Experimental and molecular pathology最新文献

{"title":"Environmental physical factors produce mitotic aberration and multicellularity in the ovarian cancer cell line SKOV3.","authors":"N Lujea, F Chiola, M De Leon Rodriguez, C Acosta, P Kunda","doi":"10.1016/j.yexmp.2024.104884","DOIUrl":"https://doi.org/10.1016/j.yexmp.2024.104884","url":null,"abstract":"<p><p>The spread of ovarian cancer (OC) to the coelomic cavity triggers the secretion and accumulation of ascitic fluid (AF). Although its biochemical composition has been well studied, less is known about the implications of physical factors such as the pH and the mechanical properties of the AF for the malignancy of tumor cells. In this work, we investigated the effect of pH and the mechanical properties of AF on cell proliferation and mitotic morphology. We employed biopsies from patients with OC and the SKOV3 cell line as an in vitro model of OC with HeLa cells as controls. Sections of each tumor were stained with HE, analyzed, and related to clinical data. AF from patients with OC exhibited an alkaline pH (ranging from 7.3 to 7.8). Compared to control conditions, the 3 AFs significantly enhanced the proliferation of SKOV3 and HeLa cells. These effects were more pronounced at a more alkaline pH. In addition, we found that AFs have different densities that correlated with a significant increase in multinucleated tumor cells and severe morphological defects in cells undergoing mitosis. In agreement with these data, we found that higher concentrations of soft agar provoked significantly higher numbers of multinucleated and morphologically abnormal SKOV3 cells with no effect on HeLa cells. We conclude that an alkaline pH and greater rigidity could enhance the metastatic potential of OC cells. We propose that these two physical factors could be parameters of clinical importance as predictors of malignancy.</p>","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":" ","pages":"104884"},"PeriodicalIF":3.6,"publicationDate":"2024-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139575028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An in-silico analysis reveals further evidence of an aggressive subset of lung carcinoids sharing molecular features of high-grade neuroendocrine neoplasms","authors":"Giuseppe Pelosi ,&nbsp;Valentina Melocchi ,&nbsp;Elisa Dama ,&nbsp;Paul Hofman ,&nbsp;Marco De Luca ,&nbsp;Adriana Albini ,&nbsp;Maria Gemelli ,&nbsp;Riccardo Ricotta ,&nbsp;Mauro Papotti ,&nbsp;Stefano La Rosa ,&nbsp;Silvia Uccella ,&nbsp;Sergio Harari ,&nbsp;Angelica Sonzogni ,&nbsp;Michael K. Asiedu ,&nbsp;Dennis A. Wigle ,&nbsp;Fabrizio Bianchi","doi":"10.1016/j.yexmp.2024.104882","DOIUrl":"10.1016/j.yexmp.2024.104882","url":null,"abstract":"<div><p>Little is known as to whether there may be any pathogenetic link between pulmonary carcinoids and neuroendocrine carcinomas (NECs). A gene signature we previously found to cluster pulmonary carcinoids, large cell neuroendocrine carcinoma (LCNEC) and small cell lung carcinoma (SCLC), and which encompassed <em>MEN1, MYC, MYCL1, RICTOR, RB1, SDHA, SRC</em> and <em>TP53 mutations or</em> copy number variations (CNVs), was used to reclassify an independent cohort of 54 neuroendocrine neoplasms (NENs) [31 typical carcinoids (TC), 11 atypical carcinoids (AC) and 12 SCLC], by means of transcriptome and mutation data. Unsupervised clustering analysis identified two histology-independent clusters, namely CL1 and CL2, where 17/42 (40.5%) carcinoids and all the SCLC samples fell into the latter. CL2 carcinoids affected survival adversely, were enriched in T to G transversions or T &gt; C/C &gt; T transitions in the context of specific mutational signatures, presented with at least 1.5-fold change (FC) increase of gene mutations including <em>TSC2</em>, <em>SMARCA2</em>, <em>SMARCA4</em>, <em>ERBB4</em> and <em>PTPRZ1</em>, differed for gene expression and showed epigenetic changes in charge of <em>MYC</em> and <em>MTORC1</em> pathways, cellular senescence, inflammation, high-plasticity cell state and immune system exhaustion. Similar results were also found in two other independent validation sets comprising 101 lung NENs (24 carcinoids, 21 SCLC and 56 LCNEC) and 30 carcinoids, respectively. We herein confirmed an unexpected sharing of molecular traits along the spectrum of lung NENs, with a subset of genomically distinct aggressive carcinoids sharing molecular features of high-grade neuroendocrine neoplasms.