Hypoxia induces downregulation of soluble guanylyl cyclase β1 by miR-34c-5p

Xu, Xiaojian; Wang, Shumin; Liu, Juan; Dou, Dou; Liu, Limei; Chen, Zhengju; Ye, Liping; Liu, Huixia; He, Qiong; Raj, J. Usha; Gao, Yuansheng

doi:10.1242/jcs.113381

Cited by 33 publications

(22 citation statements)

References 68 publications

(76 reference statements)

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“…changed only after prolonged hypoxia. MiR-34c-5p, directly targets sGCβ1 in hypoxia and is a crucial factor in the control of various physiological functions [50]. MiR-184 can inhibit hypoxia-induced apoptosis due to activation of caspase-3 and caspase-9 in cyanotic congenital heart disease [51].…”

Section: Discussionmentioning

confidence: 99%

Characteristic MicroRNA Expression Induced by δ-Opioid Receptor Activation in the Rat Liver Under Prolonged Hypoxia

Zhi

Shao

Xue

et al. 2017

Cell Physiol Biochem

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Background/Aims: Hypoxic/ischemic injury to the liver is a frequently encountered clinical problem with limited therapeutic options. Since microRNAs (miRNAs) are involved in hypoxic/ ischemic events, and δ-opioid receptor (DOR) is protective against hypoxic/ischemic injury, we asked if pharmacological activation of DOR can alter hypoxic events by regulating miRNA expression in the liver. As the first step, the present work aimed at testing the effect of DOR activation on hepatic miRNA expression in hypoxia. Methods: Male Sprague Dawley rats were exposed to hypoxia (9.5-10% O₂) for 1, 5, or 10 days with or without DOR activation. The target miRNAs were selected according to TaqMan low-density array (TLDA) data and analyzed by quantitative real-time PCR. Results: We found that: 1) 1-day hypoxia caused the upregulation of 9 miRNAs (miR-7a-5p, miR-10a-5p, miR-25-3p, miR-26b-5p, miR-122-5p, miR-128a-3p, miR-135b-5p, miR-145-5p, and miR-181a-5p) and the downregulation of 2 miRNAs (miR-34a-5p and miR-182); 2) 5 and 10-days hypoxia altered the expression of 4 miRNAs (miR-34c-5p, miR-184, miR-107-3p and miR192-5p); 3) DOR activation shifted the expression of 8 miRNAs (miR-122-5p, miR-146a-5p, miR-30e-5p, miR-128a-3p, miR-182, miR-192-5p miR-107-3p and miR-184) in normoxic condition; and 4) DOR activation modified hypoxia-induced changes in 6 miRNAs (miR-142-5p, miR-145-5p, miR-146a-5p, miR-204-5p, miR-34a-5p and miR-192-5p). Conclusion: Hypoxia significantly modifies the miRNA profile in the liver, while DOR activation can modify the hypoxic modification. Therefore, it is potentially possible to alter hypoxic/ischemic pathophysiology in the liver through DOR pharmacotherapy.

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Section: Discussionmentioning

confidence: 99%

Characteristic MicroRNA Expression Induced by δ-Opioid Receptor Activation in the Rat Liver Under Prolonged Hypoxia

Zhi

Shao

Xue

et al. 2017

Cell Physiol Biochem

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“…15,67,159 Such reduced responses have been attributed to (1) reduced expression of the β-subunit of sGC (because of increased degradation after sustained increases in cGMP level [by C-type natriuretic peptide activating particulate guanylyl cyclase or by upregulation of phosphodiesterases] or increased oxidative stress [with aging, hypertension, and diabetes mellitus]), which contains the heme-binding domain responding to NO [159][160][161] ; (2) reduced dimerization by thiol-reducing agents (eg, reduced glutathione, l-cysteine, and hydrogen sulfide) or by interaction with protein-disulfide isomerase (eg, hypoxia in the pulmonary circulation), preventing the formation of disulphide bonds between by guest on May 10, 2018 http://circres.ahajournals.org/ Downloaded from the cysteine residues of the α-and β-subunits of the enzyme, which are essential for its activity [162][163][164] ; (3) desensitization by oxidation or S-nitrosylation at Cys122 of the β-subunit caused by prolonged exposure to NO or increased oxidative stress (with the resultant formation of peroxynitrite) 165,166 ; and (4) reduced expression/activity of HO-1 (caused by allelic variants of the HO-1 gene promoter with reduced transcriptional activity or to hypoxia that stimulates its cleavage) favoring oxidation of the sGC-heme (containing Fe 3+ instead of Fe…”

