury or myocardial I/R injury via inhibition of cell apoptosis, mediated by NF-κB and PUMA signal pathway. ARTICLE HISTORY

show abstract

“…16,17 Besides, lncRNA is involved in morphine-meditated alleviation of autophage in MI/R injury, 18 indicating that lncRNAs may mediate the protective role of drugs against MI/R injury. 22,23 Several studies have shown that the expression of lncRNA MIAT can be inhibited or promoted by drugs, indicating lncRNA MIAT involves in drug-mediated inhibition or promotion of diseases progression. 22,23 Several studies have shown that the expression of lncRNA MIAT can be inhibited or promoted by drugs, indicating lncRNA MIAT involves in drug-mediated inhibition or promotion of diseases progression.…”

mentioning

confidence: 99%

“…LncRNA myocardial infarction-associated transcript (MIAT) is a widely expressed lncRNA that exerts its regulation function in cancers, diabetic retinopathy, atherosclerosis, etc [19][20][21] Recent studies have shown that down-regulation of lncRNA MIAT reduced myocardial cell apoptosis after MI/R injury, indicating targeting MIAT might protect against H/R-induced myocardial cell apoptosis or MI/R injury. 22,23 Several studies have shown that the expression of lncRNA MIAT can be inhibited or promoted by drugs, indicating lncRNA MIAT involves in drug-mediated inhibition or promotion of diseases progression. 21,24 However, whether lncRNA MIAT is involved in catechin-mediated inhibition on MI/R injury is unclear.…”

mentioning

confidence: 99%

Catechin relieves hypoxia/reoxygenation‐induced myocardial cell apoptosis via down‐regulating lncRNA MIAT

Wei

et al. 2020

J Cellular Molecular Medi

View full text Add to dashboard Cite

Background Catechin protects heart from myocardial ischaemia/reperfusion (MI/R) injury. However, whether catechin inhibits H/R‐induced myocardial cell apoptosis is largely unknown. Objective This study aims to investigate the underlying mechanism of catechin in inhibiting the apoptosis of H/R‐induced myocardial cells. Methods LncRNA MIAT expression was detected by qRT‐PCR. Cell viability of H9C2 cells was detected using CCK‐8 assay. The apoptosis of H9C2 cells was detected by flow cytometry. The interaction between CREB and MIAT promoter regions was confirmed by dual‐luciferase reporter gene assay and ChIP assay. Results In MI/R rats, catechin improved heart function and down‐regulated lncRNA MIAT expression in myocardial tissue. In H/R‐induced H9C2 cells, catechin protected against cell apoptosis, and lncRNA MIAT overexpression attenuated this protective effect of catechin. We confirmed that transcription factor CREB could bind to MIAT promoter region, and catechin suppressed lncRNA MIAT expression through up‐regulating CREB. Catechin improved mitochondrial function and relieved apoptosis through promoting Akt/Gsk‐3β activation. In addition, MIAT inhibited Akt/Gsk‐3β activation and promoted cell apoptosis in H/R‐induced H9C2 cells. Finally, we found catechin promoted Akt/Gsk‐3β activation through inhibiting MIAT expression in H/R‐induced H9C2 cells. Conclusion Catechin relieved H/R‐induced myocardial cell apoptosis through regulating CREB/lncRNA MIAT/Akt/Gsk‐3β pathway.

show abstract

Down-regulation of myocardial infarction associated transcript 1 improves myocardial ischemia-reperfusion injury in aged diabetic rats by inhibition of activation of NF-κB signaling pathway

Cited by 30 publications

References 41 publications

Silence of lncRNA MIAT protects ATDC5 cells against lipopolysaccharides challenge via up-regulating miR-132

Silence of lncRNA MIAT protects ATDC5 cells against lipopolysaccharides challenge via up-regulating miR-132

Targeting MIAT reduces apoptosis of cardiomyocytes after ischemia/reperfusion injury

Catechin relieves hypoxia/reoxygenation‐induced myocardial cell apoptosis via down‐regulating lncRNA MIAT

Contact Info

Product

Resources

About