scholarly journals MicroRNA-195 Prevents Hippocampal Microglial Polarization Towards The M1 Phenotype Induced By Chronic Brain Hypoperfusion Through Regulating CX3CL1/CX3CR1 Signalling

2020 ◽  
Author(s):  
Meng Mao ◽  
Yi Xu ◽  
Xin-Yu Zhang ◽  
Lin Yang ◽  
Xiao-bin An ◽  
...  
Keyword(s):  
Culture System ◽  
Molecular Mechanisms ◽  
Immunofluorescence Staining ◽  
Neonatal Rat ◽  
Injection Technique ◽  
Microglial Polarization ◽  
Bv2 Cells ◽  
Bilateral Carotid ◽  
M1 Phenotype

Abstract Background Microglial polarization was found respond dynamically to acute brain hypoxia induced by stroke and traumatic brain injury (TBI). However, studies on the process of microglial polarization during chronic cerebral ischaemia (CCI) are limited. Our goal is to investigate the influence of CCI on microglial polarization following chronic brain hypoperfusion (CBH) and exploit potential molecular mechanisms.Methods CBH model was performed by bilateral carotid artery ligation (2VO) in rats. Using stereotaxic injection technique, lenti-pre-miR-195 and anti-miR-195 oligonucleotide fragments (lenti-pre-AMO-195) were injeted into CA1 region of the hippocampus to construct animal models with high or low expression of miR-195. Immunofluorescence staining and flow cytometry were conducted to examine the status of microglial polarization. In vitro, Transwell co-culture system was taken to investigate the role of miR-195 on neuronal-microglial communication through CX3CL1-CX3CR1 signalling. Quantitative real-time PCR was used to detect the level of miR-195 and inflammatory factors. The protein levels of CX3CL1 and CX3CR1 were evaluated by both western blot and immunofluorescence staining.Results CBH induced by 2VO initiated microglial activation in the rat hippocampus from 1 week to 8 weeks, as evaluated by increased Iba-1 immunofluorescence, that the balance between microglial polarization towards the M1 and M2 phenotypes was shifted towards the M1 phenotype and that the expression of CX3CL1 and CX3CR1 was increased at 8 w following CBH. An in vitro study in a Transwell co-culture system demonstrated that transfection of either primary cultured neonatal rat neurons (NRNs) or microglial BV2 cells with AMO-195 induced M1 polarization of BV2 cells and increased CX3CL1 and CX3CR1 expression and that these effects were reversed by miR-195 mimics. Furthermore, overexpression of miR-195 induced by lenti-pre-miR-195 prevented the changes triggered by knockdown of endogenous miR-195 induced by lentiviral vector-mediated expression of lenti-pre-AMO-195 and 2VO surgery.Conclusions Our findings conclude that downregulation of miR-195 in the hippocampus is involved in CBH-induced microglial polarization towards M1 phenotype by governing communication between neurons and microglia through the regulation of CX3CL1 and CX3CR1 signalling. This indicates that miR-195 may provide a new strategy for clinical prevention and treatment of CBH.

A novel epithelial cell from neonatal rat lung: isolation and differentiated phenotype

1990 ◽  
Vol 259 (6) ◽  
pp. L415-L425 ◽  
Author(s):  
P. E. Roberts ◽  
D. M. Phillips ◽  
J. P. Mather
Keyword(s):  
Epithelial Cell ◽  
Molecular Mechanisms ◽  
Basal Medium ◽  
Fold Increase ◽  
Cell Types ◽  
Cell Number ◽  
Neonatal Rat ◽  
Rat Lung ◽  
Cell Type

