Publications by authors named "Haiying Yan"

13 Publications

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NEDD4L-induced β-catenin ubiquitination suppresses the formation and progression of interstitial pulmonary fibrosis inhibiting the CTHRC1/HIF-1α axis.

Int J Biol Sci 2021 25;17(13):3320-3330. Epub 2021 Jul 25.

Department of Respiratory and Critical Care Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu 611731, P.R. China.

Interstitial pulmonary fibrosis (IPF) is a severe progressive lung disease with limited therapeutic options and poor prognosis. Initially, we found the downregulated level of neural precursor cell expressed developmentally down-regulated 4-like protein (NEDD4L) in IPF-related expression microarray dataset, and this study was thus performed to explore the molecular mechanism of NEDD4L in IPF. The expression of NEDD4L was subsequently validated in lung tissues of IPF patients and mouse models. Then, mouse primary lung fibroblasts (LFs) were collected for functional experiments, with CCK-8, Transwell, and immunofluorescence assays used to examine the viability, migration, and differentiation of LFs. The findings were further assessed using mouse models. The expression of NEDD4L was down-regulated in lung tissues of IPF patients and mouse models. Overexpression of NEDD4L restricted the formation and progression of IPF in mice and attenuated the proliferative, invasive and differentiative abilities of LFs. Further, NEDD4L halted LFs activity by enhancing β-catenin ubiquitination and down-regulating the CTHRC1/HIF-1α axis. Also, experiments then validated that NEDD4L silencing repressed β-catenin ubiquitination and activated the CTHRC1/HIF-1α axis, thereby aggravating IPF in mice. NEDD4L may suppress the formation and progression of IPF through augmenting β-catenin ubiquitination and inhibiting the CTHRC1/HIF-1α axis.
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http://dx.doi.org/10.7150/ijbs.57247DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8416742PMC
July 2021

The antifungal activity of caspofungin in combination with antifungals or non-antifungals against species and in clinical therapy.

Expert Rev Anti Infect Ther 2021 Jun 28:1-18. Epub 2021 Jun 28.

Department of Clinical Pharmacy, Shandong Provincial Qianfoshan Hospital, Shandong University, Shandong Engineering and Technology Research Center for Pediatric Drug Development, Shandong Medicine and Health Key Laboratory of Clinical Pharmacy, Jinan, People's Republic of China.

: species have been regarded as global health threats due to their ability to cause invasive infections. It is challenging to treat bloodstream infections, which are associated with high mortality levels. Monotherapy with antifungals is sometimes not effective against severe infections, and combination therapy is needed in clinical practice.: This review was undertaken based on data from a PubMed search for English language reports published before March 2021 by using the terms 'caspofungin,' ' species,' 'combination therapy,' 'antifungal effect,' and 'novel antifungal agent.': Combination therapy is an empirical strategy for treating refractory infections. Caspofungin has been recommended to treat candidaemia. Caspofungin in combination therapy has some applications, while the efficacy of combination therapy in the treatment of refractory infections needs more study, such as randomized controlled trials. In addition, novel compounds or drugs with potential antifungal activities have been examined, and some of them exhibit synergistic interactions with caspofungin. Thus, the antifungal activity of caspofungin in combination with antifungals or non-antifungals against species and in clinical therapy is summarized.
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http://dx.doi.org/10.1080/14787210.2021.1941868DOI Listing
June 2021

Transcription factor YY1 inhibits the expression of THY1 to promote interstitial pulmonary fibrosis by activating the HSF1/miR-214 axis.

Aging (Albany NY) 2020 05 12;12(9):8339-8351. Epub 2020 May 12.

Department of Laboratory Medicine, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu 611731, P.R. China.

Interstitial pulmonary fibrosis (IPF) is a progressive disease of diverse etiology manifesting with proliferation of lung fibroblasts and accumulation of extracellular matrix deposition in pulmonary interstitium. Recent studies show aberrant expression of mRNAs and microRNAs (miRNAs) in human embryonic pulmonary fibroblasts (HEPFs). In this study, we investigated effects of the YY1/HSF1/miR-214/THY1 axis on the functions of HEPFs and IPF. Loss- and gain-of-function tests were conducted to identify roles of YY1, HSF1, miR-214, and THY1 in IPF. As determined by RT-qPCR or western blot assay, silencing YY1 down-regulated HSF1 expression and attenuated the expression of pro-proliferative and fibrosis markers in HEPFs. Meanwhile, viability of HEPFs was impeded by YY1 knockdown. The binding relationship between miR-214 and THY1 was verified using dual-luciferase reporter assay. In HEPFs, down-regulation of HSF1 reduced miR-214 expression to repress proliferation and fibrogenic transformation of HEPFs, while inhibition of miR-214 expression could restrain the fibrogenic transformation property of HEPFs by up-regulating THY1. Subsequently, IPF model in mice was induced by bleomycin treatment. These animal experiments validated the protective effects of YY1 knockdown against IPF-induced lung pathological manifestations, which could be reversed by THY1 knockdown. Our study demonstrates the important involvement of YY1/HSF1/miR-214/THY1 axis in the development of IPF.
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http://dx.doi.org/10.18632/aging.103142DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7244040PMC
May 2020

Corrigendum to "Antifungal activity of ribavirin used alone or in combination with fluconazole against Candida albicans is me diated by reduced virulence" [International Journal of Antimicrobial Agents (2020) 105804].