</p></div>","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":"135 ","pages":"Article 104882"},"PeriodicalIF":3.6,"publicationDate":"2024-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0014480024000017/pdfft?md5=8e18b58028ce704033d84572f79c139a&pid=1-s2.0-S0014480024000017-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139490897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction notice to “Overexpression of cortistatin alleviates oxygen/glucose-deprivation-induced ER stress and prompts neural stem cell proliferation via SSTR2” [Experimental and Molecular Pathology 113 (2020) 104351]","authors":"Xiulin Liang ,&nbsp;Qing Mao ,&nbsp;Donghong Huang ,&nbsp;Jian Tang ,&nbsp;Jinou Zheng","doi":"10.1016/j.yexmp.2023.104878","DOIUrl":"10.1016/j.yexmp.2023.104878","url":null,"abstract":"","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":"134 ","pages":"Article 104878"},"PeriodicalIF":3.6,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0014480023000291/pdfft?md5=0797031bcbde4b163b182d3b0d74ee57&pid=1-s2.0-S0014480023000291-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138470167","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “RAB5A effect on metastasis of hepatocellular carcinoma cell line via altering the pro-invasive content of exosomes” [Experimental and Molecular Pathology 120 (2021) 104632]","authors":"Gilar Gorji-bahri ,&nbsp;Hamid Reza Moghimi ,&nbsp;Atieh Hashemi","doi":"10.1016/j.yexmp.2023.104875","DOIUrl":"10.1016/j.yexmp.2023.104875","url":null,"abstract":"","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":"134 ","pages":"Article 104875"},"PeriodicalIF":3.6,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0014480023000266/pdfft?md5=45747e089facf4745939789bb527ce74&pid=1-s2.0-S0014480023000266-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71479852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Roots remain","authors":"Marco Giudici","doi":"10.1016/j.yexmp.2023.104868","DOIUrl":"10.1016/j.yexmp.2023.104868","url":null,"abstract":"","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":"134 ","pages":"Article 104868"},"PeriodicalIF":3.6,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0014480023000199/pdfft?md5=c0749998321ac7271527465891af5bc8&pid=1-s2.0-S0014480023000199-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10283424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Urinary exosomes from patients with diabetic kidney disease induced podocyte apoptosis via microRNA-145-5p/Srgap2 and the RhoA/ROCK pathway","authors":"Lulu Han ,&nbsp;Shenghai Wang ,&nbsp;Juan Li ,&nbsp;Lulu Zhao ,&nbsp;Hong Zhou","doi":"10.1016/j.yexmp.2023.104877","DOIUrl":"10.1016/j.yexmp.2023.104877","url":null,"abstract":"<div><p>Diabetic kidney disease (DKD) is a leading cause of end-stage renal disease without early diagnostic and specific therapeutic approaches. Podocyte apoptosis and loss play important roles in the pathological process of DKD. This study aimed to explore whether urinary exosomes from type 2 diabetes patients with DKD could induce podocyte apoptosis and the underlying pathological mechanisms. The exosomes were isolated from the urine samples of patients with DKD (DKD-Exo). Later, they were taken up and internalized by MPC5 cells. MPC5 cells were co-cultured with DKD-Exo (45 