A novel epithelial cell from normal neonatal rat lung has been isolated, established, and maintained for multiple passages in the absence of serum, without undergoing crisis or senescence. By careful manipulation of the nutrition/hormonal microenvironment, we have been able to select, from a heterogeneous population, a single epithelial cell type that can maintain highly differentiated features in vitro. This cell type has characteristics of bronchiolar epithelial cells. A clonal line, RL-65, has been selected and observed for greater than 2 yr in continuous culture. It has been characterized by ultrastructural, morphological, and biochemical criteria. The basal medium for this cell line is Ham's F12/Dulbecco's modified Eagle's (DME) medium plus insulin (1 micrograms/ml), human transferrin (10 micrograms/ml), ethanolamine (10(-4) M), phosphoethanolamine (10(-4) M), selenium (2.5 x 10(-8) M), hydrocortisone (2.5 x 10(-7) M), and forskolin (5 microM). The addition of 150 micrograms/ml of bovine pituitary extract to the defined basal medium stimulates a greater than 10-fold increase in cell number and a 50- to 100-fold increase in thymidine incorporation. The addition of retinoic acid results in further enhancement of cell growth and complete inhibition of keratinization. We have demonstrated a strategy that may be applicable to isolating other cell types from the lung and maintaining their differentiated characteristics for long-term culture in vitro. Such a culture system promises to be a useful model in which to study cellular events associated with differentiation and proliferation in the lung and to better understand the molecular mechanisms involved in these events.

scholarly journals Maturation of Embryonic Stem Cells Into Endothelial Cells in an In Vitro Model of Vasculogenesis

Blood ◽  
1999 ◽  
Vol 93 (4) ◽  
pp. 1253-1263 ◽  
Author(s):  
Masanori Hirashima ◽  
Hiroshi Kataoka ◽  
Satomi Nishikawa ◽  
Norihisa Matsuyoshi ◽  
Shin-Ichi Nishikawa
Keyword(s):  
Cell Adhesion ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Culture System ◽  
Molecular Mechanisms ◽  
Es Cells ◽  
Embryonic Stem ◽  
Vascular Endothelial ◽  
Cell Cell

A primitive vascular plexus is formed through coordinated regulation of differentiation, proliferation, migration, and cell-cell adhesion of endothelial cell (EC) progenitors. In this study, a culture system was devised to investigate the behavior of purified EC progenitors in vitro. Because Flk-1+ cells derived from ES cells did not initially express other EC markers, they were sorted and used as EC progenitors. Their in vitro differentiation into ECs, via vascular endothelial-cadherin (VE-cadherin)+ platelet-endothelial cell adhesion molecule-1 (PECAM-1)+ CD34−to VE-cadherin+ PECAM-1+CD34+ stage, occurred without exogenous factors, whereas their proliferation, particularly at low cell density, required OP9 feeder cells. On OP9 feeder layer, EC progenitors gave rise to sheet-like clusters of Flk-1+ cells, with VE-cadherin concentrated at the cell-cell junction. The growth was suppressed by Flt-1-IgG1 chimeric protein and dependent on vascular endothelial growth factor (VEGF) but not placenta growth factor (PIGF). Further addition of VEGF resulted in cell dispersion, indicating the role of VEGF in the migration of ECs as well as their proliferation. Cell-cell adhesion of ECs in this culture system was mediated by VE-cadherin. Thus, the culture system described here is useful in dissecting the cellular events of EC progenitors that occur during vasculogenesis and in investigating the molecular mechanisms underlying these processes.

scholarly journals Notch1 signaling stimulates proliferation of immature cardiomyocytes

2008 ◽  
Vol 183 (1) ◽  
pp. 117-128 ◽  
Author(s):  
Chiara Collesi ◽  
Lorena Zentilin ◽  
Gianfranco Sinagra ◽  
Mauro Giacca
Keyword(s):  
Notch Signaling ◽  
Cardiac Myocytes ◽  
Molecular Mechanisms ◽  
Notch Pathway ◽  
Constitutive Expression ◽  
Neonatal Rat ◽  
Proliferative Potential ◽  
Rat Cardiomyocytes

The identification of the molecular mechanisms controlling cardiomyocyte proliferation during the embryonic, fetal, and early neonatal life appears of paramount interest in regard to exploiting this information to promote cardiac regeneration. Here, we show that the proliferative potential of neonatal rat cardiomyocytes is powerfully stimulated by the sustained activation of the Notch pathway. We found that Notch1 is expressed in proliferating ventricular immature cardiac myocytes (ICMs) both in vitro and in vivo, and that the number of Notch1-positive cells in the heart declines with age. Notch1 expression in ICMs paralleled the expression of its Jagged1 ligand on non-myocyte supporting cells. The inhibition of Notch signaling in ICMs blocked their proliferation and induced apoptosis; in contrast, its activation by Jagged1 or by the constitutive expression of its activated form using an adeno-associated virus markedly stimulated proliferative signaling and promoted ICM expansion. Maintenance or reactivation of Notch signaling in cardiac myocytes might represent an interesting target for innovative regenerative therapy.

