Wenqiang Wei

Chinese Academy of Medical Sciences & Peking Union Medical College

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You‐Lin Qiao

Chinese Academy of Medical Sciences & Peking Union Medical College

Shaoping Ji

Henan University

Hongju Wang

First Affiliated Hospital of Bengbu Medical College

Christian C. Abnet

National Cancer Institute

Sanford M. Dawsey

National Cancer Institute

Fusheng Si

Saint Louis University

Ru Chen

Wenzhou Medical University

Mark J. Roth

Center for Cancer Research

Na Fang

Henan University

Philip R. Taylor

National Cancer Institute

Cooperative Institutions

Chinese Academy of Medical Sciences & Peking Union Medical College

Henan University

National Cancer Institute

Peking Union Medical College Hospital

Chinese Academy of Sciences

Sichuan University

Peking University

National Institutes of Health

Capital Medical University

Sun Yat-sen University

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Cellular senescence: Molecular mechanisms and pathogenicity

Journal of Cellular Physiology (2018)

Wenqiang Wei Shaoping Ji

Cellular senescence is the arrest of normal cell division. Oncogenic genes and oxidative stress, which cause genomic DNA damage and generation of reactive oxygen species, lead to cellular senescence. The senescence-associated secretory phenotype is a distinct feature of senescence. Senescence is normally involved in the embryonic development. Senescent cells can communicate with immune cells to invoke an immune response. Senescence emerges during the aging process in several tissues and organs. In fact, increasing evidence shows that cellular senescence is implicated in aging-related diseases, such as nonalcoholic fatty liver disease, obesity and diabetes, pulmonary hypertension, and tumorigenesis. Cellular senescence can also be induced by microbial infection. During cellular senescence, several signaling pathways, including those of p53, nuclear factor-κB (NF-κB), mammalian target of rapamycin, and transforming growth factor-beta, play important roles. Accumulation of senescent cells can trigger chronic inflammation, which may contribute to the pathological changes in the elderly. Given the variety of deleterious effects caused by cellular senescence in humans, strategies have been proposed to control senescence. In this review, we will focus on recent studies to provide a brief introduction to cellular senescence, including associated signaling pathways and pathology.

Senescence

Cellular senescence

10.1002/jcp.26956

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Citations (172)

COVID-19 and Kidney Injury: Could Renin-Angiotensin Components Crosstalk with Immune Responses?

Bernard Nsengimana Yu Jin Yuting Jia Wenqiang Wei Shaoping Ji

Coronavirus disease 2019 (COVID-19) is a global pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). To contain the virus, numerous preventive measures have been taken including isolation of patients, careful infection control, social distancing, and taking vaccine. So far, new confirmed and death cases are still increasing. SARS-CoV-2 invades cells by using the angiotensin converting enzyme 2 (ACE2). ACE2 is an essential enzyme of the renin-angiotensin system (RAS) which converts angiotensin II (Ang II) to angiotensin (1-7). ACE2 is expressed in different organs, including lung, heart, and kidney. A high number of COVID-19 patients developed kidney injury has been reported. Renal impairment and acute injury are associated with mortality of COVID-19, which is 14-16 times higher than other general patients. Acute Kidney Injury has been occured in 2.9 up to 43% of intensive care unit patients. The increasing evidence show that the components of RAS can activate the complement cascade, and cytokines production. Kidney injury caused by SARS-CoV-2 is related mainly to systemic and local inflammation. Moreover, the uncontrolled immune responses mediated by SARS-CoV-2 including hypercytokinaemia, secondary hemophagocytic lymphohistiocytosis, antibody dependent enhancement, complement system, and phagocytic cells activation can contribute in the virus pathogenesis leading to associated renal dysfunction. However, the role and crosstalk between of RAS components and immune response in mediating kidney injury remain undefined. In this review, we focus on the recent studies to provide the pathogenesis of SARS-CoV-2 interacting with RAS and immune responses to mediate kidney injury.

Pathogenesis

10.20944/preprints202107.0642.v1

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Citations (1)

Autographa californica multiple nucleopolyhedrovirus orf114 is not essential for virus replication in vitro, but its knockout reduces per os infectivity in vivo

Virus Genes (2012)

Wenqiang Wei Yin Zhou Chengfeng Lei Xiulian Sun

Autographa californica

Infectivity

Sf9

Polyhedrin

Baculoviridae

10.1007/s11262-012-0777-y

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Citations (12)

No role for human papillomavirus in esophageal squamous cell carcinoma in China

International Journal of Cancer (2009)