μg/ml) for 24 h in the presence or absence of microRNA-145-5p (miR-145-5p) inhibitor, fasudil and pcDNA-Srgap2 transfection. MiR-145-5p and Srgap2 expression was evaluated using real-time quantitative PCR. The protein levels of Srgap2, Bcl-2, Bax, and cleaved caspase-3, as well as ROCK activity were determined using Western blotting. Cell apoptosis was measured using flow cytometry and the TUNEL assay. miR-145-5p expression in MPC5 cells exposed to DKD-Exo was markedly upregulated. miR-145-5p negatively regulated Srgap2 levels. Exposure of MPC5 cells to DKD-Exo reduced Srgap2 expression and activated ROCK, which was partly reversed by the presence of the miR-145-5p inhibitor or Srgap2 overexpression. The apoptosis of MPC5 cells exposed to DKD-Exo increased significantly, which was counteracted by the addition of the miR-145-5p inhibitor and fasudil. The results showed that urinary exosomal miR-145-5p from patients with DKD induced podocyte apoptosis by inhibiting Srgap2 and activating the RhoA/ROCK pathway, suggesting that urinary exosomal miR-145-5p is involved in the pathological process of DKD and could become a noninvasive diagnostic biomarker for DKD.</p></div>","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":"134 ","pages":"Article 104877"},"PeriodicalIF":3.6,"publicationDate":"2023-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S001448002300028X/pdfft?md5=a627243501fc25972111af7d28ece93a&pid=1-s2.0-S001448002300028X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89717564","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The MC160 protein of the molluscum contagiosum virus dampens cGAS/STING-induced interferon-β activation","authors":"Brian T. Reiss,&nbsp;Lissette Bouza,&nbsp;Swagath Thomas,&nbsp;Catherine D. Suarez,&nbsp;Erik R. Hill,&nbsp;Daniel Brian Nichols","doi":"10.1016/j.yexmp.2023.104876","DOIUrl":"10.1016/j.yexmp.2023.104876","url":null,"abstract":"<div><p>Molluscum contagiosum virus (MCV) is a poxvirus that causes benign, persistent skin lesions. MCV encodes a variety of immune evasion molecules to dampen host immune responses. Two of these proteins are the MC159 and MC160 proteins. Both MC159 and MC160 contain two tandem death effector domains and share homology to the cellular FLIPs, FADD, and procaspase-8. MC159 and MC160 dampen several innate immune responses such as NF-κB activation and mitochondrial antiviral signaling (MAVS)-mediated induction of type 1 interferon (IFN). The type 1 IFN response is also activated by the cytosolic DNA sensors cyclic GMP-AMP synthase (cGAS) and stimulator of interferon genes (STING). Both cGAS and STING play a vital role in sensing a poxvirus infection. In this study, we demonstrate that there are nuanced differences between both MC160 and MC159 in terms of how the viral proteins modulate the cGAS/STING and MAVS pathways. Specifically, MC160 expression, but not MC159 expression, dampens cGAS/STING-mediated induction of IFN in HEK 293 T cells. Further, MC160 expression prevented the K63-ubiquitination of both STING and TBK1, a kinase downstream of cGAS/STING. Ectopic expression of the MC160 protein, but not the MC159 protein, resulted in a measurable decrease in the TBK1 protein levels as detected via immunoblotting. Finally, using a panel of MC160 truncation mutants, we report that the MC160 protein requires both DEDs to inhibit cGAS/STING-induced activation of IFN-β. Our model indicates MC160 likely alters the TBK1 signaling complex to decrease IFN-β activation at the molecular intersection of the cGAS/STING and MAVS signaling pathways.