scholarly journals AXL kinase-mediated astrocytic phagocytosis modulates outcomes of traumatic brain injury

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Hang Zhou ◽  
Libin Hu ◽  
Jianru Li ◽  
Wu Ruan ◽  
Yang Cao ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Molecular Mechanisms ◽  
Therapeutic Interventions ◽  
Neurological Dysfunction ◽  
Transmission Electron ◽  
Cultured Astrocytes ◽  
Bv2 Cells

Abstract Background Complex changes in the brain microenvironment following traumatic brain injury (TBI) can cause neurological impairments for which there are few efficacious therapeutic interventions. The reactivity of astrocytes is one of the keys to microenvironmental changes, such as neuroinflammation, but its role and the molecular mechanisms that underpin it remain unclear. Methods Male C57BL/6J mice were subjected to the controlled cortical impact (CCI) to develop a TBI model. The specific ligand of AXL receptor tyrosine kinase (AXL), recombinant mouse growth arrest-specific 6 (rmGas6) was intracerebroventricularly administered, and selective AXL antagonist R428 was intraperitoneally applied at 30 min post-modeling separately. Post-TBI assessments included neurobehavioral assessments, transmission electron microscopy, immunohistochemistry, and western blotting. Real-time polymerase chain reaction (RT-PCR), siRNA transfection, and flow cytometry were performed for mechanism assessments in primary cultured astrocytes. Results AXL is upregulated mainly in astrocytes after TBI and promotes astrocytes switching to a phenotype that exhibits the capability of ingesting degenerated neurons or debris. As a result, this astrocytic transformation promotes the limitation of neuroinflammation and recovery of neurological dysfunction. Pharmacological inhibition of AXL in astrocytes significantly decreased astrocytic phagocytosis both in vivo and in primary astrocyte cultures, in contrast to the effect of treatment with the rmGas6. AXL activates the signal transducer and activator of the transcription 1 (STAT1) pathway thereby further upregulating ATP-binding cassette transporter 1 (ABCA1). Moreover, the supernatant from GAS6-depleted BV2 cells induced limited enhancement of astrocytic phagocytosis in vitro. Conclusion Our work establishes the role of AXL in the transformation of astrocytes to a phagocytic phenotype via the AXL/STAT1/ABCA1 pathway which contributes to the separation of healthy brain tissue from injury-induced cell debris, further ameliorating neuroinflammation and neurological impairments after TBI. Collectively, our findings provide a potential therapeutic target for TBI.

scholarly journals Melatonin reduces neuroinflammation and improves axonal hypomyelination by modulating M1/M2 microglia polarization via JAK2-STAT3-telomerase pathway in postnatal rats exposed to lipopolysaccharide

2021 ◽  
Author(s):  
Qiuping Zhou ◽  
Lanfen Lin ◽  
Haiyan Li ◽  
Shuqi Jiang ◽  
Huifang Wang ◽  
...  
Keyword(s):  
Inflammatory Mediators ◽  
Periventricular White Matter ◽  
Microglial Polarization ◽  
Proinflammatory Mediators ◽  
M2 Microglia ◽  
Microglia Polarization ◽  
M1 Phenotype ◽  
Anti Inflammatory ◽  
Postnatal Rats