Jill Koshiol Wenqiang Wei Aimée R. Kreimer Wen Chen Patti E. Gravitt

Abstract Certain regions of China have high rates of esophageal squamous cell carcinoma (ESCC). Previous studies of human papillomavirus (HPV), a proposed causal factor, have produced highly variable results. We attempted to evaluate HPV and ESCC more definitively using extreme care to prevent DNA contamination. We collected tissue and serum in China from 272 histopathologically‐confirmed ESCC cases with rigorous attention to good molecular biology technique. We tested for HPV DNA in fresh‐frozen tumor tissue using PCR with PGMY L1 consensus primers and HPV16 and 18 type‐specific E6 and E7 primers, and in formalin‐fixed paraffin‐embedded tumor tissue using SPF 10 L1 primers. In HPV‐positive cases, we evaluated p16 INK4a overexpression and HPV E6/E7 seropositivity as evidence of carcinogenic HPV activity. β‐globin, and thus DNA, was adequate in 98.2% of the frozen tumor tissues (267/272). Of these, 99.6% (95% confidence interval (CI) = 97.9–100.0%) were negative for HPV DNA by PGMY, and 100% (95% CI = 98.6–100%) were negative by HPV16/18 E6/E7 PCR. In the corresponding formalin‐fixed paraffin‐embedded tumor specimens, 99.3% (95% CI = 97.3–99.9%) were HPV negative by SPF 10 . By PGMY, 1 case tested weakly positive for HPV89, a noncancer causing HPV type. By SPF 10 , 2 cases tested weakly positive: 1 for HPV16 and 1 for HPV31. No HPV DNA‐positive case had evidence of HPV oncogene activity as measured by p16 INK4a overexpression or E6/E7 seropositivity. This study provides the most definitive evidence to date that HPV is not involved in ESCC carcinogenesis in China. HPV DNA contamination cannot be ruled out as an explanation for high HPV prevalence in ESCC tissue studies with less stringent tissue procurement and processing protocols.

10.1002/ijc.25023

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Citations (80)

[A prospective study on the relationship between nutrition intervention and incidence of malignant tumors in Lin County, China].

PubMed (2007)

Xiu‐Di Sun Jin‐Hu Fan Wen Chen Wenqiang Wei You‐Lin Qiao

To analyze the tendency in the incidence of malignant tumors in nutrition-intervened population of Lin County.Subjects who had been enrolled in the General Population Trial, Lin County Nutrition Intervention Trial were followed up and the data of malignant tumors were collected with collaboration of National Cancer Institute/National Institute of Health. Incidences of malignant tumors during and after nutrition intervention were calculated and compared.Esophageal cancer, cardiac cancer, and stomach cancer were constantly the three leading cancers, accounting for 84.06% and 83.74% of the malignant tumors in men and women, respectively. The incidences of lung cancer and liver cancer in men showed increasing tendencies, while similar tendencies were found in those of stomach cancer, colorectal cancer, and liver cancer in women. With the prolonging of the follow-up, the incidences of upper digestive tract cancers declined (except stomach cancer in women).The upper digestive tract cancers remain the leading malignant tumors, although their incidences may decline with longer-term follow-up. Prevention and control of tumors in Lin County should still be focused on the esophageal cancer, cardiac cancer, and stomach cancer, as well as lung cancer and liver cancer.

Liver Cancer

Stomach cancer

Gastrointestinal cancer

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Silencing EPB41 Gene Expression Leads to Cell Cycle Arrest, Migration Inhibition, and Upregulation of Cell Surface Antigen in DC2.4 Cells

Medical Science Monitor (2020)

Qing Zhao Yongqiang Li Yanhong Li Xin‐Ying Ji Huimin Li

BACKGROUND:Protein 4.1R (EPB41) is the main cytoskeleton component of the erythrocyte membrane and may be involved in cell migration and adhesion. Previous research discovered overexpression of 4.1R in the thymus of patients with myasthenia gravis (MG). The protein 4.1R on dendritic cells may play a pivotal role in MG pathogenesis.This research investigated the effects of small interfering RNA 4.1R-siRNA on cell migration, cell cycle, and surface antigen expression of DC2.4 mouse dendritic cells, thus providing a new direction for the study of MG pathogenesis. MATERIAL AND METHODS:Three 4.1R-specific siRNAs were designed, and the expression of 4.1R was detected by real-time PCR at the mRNA level and Western blot analysis at the protein level to select out the most efficient siRNAs. Changes in cell morphology were observed and cell migration ability was analyzed by Transwell assay. Cell cycle and surface antigen were both analyzed by flow cytometry. RESULTS:The cell bodies of DC2.4 diminished, the synapses were increased, and protuberance became more obvious after being transfected with 4.1R-siRNA. After knockdown of 4.1R, cell migration ability decreased and the proportion of cells in S phase significantly increased (both P<0.05). The expression levels of MHCII, CD80, and CD86 were all increased in DC2.4 cells (all <0.05). CONCLUSIONS:Silencing the expression of 4.1R in dendritic cells resulted in inhibition of migration ability, cell cycle arrest, and increase in surface antigens, which suggest that 4.1R participates in MG autoimmunity.