Section: Reduced Vasodilator Responsementioning

confidence: 99%

Thirty Years of Saying NO

Vanhoutte

Zhao

et al. 2016

Circulation Research

321

156

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T he historical demonstration by Furchgott and Zawadzki 1 that removal of the endothelium abrogates the in vitro vasodilator effect of acetylcholine has led to the identification 30 years ago of nitric oxide (NO) as a major endogenous local regulator of vascular tone. [2][3][4][5][6][7][8][9][10] When the ability of endothelial cells to produce NO is blunted, the ensuing vascular dysfunction sets the stage for the occurrence of cardiovascular disease in general, and atherosclerosis in particular. [11][12][13][14][15] This review focuses, stepby-step, on the bioavailability (production, action, and disposition) of endothelium-derived NO as local regulator of vascular tone in health and disease. Obviously, there is much more than NO in the control of the degree of contraction of underlying vascular smooth muscle cells exerted by the endothelial cells. Indeed, they generate also prostacyclin and hyperpolarizing signals (initiating endothelium-dependent hyperpolarization [EDH] and thus relaxation) and produce vasoconstrictor mediators (endothelium-derived contracting factors and the peptide endothelin-1); those have been discussed elsewhere in detail. 15-22 Endothelial Sources of NO NO SynthaseThree NO synthase (NOS) isozymes, which are encoded by different genes, catalyze the production of NO from l-arginine: neuronal NOS (or NOS-1), cytokine-inducible NOS (iNOS or NOS-2), and endothelial NOS (eNOS or NOS-3).6,23-25 Although iNOS can be induced (by lipopolysaccharides and inflammatory cytokines) and neuronal NOS can be present in the blood vessel

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“…Sp1 also forms a complex with HDAC4 to downregulate miR-200a expression in hepatocellular carcinoma and contributes to cell proliferation and migration [28]. In addition, Sp1 is an activator of miR-34c, miR-132 and miR-365 expression [29-31]. However, no studies have assessed whether Sp1 regulates the expression of miRNAs involved in lung tumorigenesis.…”

Section: Introductionmentioning

confidence: 99%

Sp1-mediated microRNA-182 expression regulates lung cancer progression

et al. 2014

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Our recent study indicated that overexpression of Sp1 enhances the proliferation of lung cancer cells, while represses metastasis. In this study, we found that the transcriptional activity of FOXO3 was increased, but its protein levels decreased following Sp1 expression. Sp1 increased expression of miR-182, which was then recruited to the 3'-untranslated region of FOXO3 mRNA to silence its translational activity. Knockdown of miR-182 inhibited lung cancer cells growth, but enhanced the invasive and migratory abilities of these cells through increased N-cadherin expression. Repression of FOXO3 expression in the miR-182 knockdown cells partially reversed this effect, suggesting that miR-182 promotes cancer cell growth and inhibits cancer metastatic activity by regulating the expression of FOXO3. The expression of several cancer metastasis-related genes such as ADAM9, CDH9 and CD44 was increased following miR-182 knockdown. In conclusion, in the early stages of lung cancer progression, Sp1 stimulates miR-182 expression, which in turn decreases FOXO3 expression. This stimulates proliferation and tumor growth. In the late stages, Sp1 and miR-182 decline, thus increasing FOXO3 expression, which leads to lung metastasis.

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Hypoxia induces downregulation of soluble guanylyl cyclase β1 by miR-34c-5p

Cited by 33 publications

References 68 publications

Characteristic MicroRNA Expression Induced by δ-Opioid Receptor Activation in the Rat Liver Under Prolonged Hypoxia

Characteristic MicroRNA Expression Induced by δ-Opioid Receptor Activation in the Rat Liver Under Prolonged Hypoxia

Thirty Years of Saying NO

Sp1-mediated microRNA-182 expression regulates lung cancer progression

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