Abstract Microglia activation and associated inflammation are implicated in the periventricular white matter damage (PWMD) in septic postnatal rats. This study investigated whether melatonin would mitigate inflammation and alleviate the axonal hypomyelination in the corpus callosum in septic postnatal rats. We further explored if this might be through modulating microglial polarization from M1 phenotype to M2 through JAK2/STAT3/telomerase pathway. We reported here that melatonin, indeed, not only can it reduce the neurobehavioral disturbances in LPS injected rats, but it can also dampen microglia mediated inflammation. Thus, in LPS + melatonin group, expression of proinflammatory mediators in M1 phenotype microglia was downregulated. As opposed to this, M2 microglia were increased which was accompanied by upregulated expression of anti-inflammatory mediators along with TERT or MT1. In parallel to this was decreased NG2 expression but increased expression of myelin and neurofilament proteins. That melatonin can improve hypomyelination was confirmed by electron microscopy. In vitro in primary microglia stimulated by LPS, melatonin decreased the expression of proinflammatory mediators significantly; but it increased expression of anti-inflammatory mediators. Additionally, the expression levels of p-JAK2 and p-STAT3 were significantly elevated in microglia after melatonin treatment. Remarkably, the melatonin effects on LPS treated microglia was blocked by melatonin receptor, JAK2, STAT3 and telomerase reverse transcriptase inhibitors, respectively. Taken together, it is concluded that melatonin can attenuate PWMD through shifting M1 microglia towards M2 via MT1/JAK2/STAT3/telomerase pathway. The results suggest a new therapeutic strategy whereby melatonin may be adopted to convert microglial polarization that would ultimately contribute to attenuation of PWMD.

scholarly journals Calgranulin C Has Filariacidal and Filariastatic Activity

1999 ◽  
Vol 67 (12) ◽  
pp. 6631-6636 ◽  
Author(s):  
John D. Gottsch ◽  
Steven W. Eisinger ◽  
Sammy H. Liu ◽  
Alan L. Scott
Keyword(s):  
Culture System ◽  
Molecular Mechanisms ◽  
Inflammatory Responses ◽  
Parasite Burden ◽  
Immunohistochemical Analysis ◽  
Host Responses ◽  
Dose Dependent Fashion ◽  
Antifilarial Activity ◽  
Larval Parasites

ABSTRACT The calgranulins are a family of calcium- and zinc-binding proteins produced by neutrophils, monocytes, and other cells. Calgranulins are released during inflammatory responses and have antimicrobial activity. Recently, one of the calgranulins, human calgranulin C (CaGC), has been implicated as an important component of the host responses that limit the parasite burden during filarial nematode infections. The goal of this work was to test the hypothesis that human CaGC has biologic activity against filarial parasites. Brugia malayi microfilariae and adults were exposed in vitro to 0.75 to 100 nM recombinant human CaGC. Recombinant CaGC affected adult and larval parasites in a dose-dependent fashion. Microfilariae were more sensitive to the action of CaGC than were adult parasites. At high levels, CaGC was both macrofilariacidal and microfilariacidal. At lower levels, the percentage of parasites killed was dependent on the level of CaGC in the culture system. The larvae not killed had limited motility. The filariastatic effect of low-level CaGC was reversed when the CaGC was removed from the culture system. Immunohistochemical analysis demonstrated that human CaGC accumulated in the cells of the hypodermis-lateral chord of adult and larval parasites. The antifilarial activity of CaGC was not due to the sequestration of zinc. Thus, the cellular and molecular mechanisms that result in the production and release of CaGC in humans may play a key role in the regulation of filarial parasite numbers.

scholarly journals MAPK14-TFEB pathways promote microglia activation through inhibiting CMA-mediated NLRP3 degradation in Parkinson's disease

2020 ◽  
Author(s):  
Jialong Chen ◽  
Kanmin Mao ◽  
Honglin Yu ◽  
Yue Wen ◽  
Hua She ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Nlrp3 Inflammasome ◽  
Molecular Mechanisms ◽  
Lewy Bodies ◽  
Microglia Activation ◽  
Substantia Nigra Pars Compacta ◽  
Mice Model ◽  
Bv2 Cells