</p></div>","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":"134 ","pages":"Article 104876"},"PeriodicalIF":3.6,"publicationDate":"2023-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0014480023000278/pdfft?md5=33bae6cd6c463817b8ba12cb4dd26e62&pid=1-s2.0-S0014480023000278-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61561763","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SARS-CoV-2 hampers dopamine production in iPSC-derived dopaminergic neurons","authors":"G. Cappelletti ,&nbsp;E.V. Carsana ,&nbsp;G. Lunghi ,&nbsp;S. Breviario ,&nbsp;C. Vanetti ,&nbsp;A.B. Di Fonzo ,&nbsp;E. Frattini ,&nbsp;M. Magni ,&nbsp;S. Zecchini ,&nbsp;M. Clerici ,&nbsp;M. Aureli ,&nbsp;C. Fenizia","doi":"10.1016/j.yexmp.2023.104874","DOIUrl":"10.1016/j.yexmp.2023.104874","url":null,"abstract":"<div><p>An increasing number of patients experiences prolonged symptoms, whose profile and timeline remain uncertain, a condition that has been defined as post COVID. The majority of recovered hospitalized patients manifests at least one persistent symptom even sixty days after the first clinical manifestation's onset. Particularly, in light of the COVID-19-related symptomatology, it has been hypothesized that SARS-CoV-2 might affect the dopamine pathway. However, no scientific evidence has been produced so far.</p><p>To this end, human iPSC-derived dopaminergic neurons were infected with EU, Delta and Omicron SARS-CoV-2 variants. The infection with EU and Delta variants, but not with Omicron, results in a reduced intracellular content and extracellular release of dopamine. Indeed, the tyrosine hydroxylase was found to be significantly upregulated at the mRNA level, while being greatly reduced at the protein level. The major downstream synthetic enzyme DOPA-decarboxylase and the dopamine transporter were significantly downregulated both at the mRNA and protein level. Notably, <em>in vitro</em> SARS-CoV-2 infection was also associated with an altered MAP2 and TAU expression and with an increased presence of neuronal stress markers.</p><p>These preliminary observations suggest that the dopamine metabolism and production are affected by SARS-CoV-2, partially explaining some of the neurological symptoms manifested.</p></div>","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":"134 ","pages":"Article 104874"},"PeriodicalIF":3.6,"publicationDate":"2023-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41117260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of integrin alpha v/beta 5 mitigates the protective effect induced by irisin in hemorrhage","authors":"Lijiang Wang ,&nbsp;Supaporn Kulthinee ,&nbsp;John Slate-Romano ,&nbsp;Thomas Zhao ,&nbsp;Hamsa Shanmugam ,&nbsp;Patrycja M Dubielecka ,&nbsp;Ling X. Zhang ,&nbsp;Gangjian Qin ,&nbsp;Shougang Zhuang ,&nbsp;Y. Eugene Chin ,&nbsp;Ting C. Zhao","doi":"10.1016/j.yexmp.2023.104869","DOIUrl":"10.1016/j.yexmp.2023.104869","url":null,"abstract":"<div><h3>Introduction</h3><p>Irisin plays an important role in regulating tissue stress, cardiac function, and inflammation. Integrin αvβ5 was recently identified as a receptor for irisin to elicit its physiologic function. It remains unknown whether integrin αvβ5 is required for irisin's function in modulating the physiologic response to hemorrhage. The objective of this study is to examine if integrin αvβ5 contributes to the effects of irisin during the hemorrhagic response.</p></div><div><h3>Methods</h3><p>Hemorrhage was induced in mice by achieving a mean arterial blood pressure of 35–45 mmHg for one hour, followed by two hours of resuscitation. Irisin (0.5  μg/kg) was administrated to assess its pharmacologic effects in hemorrhage. Cilengitide, a cyclic Arg-Gly-Asp peptide (cRGDyK) which is an inhibitor of integrin αvβ5, or control RGDS (1 mg/kg) was administered with irisin. In another cohort of mice, the irisin-induced protective effect was examined after knocking down integrin β5 with nanoparticle delivery of integrin β5 sgRNA using CRSIPR/Cas-9 gene editing. Cardiac function and hemodynamics were measured using echocardiography and femoral artery catheterization, respectively. Systemic cytokine releases were measured using Enzyme-linked immunosorbent assay (ELISA). Histological analyses were used to determine tissue damage in myocardium, skeletal muscles, and lung tissues. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) was carried out to assess apoptosis in tissues.</p></div><div><h3>Results</h3><p>Hemorrhage induced reduction of integrin αvβ5 in skeletal muscles and repressed recovery of cardiac performance and hemodynamics. Irisin treatment led to significantly improved cardiac function, which was abrogated by treatment with Cilengitide or knockdown of integrin β5. Furthermore, irisin resulted in a marked suppression of tumor necrosis factor-α (TNF-α) and interleukin-1 (IL-1), muscle edema, and inflammatory cells infiltration in myocardium and skeletal muscles, which was attenuated by Cilengitide or knockdown of integrin β5. Irisin-induced reduction of apoptosis in the myocardium, skeletal muscles, and lung, which were attenuated by either the inhibition of integrin αvβ5, or knockdown of integrin β5.</p></div><div><h3>Conclusion</h3><p>Integrin αvβ5 plays an important role for irisin in modulating the protective effect during hemorrhage.</p></div>","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":"134 ","pages":"Article 104869"},"PeriodicalIF":3.6,"publicationDate":"2023-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10202573","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of bisphenol A on murine salivary glands and human tumor cell lines","authors":"Gabriela Kelly da Silva ,&nbsp;José Alcides Almeida de Arruda ,&nbsp;Tatiana Fernandes Araújo Almeida ,&nbsp;Sicília Rezende Oliveira ,&nbsp;Paula Alves da Silva Rocha ,&nbsp;Ricardo Alves Mesquita ,&nbsp;Zenilda de Lourdes Cardeal ,&nbsp;Helvécio Costa Menezes ,&nbsp;Ivana Márcia Alves Diniz ,&nbsp;Soraia Macari ,&nbsp;Andréia Machado Leopoldino ,&nbsp;Tarcília Aparecida Silva","doi":"10.1016/j.yexmp.2023.104870","DOIUrl":"10.1016/j.yexmp.2023.104870","url":null,"abstract":"<div><p>Bisphenol A (BPA) is an endocrine-disrupting chemical with a potential role in endocrine cancers. However, the effects of BPA on the salivary glands have been barely explored. We investigated the impact of <em>in vivo</em> sub-chronic exposure to BPA and its <em>in vitro</em> effects on human salivary gland mucoepidermoid carcinoma cell lines. Male and female mice were exposed to BPA (30 mg/kg/day). Sublingual and submandibular salivary glands from an estrogen-deficiency model were also analyzed. BPA concentration in salivary glands was evaluated by gas chromatography coupled to ion trap mass spectrometry. Immunohistochemical analysis using anti-p63 and anti-α-SMA antibodies was performed on mouse salivary gland tissues. Gene expression of estrogen receptors alpha and beta, P63 and α-SMA was quantified in mouse salivary gland and/or mucoepidermoid (UM-HMC-1 and UM-HMC-3A) cell lines. Cell viability, p63 and Ki-67 immunostaining were evaluated <em>in vitro</em>. BPA disrupted the tissue architecture of the submandibular and sublingual glands, particularly in female mice, and increased the expression of estrogen receptors and p63, effects that were accompanied by significant BPA accumulation in these tissues. Conversely, ovariectomy slightly impacted BPA-induced morphological changes. <em>In vitro</em>, BPA did not affect the proliferation of neoplastic cells, but augmented the expression of p63 and estrogen receptors. The present data highlight a potential harmful effect of BPA on salivary gland tissues, particularly in female mice, and salivary gland tumor cells. Our findings suggest that estrogen-dependent pathways may orchestrate the effects of BPA in salivary glands.</p></div>","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":"134 ","pages":"Article 104870"},"PeriodicalIF":3.6,"publicationDate":"2023-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10293946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}