Publications by authors named "Guomin Hu"

6 Publications

  • Page 1 of 1

The Prevalence of Thrice, Twice, and Once Human Papillomavirus DNA Positivity in Older Chinese Women.

Front Med (Lausanne) 2020 2;7:391. Epub 2020 Sep 2.

Minhang District Maternal and Child Health Hospital, Shanghai, China.

Human papillomavirus (HPV) DNA detection in cervical samples is widely used to identify HPV infection; however, there is little detailed evaluation of the characteristics of HPV prevalence by repeated DNA detection in community populations. Beginning in 2014, a Papanicolaou (Pap) smear and HPV cotesting program was implemented among older women living in the Minhang district of Shanghai. This report uses information from 225,000 participants, who provided person-time data. Of these, 632 subjects had 3 repeated visits and at least one HPV DNA-positive result in the last 5 years. All 16 genotypes of HPV displayed thrice, twice, and once positivity results in 3 repeated tests and differed by proportions among and within genotypes. HPV52 and 58 are the two most dominant genotypes in total and in thrice positive person-time. The thrice positive person-time exceeded 50% in each of HPV58-, 35-, 52-, 56-, 18-, 68-, 31-, and 16-infected women. The single positive person-time ratio ranged from 7.9% (HPV35) to 38.9% (HPV11). Age differed among and within genotypes in thrice, twice, and once positive women. The average age of HPV-free controls was 59.0 ± 7.2 yo, which is close to the median of average ages for thrice and twice positive women and is older than most average ages for once positive women. The percentages of negative results for intraepithelial lesion or malignancy (NILM) for thrice HPV52-, 58-, 16-, 56-, and 59-positive women were significantly lower than the percentage of NILM for HPV-free women. Thrice and/or twice HPV DNA positivity are common in HPV-infected women and tend to occur in older women.
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http://dx.doi.org/10.3389/fmed.2020.00391DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7492668PMC
September 2020

Pathological matrix stiffness promotes cardiac fibroblast differentiation through the POU2F1 signaling pathway.

Sci China Life Sci 2021 Feb 29;64(2):242-254. Epub 2020 Jun 29.

Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital; NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education; Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing, 100191, China.

Cardiac fibroblast (CF) differentiation into myofibroblasts is a crucial cause of cardiac fibrosis, which increases in the extracellular matrix (ECM) stiffness. The increased stiffness further promotes CF differentiation and fibrosis. However, the molecular mechanism is still unclear. We used bioinformatics analysis to find new candidates that regulate the genes involved in stiffness-induced CF differentiation, and found that there were binding sites for the POU-domain transcription factor, POU2F1 (also known as Oct-1), in the promoters of 50 differentially expressed genes (DEGs) in CFs on the stiffer substrate. Immunofluorescent staining and Western blotting revealed that pathological stiffness upregulated POU2F1 expression and increased CF differentiation on polyacrylamide hydrogel substrates and in mouse myocardial infarction tissue. A chromatin immunoprecipitation assay showed that POU2F1 bound to the promoters of fibrosis repressors IL1R2, CD69, and TGIF2. The expression of these fibrosis repressors was inhibited on pathological substrate stiffness. Knockdown of POU2F1 upregulated these repressors and attenuated CF differentiation on pathological substrate stiffness (35 kPa). Whereas, overexpression of POU2F1 downregulated these repressors and enhanced CF differentiation. In conclusion, pathological stiffness upregulates the transcription factor POU2F1 to promote CF differentiation by inhibiting fibrosis repressors. Our work elucidated the crosstalk between CF differentiation and the ECM and provided a potential target for cardiac fibrosis treatment.
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http://dx.doi.org/10.1007/s11427-019-1747-yDOI Listing
February 2021

Paired box 6 inhibits cardiac fibroblast differentiation.

Biochem Biophys Res Commun 2020 07 3;528(3):561-566. Epub 2020 Jun 3.

Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing, 100191, China. Electronic address:

Cardiac fibroblast (CF) differentiation plays a crucial role in cardiac fibrosis, which is a specific manifestation distinguishing pathological cardiac hypertrophy from physiological hypertrophy. The DNA-binding activity of paired box 6 (Pax6) has been shown to be oppositely regulated in physiological and pathological hypertrophy; however, it remains unclear whether Pax6 is involved in CF differentiation during cardiac fibrosis. We found that Pax6 is expressed in the heart of and CFs isolated from adult mice. Moreover, angiotensin II (Ang II) induced the downregulation of Pax6 mRNA and protein expression in fibrotic heart tissue and cardiac myofibroblasts. Pax6 knockdown in CFs promoted the expression of the myofibroblast marker α-smooth muscle actin (α-SMA) and the synthesis of the extracellular matrix (ECM) proteins collagen I and fibronectin. Furthermore, we validated the ability of Pax6 to bind to the promoter regions of Cxcl10 and Il1r2 and the intronic region of Tgfb1. Pax6 knockdown in CFs decreased CXC chemokine 10 (CXCL10) and interleukin-1 receptor 2 (IL-1R2) expression and increased transforming growth factor β1 (TGFβ1) expression, mimicking the effects of Ang II. In conclusion, Pax6 exerts an inhibitory effect on CF differentiation and ECM synthesis by transcriptionally activating the expression of the anti-fibrotic factors CXCL10 and IL-1R2 and repressing the expression of the pro-fibrotic factor TGFβ1. Therefore, maintaining Pax6 expression in CFs is essential for preventing CF differentiation, and provides a new therapeutic target for cardiac fibrosis.
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http://dx.doi.org/10.1016/j.bbrc.2020.05.146DOI Listing
July 2020

Naringenin attenuates non-alcoholic fatty liver disease by down-regulating the NLRP3/NF-κB pathway in mice.

Br J Pharmacol 2020 04 30;177(8):1806-1821. Epub 2020 Jan 30.

Peking University Institute of Cardiovascular Sciences, Peking University Health Science Center, Beijing, China.

Background And Purpose: Naringenin, a flavonoid compound with strong anti-inflammatory activity, attenuated non-alcoholic fatty liver disease (NAFLD) induced by a methionine-choline deficient (MCD) diet in mice. However, the mechanisms underlying this suppression of inflammation and NAFLD remain unknown.

Experimental Approach: WT and NLRP3 mice were fed with MCD diet for 7 days to induce NAFLD and were given naringenin by gavage at the same time. in vitro experiments used HepG2 cells, primary hepatocytes, and Kupffer cells (KCs) stimulated by LPS or LPS plus oleic acid (OA).

Key Results: Treating WT mice with naringenin (100 mg·kg ·day ) attenuated hepatic lipid accumulation and inflammation in the livers of mice given the MCD diet. NLRP3 mice showed less hepatic lipid accumulation than WT mice, but naringenin did not ameliorate hepatic lipid accumulation further in NLRP3 mice. Treating the HepG2 cells with naringenin or NLRP3 inhibitor MCC950 reduced lipid accumulation. Naringenin inhibited activation of the NLRP3/NF-κB pathway stimulated by OA together with LPS. In KCs isolated from WT mice, naringenin inhibited NLRP3 expression. Naringenin also inhibited lipid deposition, NLRP3 and IL-1β expression in WT hepatocytes but was not effective in NLRP3 hepatocytes. After re-expressing NLRP3 in NLRP3 hepatocytes by adenovirus, the anti-lipid deposition effect of naringenin was restored.

Conclusion And Implications: Naringenin prevented NAFLD via down-regulating the NLRP3/NF-κB signalling pathway both in KCs and in hepatocytes, thus attenuating inflammation in the mice livers.
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http://dx.doi.org/10.1111/bph.14938DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7070172PMC
April 2020

β-adrenergic receptor activation induces TGFβ1 expression in cardiomyocytes via the PKG/JNK/c-Jun pathway.