Int J Antimicrob Agents 2020 03 8;55(3):105917. Epub 2020 Feb 8.

Department of Pharmacy, Shandong Provincial Qianfoshan Hospital, the First Hospital Affiliated with Shandong First Medical University, Jinan, Shandong Province, China. Electronic address:

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http://dx.doi.org/10.1016/j.ijantimicag.2020.105917DOI Listing
March 2020

Proton pump inhibitors act synergistically with fluconazole against resistant Candida albicans.

Sci Rep 2020 01 16;10(1):498. Epub 2020 Jan 16.

Department of Pharmacy, Shandong Provincial Qianfoshan Hospital, the First Hospital Affiliated with Shandong First Medical University, Ji'nan, 250014, Shandong Province, P.R. China.

The incidence of resistant Candida isolates, especially Candida albicans, has increased continuously. To overcome the resistance, research on antifungal agent sensitizers has attracted considerable attention. Omeprazole and lansoprazole were found to inhibit the growth of sensitive C. albicans and hyphae formation in a high dose, respectively. This study aimed to determine the interactions of common clinically proton pump inhibitors (PPIs) and fluconazole both in vitro and in vivo and to further explore the possible mechanisms. In vitro, the tested PPIs all acted synergistically with fluconazole against both resistant C. albicans planktonic cells and biofilms preformed for ≤12 h with the minimum inhibitory concentration of fluconazole decreased from >512 μg/mL to 1-4 μg/mL. In vivo, PPIs plus fluconazole prolonged the survival rate of infected Galleria mellonella larvae by two-fold compared with that for the fluconazole monotherapy group and significantly reduced the tissue damage of infected larvae. Mechanism studies showed that PPIs significantly suppressed efflux pump activity, which is the common resistance mechanism of C. albicans, and significantly inhibited the virulence factors: phospholipase activity and morphology switching. These findings will provide new insights into antifungal agent discovery and potential approaches for the treatment of candidiasis caused by resistant C. albicans.
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http://dx.doi.org/10.1038/s41598-019-57174-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6965112PMC
January 2020

The Role of MicroRNAs in the Pathogenesis of Diabetic Nephropathy.

Int J Endocrinol 2019 1;2019:8719060. Epub 2019 Dec 1.

Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu 610075, Sichuan, China.

Diabetic nephropathy (DN) is one of the most common microvascular complications in diabetic patients; it is also an important cause of renal dysfunction, renal fibrosis, and end-stage renal disease. Unfortunately, the pathogenesis of DN is complex and has not yet been fully elucidated; hence, the pathogenesis of DN to determine effective treatments of crucial importance is deeply explored. Early DN research focuses on hemodynamic changes and metabolic disorders, and recent studies have shown the regulatory role of microRNAs (miRNAs) in genes, which may be a new diagnostic marker and therapeutic target for diabetic nephropathy. In this review, we summarize the recent advances in the clinical value and molecular mechanisms of miRNAs in DN, providing new ideas for the diagnosis and treatment of DN.
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http://dx.doi.org/10.1155/2019/8719060DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6914872PMC
December 2019

Antifungal activity of ribavirin used alone or in combination with fluconazole against Candida albicans is mediated by reduced virulence.

Int J Antimicrob Agents 2020 Jan 9;55(1):105804. Epub 2019 Oct 9.

Department of Pharmacy, Shandong Provincial Qianfoshan Hospital, the First Hospital Affiliated with Shandong First Medical University, Jinan, Shandong Province, China. Electronic address:

