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Mou JY, Ma ZW, Zhang MY, Yuan Q, Wang ZY, Liu QH, Li F, Liu Z, Wang L. Structural abnormality of hepatic glycogen in rat liver with diethylnitrosamine-induced carcinogenic injury. Int J Biol Macromol 2024; 260:129432. [PMID: 38228208 DOI: 10.1016/j.ijbiomac.2024.129432] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/18/2023] [Revised: 01/01/2024] [Accepted: 01/09/2024] [Indexed: 01/18/2024]
Abstract
Growing evidence confirms associations between glycogen metabolic re-wiring and the development of liver cancer. Previous studies showed that glycogen structure changes abnormally in liver diseases such as cystic fibrosis, diabetes, etc. However, few studies focus on glycogen molecular structural characteristics during liver cancer development, which is worthy of further exploration. In this study, a rat model with carcinogenic liver injury induced by diethylnitrosamine (DEN) was successfully constructed, and hepatic glycogen structure was characterized. Compared with glycogen structure in the healthy rat liver, glycogen chain length distribution (CLD) shifts towards a short region. In contrast, glycogen particles were mainly present in small-sized β particles in DEN-damaged carcinogenic rat liver. Comparative transcriptomic analysis revealed significant expression changes of genes and pathways involved in carcinogenic liver injury. A combination of transcriptomic analysis, RT-qPCR, and western blot showed that the two genes, Gsy1 encoding glycogen synthase and Gbe1 encoding glycogen branching enzyme, were significantly altered and might be responsible for the structural abnormality of hepatic glycogen in carcinogenic liver injury. Taken together, this study confirmed that carcinogenic liver injury led to structural abnormality of hepatic glycogen, which provided clues to the future development of novel drug targets for potential therapeutics of carcinogenic liver injury.
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Affiliation(s)
- Jing-Yi Mou
- Department of Clinical Medicine, School of 1(st) Clinical Medicine, Xuzhou Medical University, Xuzhou, Jiangsu Province, China
| | - Zhang-Wen Ma
- Department of Pharmaceutical Analysis, School of Pharmacy, Xuzhou Medical University, Xuzhou, Jiangsu Province, China
| | - Meng-Ying Zhang
- School of Medical Informatics and Engineering, Xuzhou Medical University, Xuzhou, Jiangsu Province, China
| | - Quan Yuan
- School of Medical Informatics and Engineering, Xuzhou Medical University, Xuzhou, Jiangsu Province, China
| | - Zi-Yi Wang
- School of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, Queensland, Australia
| | - Qing-Hua Liu
- State Key Laboratory of Quality Research in Chinese Medicines, Macau University of Science and Technology, Taipa, Macau SAR, China
| | - Fen Li
- Laboratory Medicine, The Fifth People's Hospital of Huai'an, Huai'an, Jiangsu Province, China
| | - Zhao Liu
- Department of Clinical Medicine, School of 1(st) Clinical Medicine, Xuzhou Medical University, Xuzhou, Jiangsu Province, China; Department of Thyroid and Breast Surgery, Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, China.
| | - Liang Wang
- School of Medical Informatics and Engineering, Xuzhou Medical University, Xuzhou, Jiangsu Province, China; Laboratory Medicine, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong Province, China; School of Agriculture and Food Sciences, The University of Queensland, Brisbane, Queensland, Australia.
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2
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Abdalla MMI. Serum resistin and the risk for hepatocellular carcinoma in diabetic patients. World J Gastroenterol 2023; 29:4271-4288. [PMID: 37545641 PMCID: PMC10401662 DOI: 10.3748/wjg.v29.i27.4271] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/26/2023] [Revised: 06/11/2023] [Accepted: 06/27/2023] [Indexed: 07/13/2023] Open
Abstract
Hepatocellular carcinoma (HCC), the predominant type of liver cancer, is a major contributor to cancer-related fatalities across the globe. Diabetes has been identified as a significant risk factor for HCC, with recent research indicating that the hormone resistin could be involved in the onset and advancement of HCC in diabetic individuals. Resistin is a hormone that is known to be involved in inflammation and insulin resistance. Patients with HCC have been observed to exhibit increased resistin levels, which could be correlated with more severe disease stages and unfavourable prognoses. Nevertheless, the exact processes through which resistin influences the development and progression of HCC in diabetic patients remain unclear. This article aims to examine the existing literature on the possible use of resistin levels as a biomarker for HCC development and monitoring. Furthermore, it reviews the possible pathways of HCC initiation due to elevated resistin and offers new perspectives on comprehending the fundamental mechanisms of HCC in diabetic patients. Gaining a better understanding of these processes may yield valuable insights into HCC’s development and progression, as well as identify possible avenues for prevention and therapy.