CD80

CD86

10.12659/msm.920594

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Citations (2)

Progress in Research on SARS-CoV-2 Infection Causing Neurological Diseases and Its Infection Mechanism

Frontiers in Neurology (2021)

Lintao Wang Zhiguang Ren Li Ma Yanjie Han Wenqiang Wei

COVID-19 has spread rapidly worldwide since its outbreak and has now become a major public health problem. More and more evidence indicates that SARS-CoV-2 may not only affect the respiratory system but also cause great harm to the central nervous system. Therefore, it is extremely important to explore in-depth the impact of SARS-CoV-2 infection on the nervous system. In this paper, the possible mechanisms of SARS-CoV-2 invading the central nervous system during COVID-19, and the neurological complications caused by SARS-CoV-2 infection were reviewed.

Coronavirus

10.3389/fneur.2020.592888

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Citations (11)

Serum pepsinogens and risk of esophageal squamous dysplasia

International Journal of Cancer (2008)

Farin Kamangar Léna Diaw Wenqiang Wei Christian C. Abnet Guoqing Wang

Pepsinogens are a class of endopeptidases that are secreted by the gastric epithelium and released into the circulation. Low serum pepsinogen I (PGI) and low serum pepsinogen I/pepsinogen II ratio (PGI/II ratio) are markers of gastric fundic atrophy, and have recently been shown to be associated with increased risk of esophageal squamous cell carcinoma (ESCC). We conducted the current study to test whether these markers are also associated with esophageal squamous dysplasia (ESD), the precursor lesion of ESCC. We measured serum PGI and PGII, using enzyme-linked immunosorbent assays, in 125 case subjects (patients with moderate or severe ESD) and 250 sex-matched control subjects (no ESD) selected from an endoscopic screening study in Linxian, China. We used conditional logistic regression models adjusted for age, smoking and place of residence to calculate odds ratios (ORs) and 95% confidence intervals (95% CIs). Serum PGI showed no statistically significant association with ESD, whether analyzed as a dichotomous, ordinal (quartiles) or continuous variable. Lower serum PGI/II ratio, however, showed a dose-response association with increased risk of ESD, with an adjusted OR (95% CI) of 2.12 (1.08-4.18), comparing the lowest versus the highest quartile. The association between the lower serum PGI/II ratio and log OR of ESD was nearly linear, and the p-value for the continuous association was 0.03. Lower serum PGI/II ratio was linearly associated with higher risk of ESD. This result is consistent with recent findings that gastric atrophy may increase the risk of ESCC.

Quartile

Atrophic gastritis

Pepsin

10.1002/ijc.23918

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Citations (43)

Coping with esophageal cancer approaches worldwide

Annals of the New York Academy of Sciences (2014)

Richard G.H. Cotton Rupert Langer Trevor Leong Jan Martínek Vikash Sewram

The following, from the 12th OESO World Conference: Cancers of the Esophagus, includes commentaries on approaches to the epidemiology, diagnosis, and treatment of esophageal cancer in Europe, South Africa, Kenya, Australia, and China; the molecular classification of esophageal cancers (including cancers at the gastroesophageal junction); the Japanese classification; the scope of the Human Variome Project; and the topographic–anatomic subclassification of adenocarcinomas of the gastroesophageal junction.

Scope (computer science)

10.1111/nyas.12522

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Citations (15)

Coronavirus accessory protein ORF3 biology and its contribution to viral behavior and pathogenesis

iScience (2023)

Fusheng Si Shuai Song Ruisong Yu Zhen Li Wenqiang Wei

Coronavirus porcine epidemic diarrhea virus (PEDV) is classified in the genus Alphacoronavirus, family Coronaviridae that encodes the only accessory protein, ORF3 protein. However, how ORF3 contributes to viral pathogenicity, adaptability, and replication is obscure. In this review, we summarize current knowledge and identify gaps in many aspects of ORF3 protein in PEDV, with emphasis on its unique biological features, including membrane topology, Golgi retention mechanism, potential intrinsic disordered property, functional motifs, protein glycosylation, and codon usage phenotypes related to genetic evolution and gene expression. In addition, we propose intriguing questions related to ORF3 protein that we hope to stimulate further studies and encourage collaboration among virologists worldwide to provide constructive knowledge about the unique characteristics and biological functions of ORF3 protein, by which their potential role in clarifying viral behavior and pathogenesis can be possible.

Coronavirus

Coronaviridae

10.1016/j.isci.2023.106280

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Citations (17)