The incidence of fungal infections has increased continuously in recent years, and drug resistance, especially resistance to fluconazole (FLC), has emerged. To overcome this challenge, research on the antifungal activities of non-antifungal agents has gained more attention. In this study, we determined the anti-Candida activity of ribavirin (RBV), an antiviral drug commonly used in the clinic, and found that RBV displayed potent antifungal activity when used alone or in combination with FLC in vitro and in vivo. In vitro, the MIC values of RBV were 2-4 µg/mL for FLC-susceptible Candida albicans and 8 µg/mL for FLC-resistant C. albicans. When RBV at a dose of 1 µg/mL was combined with FLC, significant synergistic effects were exhibited against FLC-resistant C. albicans, and the MICs of FLC decreased from >512 µg/mL to 0.25-1 µg/mL. Synergism was also exhibited against C. albicans biofilms. In vivo, RBV plus FLC significantly improved the survival of infected Galleria mellonella larvae compared with the FLC-treated group over a 4-day period and attenuated the damage of FLC-resistant C. albicans to G. mellonella larvae tissue. Furthermore, mechanistic studies indicated that the antifungal effects of RBV used alone or in combination with FLC might be associated with inhibition of biofilm formation, reduced extracellular phospholipase activity and inhibition of hyphal growth, but is not related to promotion of FLC uptake and inhibition of FLC efflux. These results provide a promising direction for overcoming drug resistance and for expanding the clinical application of existing drugs.
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http://dx.doi.org/10.1016/j.ijantimicag.2019.09.008DOI Listing
January 2020

Anti- activity of existing antibiotics and their derivatives when used alone or in combination with antifungals.

Future Microbiol 2019 Aug 9. Epub 2019 Aug 9.

Department of Pharmacy, Shandong Provincial Qianfoshan Hospital, the First Hospital Affiliated with Shandong First Medical University, Jinan 250014, People's Republic of China.

Fungal infections are a growing challenge in immunocompromised patients, especially candidiasis. The prolonged use of traditional antifungals to treat infection has caused the emergence of drug resistance, especially fluconazole. Therefore, new therapeutic strategies for infection are warranted. Recently, attention has been paid to the anti- activity of antibiotics and their derivatives. Studies revealed that a series of antibiotics/derivatives displayed potential anti- activity and some of them could significantly increase the susceptibility of antifungals. Interestingly, the derivatives of aminoglycosides were even more active than fluconazole/itraconazole/posaconazole. This article reviews the anti- activities and mechanisms of antibiotics/derivatives used alone or in combination with antifungals. This review will helpfully provide novel insights for overcoming resistance and discovering new antifungals.
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http://dx.doi.org/10.2217/fmb-2019-0076DOI Listing
August 2019

Next-generation sequencing improves molecular epidemiological characterization of thalassemia in Chenzhou Region, P.R. China.

J Clin Lab Anal 2019 May 27;33(4):e22845. Epub 2019 Feb 27.

Center of Prenatal Diagnosis, Chenzhou No. 1 People's Hospital, Chenzhou, China.

Objectives: Thalassemia is a highly prevalent monogenic inherited disease in southern China. It is important to collect epidemiological data comprehensively for proper prevention and treatment.

Methods: In this study, blood samples collected from 15 807 residents of Chenzhou were primarily screened by hematological tests. A total of 3973 samples of suspected thalassemia carriers were further characterized by combined next-generation sequencing (NGS) and Gap-PCR.

Results: In total, 1704 subjects were diagnosed as thalassemia carriers with a total prevalence rate of 10.78%, including 943 α-thalassemia carriers, 708 β-thalassemia carriers, and 53 composite α and β-thalassemia carriers. The prevalence rates of α-thalassemia, β-thalassemia, and composite α and β-thalassemia were 5.97%, 4.48%, and 0.34%, respectively. Meanwhile, we characterized 19 α-thalassemia variations and 21 β-thalassemia variations in thalassemia carriers. Approximately 2.88% of thalassemia carriers would be missed by traditional genetic analysis. In addition, four novel thalassemia mutations and one novel abnormal hemoglobin mutation were identified.

Conclusions: Our data suggest a high prevalence of thalassemia and a diverse spectrum of thalassemia-associated variations in Chenzhou. Also, combined NGS and Gap-PCR is an effective thalassemia screening method. Our findings might be helpful for prevention and treatment of thalassemia in this region.
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http://dx.doi.org/10.1002/jcla.22845DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6528559PMC
May 2019

Association of high normal HbA1c and TSH levels with the risk of CHD: a 10-year cohort study and SVM analysis.

Sci Rep 2017 03 27;7:45406. Epub 2017 Mar 27.

Department of Health Administration, Affiliated Central Hospital of Xinxiang Medical University, Xinxiang Central Hospital, Xinxiang, Henan, China.