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Affiliation(s)
- Mona Mohamed Ibrahim Abdalla
- Department of Human Biology, School of Medicine, International Medical University, Bukit Jalil 57000, Kuala Lumpur, Malaysia
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3
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Vachher M, Bansal S, Kumar B, Yadav S, Arora T, Wali NM, Burman A. Contribution of organokines in the development of NAFLD/NASH associated hepatocellular carcinoma. J Cell Biochem 2022; 123:1553-1584. [PMID: 35818831 DOI: 10.1002/jcb.30252] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/30/2021] [Revised: 03/17/2022] [Accepted: 03/29/2022] [Indexed: 12/16/2022]
Abstract
Globally the incidence of hepatocellular carcinoma (HCC) is on an upsurge. Evidence is accumulating that liver disorders like nonalcoholic fatty liver disease (NAFLD) and its more progressive form nonalcoholic steatohepatitis (NASH) are associated with increased risk of developing HCC. NAFLD has a prevalence of about 25% and 50%-90% in obese population. With the growing burden of obesity epidemic worldwide, HCC presents a major healthcare burden. While cirrhosis is one of the major risk factors of HCC, available literature suggests that NAFLD/NASH associated HCC also develops in minimum or noncirrhotic livers. Therefore, there is an urgent need to understand the pathogenesis and risk factors associated with NAFLD and NASH related HCC that would help in early diagnosis and favorable prognosis of HCC secondary to NAFLD. Adipokines, hepatokines and myokines are factors secreted by adipocytes, hepatocytes and myocytes, respectively, playing essential roles in cellular homeostasis, energy balance and metabolism with autocrine, paracrine and endocrine effects. In this review, we endeavor to focus on the role of these organokines in the pathogenesis of NAFLD/NASH and its progression to HCC to augment the understanding of the factors stimulating hepatocytes to acquire a malignant phenotype. This shall aid in the development of novel therapeutic strategies and tools for early diagnosis of NAFLD/NASH and HCC.
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Affiliation(s)
- Meenakshi Vachher
- Department of Biochemistry, Institute of Home Economics, University of Delhi, Delhi, India
| | - Savita Bansal
- Department of Biochemistry, Institute of Home Economics, University of Delhi, Delhi, India
| | - Bhupender Kumar
- Department of Biochemistry, Institute of Home Economics, University of Delhi, Delhi, India
| | - Sandeep Yadav
- Department of Biochemistry, Institute of Home Economics, University of Delhi, Delhi, India
| | - Taruna Arora
- Department of Biochemistry, Institute of Home Economics, University of Delhi, Delhi, India
| | - Nalini Moza Wali
- Department of Biochemistry, Institute of Home Economics, University of Delhi, Delhi, India
| | - Archana Burman
- Department of Biochemistry, Institute of Home Economics, University of Delhi, Delhi, India
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4
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Patoulias D. Serum Resistin as a Biomarker in Nonalcoholic Fatty Liver Disease: Is This a Road to be Taken? J Clin Transl Hepatol 2021; 9:454-455. [PMID: 34447672 PMCID: PMC8369027 DOI: 10.14218/jcth.2021.00236] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/20/2021] [Revised: 07/05/2021] [Accepted: 07/12/2021] [Indexed: 12/04/2022] Open
Affiliation(s)
- Dimitrios Patoulias
- Second Propedeutic Department of Internal Medicine, Aristotle University of Thessaloniki, General Hospital “Hippokration”, Thessaloniki, Greece
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5
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Conway RBN, Sudenga S, McClain D, Blot WJ. Diabetes and liver cancer risk: A stronger effect in Whites than Blacks? J Diabetes Complications 2021; 35:107816. [PMID: 33323327 PMCID: PMC8045414 DOI: 10.1016/j.jdiacomp.2020.107816] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/13/2020] [Revised: 11/10/2020] [Accepted: 11/11/2020] [Indexed: 10/22/2022]
Abstract
BACKGROUND Both diabetes and liver cancer are overrepresented among African Americans, but limited information is available on the interrelationship of these two diseases among African Americans. We examined the association of diabetes with the incidence of liver cancer and whether this varied by participant self-reported race/ethnicity. METHODS Using the Southern Community Cohort Study, we conducted a cancer follow up (2002-2016) of a cohort of mostly low-income participants aged 40-79 with diabetes (n = 15,879) and without diabetes (n = 59,077) at study baseline. Cox regression was used to compute Hazard Ratios (HR) and 95% CIs for the risk of incident liver cancer. RESULTS With 790,132 person years of follow up, 320 incident cases of liver cancer were identified. In analyses controlling for age, sex, race, BMI, current and former smoking, total alcohol consumption, family history of liver cancer, any hepatitis infection, hyperlipidemia and socioeconomic factors, the association between diabetes and risk of liver cancer differed significantly (pinteraction = 0.0001) between participants identifying as Black/African American (AA) or White/European American (EA). Diabetes was associated with 5.3-fold increased cancer risk among EAs (HR 5.4, 95% CI 3.2-9.3) vs an 80% increase (HR 1.8, 95% CI 1.3-2.5) among AAs. Furthermore, controlling for diabetes greatly attenuated the higher risk of liver cancer among AAs; indeed, while the cancer risk among those without diabetes was twice as high among AAs than EAs (HR = 2.0, 95% CI = 1.4-2.9), no excess in AAs was observed among those with diabetes (HR = 0.7, 95% CI = 0.4-1.1). CONCLUSION While liver cancer risk in general is greater in AAs than EAs and diabetes increases this risk in both racial/ethnic groups, diabetes appears to impact liver cancer to a much greater extent among EAs. The findings raise the possibility of racially different mechanisms and impacts of diabetes on this often fatal cancer among AAs and EAs.