Biochem Biophys Res Commun 2018 09 6;503(1):146-151. Epub 2018 Jun 6.

The 3rd Department of Cardiology, The First Affiliated Hospital of the Medical College, Shihezi University, Shihezi City, Xinjiang, 832008, China. Electronic address:

In heart failure, the expression of cardiac β-adrenergic receptors (β-ARs) increases. However, the precise role of β-AR signaling within cardiomyocytes remains unclear. Transforming growth factor β1 (TGFβ1) is a crucial cytokine mediating the cardiac remodeling that plays a causal role in the progression of heart failure. Here, we set out to determine the effect of β-AR activation on TGFβ1 expression in rat cardiomyocytes and examine the underlying mechanism. The selective β-AR agonist BRL37344 induced an increase in TGFβ1 expression and the phosphorylation of c-Jun N-terminal kinase (JNK) and c-Jun in β-AR-overexpressing cardiomyocytes. Those effects of BRL37344 were suppressed by a β-AR antagonist. Moreover, the inhibition of JNK and c-Jun activity by a JNK inhibitor and c-Jun siRNA blocked the increase in TGFβ1 expression upon β-AR activation. A protein kinase G (PKG) inhibitor also attenuated β-AR-agonist-induced TGFβ1 expression and the phosphorylation of JNK and c-Jun. In conclusion, the β-AR activation in cardiomyocytes increases the expression of TGFβ1 via the PKG/JNK/c-Jun pathway. These results help us further understand the role of β-AR signaling in heart failure.
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http://dx.doi.org/10.1016/j.bbrc.2018.05.200DOI Listing
September 2018

Nucleated Red Blood Cell Count in Maternal Peripheral Blood and Hypertensive Disorders in Pregnant Women.

Am J Med Sci 2016 Feb;351(2):140-6

The Department of Obstetrics and Gynecology, First Affiliated Hospital, Second Military Medical University, Shanghai, China (RG, LL).

Objective: We investigated the correlations of nucleated red blood cell (NRBC) counts with hypertensive disorders in pregnancy (HDP) and fetal umbilical blood flow velocity.

Materials And Methods: We recruited 282 patients with HDP as experimental group including 107 with mild pre-eclampsia (A1 group), 100 with severe pre-eclampsia (A2 group) and 75 with eclampsia (A3 group), and 215 normal pregnant women as control group. Maternal peripheral venous blood was collected and isolated cells were stained with Wright-Giemsa. We estimated NRBC counts according to laboratory routine and Doppler ultrasound examinations were employed to measure the systolic/diastolic (S/D) ratios of fetal ductus venosus, umbilical artery and middle cerebral artery.

Results: The NRBC counts in A1, A2 and A3 groups were higher than control group (all P < 0.01). The S/D ratios in control, A1, A2 and A3 groups increased orderly (P < 0.05). Receiver operating characteristic curve analysis demonstrated that the sensitivity and specificity of NRBC count and S/D ratios in diagnosing HDP were 96.50% and 96.28%; 93.60% and 98.14%; 94.30% and 94.88% 99.30% and 100%, respectively. Pearson and Spearman correlation analysis revealed that the NRBC and S/D ratios were correlated with gestational age at birth, amniotic fluid volume, premature birth, mechanical ventilation, neonatal intensive care unit admission, neonatal asphyxia, birth weight, fetal distress, APGAR score, pH value, arterial oxygenation tension, bicarbonate and base excess (all P < 0.05). The NRBC count was positively associated with the S/D ratios (all P < 0.05).

Conclusions: Our results provide evidence that NRBC count in patients with HDP increased significantly, showing positive correlations with umbilical S/D ratios.
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http://dx.doi.org/10.1016/j.amjms.2015.11.008DOI Listing
February 2016
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