Abstract Background Parkinson’s disease (PD) is characterized by the degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc), accompanied by chronic neuroinflammation, autophagy dysfunction and SNCA(α-synuclein) accumulation in the form of Lewy bodies. Previous studies show that misfolded SNCA upregulate the inflammatory cascade through NOX activation, which elevated ROS production in microglial cell. However, it’s still not elucidated about the molecular mechanisms between autophagy deficiency and neuroinflammation induced by SNCA accumulation in microglia.Methods We overexpress mice and BV2 cells with SNCAA53T mutant as models of early-onset Parkinson's disease and identified the mechanisms that MAPK14-TFEB pathways promote microglia activation through inhibiting CMA-mediated NLRP3 degradation in Parkinson's disease by a series of methods of molecular biology. The results of pathology and animal behavior showed that the inhibition of MAPK14 and NLRP3 had protective effect on Parkinson's disease model.Results Here, we report that MAPK14 (p38α) activates NLRP3 inflammasome via inhibiting TFEB in BV2 cells. Transcription Factor EB (TFEB) signaling negatively regulates NLRP3 inflammasome through increasing LAMP2A expression, which binds to NLRP3 and promotes its degradation via chaperone-mediated autophagy(CMA). Importantly, both MAPK14 inhibitor SB203580 and NLRP3 inhibitor MCC950 not only prevents neurodegeneration in vitro, but also alleviates movement impairment and SNCA/α-synuclein abnormal accumulation in SNCAA53T-tg mice model of Parkinson’s disease.Conclusion Our research reveals an endogenous regulatory mechanism of NLRP3 turnover and microglia-dopaminergic neuron interaction, which may be a potential therapeutic strategy for Parkinson’s disease.

scholarly journals MiR-124 Promotes Microglial M2 Polarization Through TLR4/MyD88/NF-κB p65/NLRP3 Signaling In Palmitic Acid Treated-BV2 Cells

2021 ◽  
Author(s):  
Caixia Yang ◽  
Guanghong Sui ◽  
Zheng Chen ◽  
Feng Wang
Keyword(s):  
Palmitic Acid ◽  
High Fat Diet ◽  
Signaling Proteins ◽  
High Fat ◽  
Microglial Polarization ◽  
M2 Polarization ◽  
Bv2 Cells ◽  
Vitro Model ◽  
Nlrp3 Expression

Abstract AimNeuroinflammation is an explanation why obesity or high-fat diet induce central nervous system disorders. MiR-124, as a highly expressed microRNA in brain, might alleviate neuroinflammation through regulating microglial M1/M2 polarization, but its mechanism is unclear. The aim of the study was to explore whether miR-124 exerted its effect mentioned above through TLR4/MyD88/NF-κB p65/NLRP3 signaling in palmitic acid treated-microglia.MethodsPrepared BV2 cells were treated with palmitic acid to establish an in vitro model of high-fat diet. MiR-124 mimic and inhibitor were adopted to up-regulate and down-regulate the expression of miR-124. TAK-242 and NLRP3 siRNA were used to down-regulate the expression of TLR4 and NLRP3. Expression of miR-124, signaling proteins (TLR4, MyD88, NF-κB p65), inflammasome markers (NLRP3, IL-1β) and microglial polarization markers (CD206, Arg-1, CD86, iNOS) was measured by qPCR and western blotting. Pyroptosis rate was assessed using flow cytometry.ResultsFirst, palmitic acid up-regulated the TLR4/MyD88/NF-κB p65 signaling, increased the NLRP3 expression, elevated the pyroptosis rate and inhibited the M2 polarization in BV2 cells. Second, miR-124 mimic and inhibitor separately alleviated and aggravated the effect of palmitic acid on microglial polarization and NLRP3 expression. MiR-124 mimic also down-regulated the TLR4/MyD88/NF-κB p65 signaling. Third, TAK-242 did not affect the expression of miR-124, but can simulate the protective effect of miR-124 mimic on microglial polarization and NLRP3 expression. Fourth, NLRP3 siRNA can also promoted M2 polarization in BV2 cells.ConclusionMiR-124 promoted microglial M2 polarization through TLR4/MyD88/NF-κB p65/NLRP3 signaling in palmitic acid treated-BV2 cells

scholarly journals Bioconversion of norethisterone, a progesterone receptor agonist into estrogen receptor agonists in osteoblastic cells

2008 ◽  
Vol 200 (2) ◽  
pp. 199-206 ◽  
Author(s):  
Ana E Lemus ◽  
Juana Enríquez ◽  
Ángeles Hernández ◽  
René Santillán ◽  
Gregorio Pérez-Palacios
Keyword(s):  
Estrogen Receptor ◽  
Progesterone Receptor ◽  
Molecular Mechanisms ◽  
Bone Cells ◽  
Neonatal Rat ◽  
Osteoblastic Cells ◽  
Osteoblastic Cell ◽  
Competition Analysis ◽  
Cell Proliferation And Differentiation