This study aimed to determine the association between the clinical reference range of serum glycated hemoglobin A1c (HbA1c) and thyrotropin (TSH) and the risk of coronary heart disease (CHD) in non-diabetic and euthyroid patients. We examined baseline HbA1c and TSH in 538 healthy participants, and then analyzed the associations and potential value of these indicators for predicting CHD using Cox proportional hazard and support vector machine analyses. During the median follow-up of 120 months, 39 participants later developed CHD. The baseline HbA1c and TSH within the reference range were positively associated with CHD risk. No correlation and interaction were found between the baseline HbA1c and TSH for the development of CHD. Disease event-free survival varied among participants with different baseline HbA1c quintiles, whereas disease event-free survival was similar for different TSH tertiles. The combination of these baselines showed sensitivity of 87.2%, specificity of 92.7%, and accuracy of 92.3% for identifying the participants who will later develop CHD. Relatively high but clinically normal HbA1c and TSH levels may increase the risk of CHD. Therefore, the combination of these indicators can serve as a biomarker for identifying healthy individuals from those who would later develop CHD.
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http://dx.doi.org/10.1038/srep45406DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5366946PMC
March 2017

Clinical and genomic evaluation of a Chinese patient with a novel deletion associated with Phelan-McDermid syndrome.

Oncotarget 2016 Dec;7(49):80327-80335

BGI-Shenzhen, Shenzhen, China.

Phelan-McDermid syndrome is a neurodevelopmental disorder caused by the terminal deletion of chromosome 22 (22q13) followed by the loss of function of the SHANK3 gene. Various terminal deletions of chromosome 22q13 are associated with Phelan-McDermid with a spectrum of phenotypic severity. Here, we have done a clinical molecular study of a Chinese proband with Phelan-McDermid syndrome. Both the proband and her younger brother are associated with this syndrome while their parents are phenotypically normal. We used a karyotype in order to detect the genotype of the proband and her younger brother. We have also used whole genome low-coverage paired-end next generation sequencing to determine whether the parent is the carrier of translocation with terminal 22q13 deletions. We found that both proband and her younger brother are comprises of a novel deletion of 22q13.31q13.33, harboring genes were associated with several clinical phenotype such as severity of speech delay, neonatal hypotonia, delayed in age of walking, male genital anomalies, dysplastic toenails, large and fleshy hands, macrocephaly, short stature, facial asymmetry, and atypical reflexes. Probands and her younger brother inherited this translocation from their mother whereas their father is genotypically normal. In conclusion, our present study expands the deletion spectrum and report a novel deletion associated with Phelan-McDermid syndrome.
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http://dx.doi.org/10.18632/oncotarget.12552DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5348323PMC
December 2016

miR-122 inhibits metastasis and epithelial-mesenchymal transition of non-small-cell lung cancer cells.

Onco Targets Ther 2015 29;8:3175-84. Epub 2015 Oct 29.

Department of Pulmonary Neoplasm Internal Medicine, Affiliated Hospital of Academy of the Military Medical Sciences, Beijing, People's Republic of China.

miR-122 may function as a novel tumor suppressor. Expression of miR-122 could suppress the proliferation of multi-kinds of human cancer cell lines. In this work, expression of miR-122 via adenoviral vector in non-small-cell lung cancer (NSCLC) cells reduces the number of invasion and migration cells. miR-122 attenuates the epithelial-mesenchymal transition process, which mediates cancer cells metastasis in NSCLC cells A549 and H460. The mechanisms data reveals that miR-122 would disrupt the epithelial-mesenchymal transition process by downregulating PI3K/AKT activation via reducing endogenous expression of insulin-like growth factor 1 receptor. These data highlight the detailed roles and potential application of miR-122 in NSCLC cells.
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http://dx.doi.org/10.2147/OTT.S91696DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4631421PMC
November 2015

Over-expressed RPL34 promotes malignant proliferation of non-small cell lung cancer cells.

Gene 2016 Jan 23;576(1 Pt 3):421-8. Epub 2015 Oct 23.

Department of Pulmonary Oncology, Affiliated Hospital, Academy of Military Medical Science, No. 8 East Avenue, Fengtai District, Beijing 100071, China. Electronic address:

Ribosomal protein L34 (RPL34) was reported to be involved in the regulation of cell proliferation of prokaryotes, plant and animal cells. In the present study, we analyze the expression and function of RPL34 in NSCLC. Immunohistochemical analysis, qPCR and Western blot were used to detect the expression of RPL34 in NSCLC tissues and cells lines. Flow cytometry was used to detect cell activity of NSCLC cell line H1299 under lentivirus-mediated RNAi on RPL34. Cell proliferation and colony formation assays were used to analyze the role of RPL34 in NSCLC cell proliferation. We found that expression of ribosomal protein RPL34 was significantly up-regulated in NSCLC tissues compared to adjacent normal tissues. Lentivirus-mediated shRNA knockdown of RPL34 in NSCLC cell line H1299 resulted in a strong decrease of proliferation, and a moderate but significant increase of apoptosis and S-phase arrest. These data indicate that over-expressed RPL34 may promote malignant proliferation of NSCLC cells, thus playing an important role in development and progress of NSCLC.
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http://dx.doi.org/10.1016/j.gene.2015.10.053DOI Listing
January 2016
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