A number of clinical studies have demonstrated that norethisterone (NET), a potent synthetic progestin, restores postmenopausal bone loss, although its mode of action on bone cells is not fully understood, while the effect of naturally occurring progesterone in bone has remained controversial. A recent report claims that the potent effects of NET on osteoblastic cell proliferation and differentiation, mimicking the action of estrogens, are mediated by non-phenolic NET derivatives. To determine whether osteoblasts possess the enzymes required to bioconvert a progesterone receptor (PR) agonist into A-ring reduced metabolites with affinity to bind estrogen receptor (ER), we studied the in vitro metabolism of [3H]-labeled NET in cultured neonatal rat osteoblasts and the interaction of its metabolic conversion products with cytosolic –osteoblast ER, employing a competition analysis. Results indicated that NET was extensively bioconverted (36.4%) to 5α-reduced metabolites, including 5α-dihydro NET, 3α,5α-tetrahydro NET (3α,5α-NET) and 3β,5α-tetrahydro NET (3β,5α-NET), demonstrating the activities of 5α-steroid reductase and two enzymes of the aldo-keto reductases family. Expression of Srd5a1 in neonatal osteoblast was well demonstrated, whereas Srd5a2 expression was not detected. The most striking finding was that 3β,5α-NET and 3α,5α-NET were efficient competitors of [3H]-estradiol for osteoblast ER binding sites, exhibiting affinities similar to that of estradiol. The results support the concept that the interplay of 5α-steroid reductase and aldo-keto reductases in osteoblastic cells, acting as an intracrine modulator system is capable to bioconvert a PR agonist into ER agonists, offering an explanation of the molecular mechanisms NET uses to enhance osteoblastic cell activities.

Abstract 342: Implication Of Mir-98 In The Cardiac Vulnerability Of Pregnancy To Ischemia Reperfusion Injury

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Jingyuan Li ◽  
Zoltan Pierre Arany ◽  
Mansoureh Eghbali
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Late Pregnancy ◽  
Neonatal Rat ◽  
Tunel Staining

We have recently reported that the late-pregnant(LP) rodent is more prone to myocardial ischemia-reperfusion (I/R) injury compared to non-pregnant(NP). However, the underlying molecular mechanisms involved in the higher susceptibility of LP to IR injury are not quite clear. The objective of this study was to investigate the role of miRNA-98(miR-98) in higher cardiac vulnerability to I/R injury in late pregnancy. NP and LP(19 days of pregnancy Sprague-Dawley rats were subjected to 45 min myocardial ischemia followed by 3 hr reperfusion in vivo (I/R group). NP and LP rats which were not subjected to I/R injury served as controls. MicroRNA microarray expression were performed. In vitro, miR-98 was knocked down or overexpressed in neonatal rat ventricular myocytes(NRVMs). Forty eight hour post-transfection, the cells were subjected to 3 hr hypoxia followed by 12 hr reoxygenation. The apoptosis was detected by TUNEL staining, and the western blot was performed to validate the computational predicted targets genes, PGC-1α and STAT3. The miRNA expression profile showed that several miRNAs were differentially expressed in LP sham compared to NP sham, particularly, miR-98 which was significantly upregulated 1.7 fold in LP sham vs NP sham. Interestingly, miR-98 was upregulated even higher (2.3 folds) in LP rats when subjected to ischemia/reperfusion injury compared to NP I/R, suggesting that both ischemia reperfusion and late pregnancy regulate miR-98. Knock down of miRNA-98 in NRVMs significantly reduced apoptosis by ~50%, while over-expression of miR98 resulted in a two fold increase in apoptosis. In-vitro overexpression of miR98-KD in NRVMS resulted in the a significant upregulation of PGC-1α(normalized to scramble control, 1.34±0.04, P<0.05) and STAT3(normalized to scramble control, 1.28±0.05, P<0.05), whereas overexpression of miR-98 resulted in downregulation of both target genes(normalized to scramble control, 0.75±0.02 in PGC-1α; 0.5±0.03 in STAT3, both P<0.05). In conclusion, induction of miR-98 by pregnancy possibly through downregulating PGC-1α and STAT3 may at least in part underlie the greater cardiac vulnerability to I/R injury in late pregnancy.

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