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Affiliation(s)
- Rebecca Baqiyyah N Conway
- School of Community and Rural Health, University of Texas Health Science Center at Tyler, Tyler, TX, United States of America.
| | - Staci Sudenga
- Division of Epidemiology, Vanderbilt University Medical Center, Nashville, TN, United States of America
| | - Donald McClain
- Section of Endocrinology and Metabolism, Wake Forest School of Medicine, Winston-Salem, NC, United States of America
| | - William J Blot
- Division of Epidemiology, Vanderbilt University Medical Center, Nashville, TN, United States of America
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Kucukoglu O, Sowa JP, Mazzolini GD, Syn WK, Canbay A. Hepatokines and adipokines in NASH-related hepatocellular carcinoma. J Hepatol 2021; 74:442-457. [PMID: 33161047 DOI: 10.1016/j.jhep.2020.10.030] [Citation(s) in RCA: 81] [Impact Index Per Article: 20.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/26/2020] [Revised: 10/26/2020] [Accepted: 10/28/2020] [Indexed: 12/12/2022]
Abstract
The incidence of hepatocellular carcinoma (HCC) is increasing in industrialised societies; this is likely secondary to the increasing burden of non-alcoholic fatty liver disease (NAFLD), its progressive form non-alcoholic steatohepatitis (NASH), and the metabolic syndrome. Cumulative studies suggest that NAFLD-related HCC may also develop in non-cirrhotic livers. However, prognosis and survival do not differ between NAFLD- or virus-associated HCC. Thus, research has increasingly focused on NAFLD-related risk factors to better understand the biology of hepatocarcinogenesis and to develop new diagnostic, preventive, and therapeutic strategies. One important aspect thereof is the role of hepatokines and adipokines in NAFLD/NASH-related HCC. In this review, we compile current data supporting the use of hepatokines and adipokines as potential markers of disease progression in NAFLD or as early markers of NAFLD-related HCC. While much work must be done to elucidate the mechanisms and interactions underlying alterations to hepatokines and adipokines, current data support the possible utility of these factors - in particular, angiopoietin-like proteins, fibroblast growth factors, and apelin - for detection or even as therapeutic targets in NAFLD-related HCC.
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Affiliation(s)
- Ozlem Kucukoglu
- Department of Gastroenterology, Hepatology, and Infectious Diseases, Otto-von-Guericke University Magdeburg, 39120 Magdeburg, Germany
| | - Jan-Peter Sowa
- Department of Medicine, Ruhr University Bochum, University Hospital Knappschaftskrankenhaus Bochum, 44892 Bochum, Germany
| | - Guillermo Daniel Mazzolini
- Laboratory of Gene Therapy, Instituto de Investigaciones en Medicina Traslacional, CONICET-Universidad Austral, Buenos Aires 999071, Argentina; Liver Unit, Hospital Universitario Austral, Universidad Austral, Argentina
| | - Wing-Kin Syn
- Section of Gastroenterology, Ralph H. Johnson Veterans Affairs Medical Center, Charleston, SC, USA; Division of Gastroenterology and Hepatology, Medical University of South Carolina, Charleston, SC, USA; Department of Physiology, Faculty of Medicine and Nursing, University of Basque Country UPV/EHU, 48940 Leioa, Vizcaya, Spain
| | - Ali Canbay
- Department of Gastroenterology, Hepatology, and Infectious Diseases, Otto-von-Guericke University Magdeburg, 39120 Magdeburg, Germany; Department of Medicine, Ruhr University Bochum, University Hospital Knappschaftskrankenhaus Bochum, 44892 Bochum, Germany.
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7
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Chang ML, Yang Z, Yang SS. Roles of Adipokines in Digestive Diseases: Markers of Inflammation, Metabolic Alteration and Disease Progression. Int J Mol Sci 2020; 21:E8308. [PMID: 33167521 PMCID: PMC7663948 DOI: 10.3390/ijms21218308] [Citation(s) in RCA: 55] [Impact Index Per Article: 11.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/13/2020] [Revised: 10/30/2020] [Accepted: 11/01/2020] [Indexed: 12/13/2022] Open
Abstract
Adipose tissue is a highly dynamic endocrine tissue and constitutes a central node in the interorgan crosstalk network through adipokines, which cause pleiotropic effects, including the modulation of angiogenesis, metabolism, and inflammation. Specifically, digestive cancers grow anatomically near adipose tissue. During their interaction with cancer cells, adipocytes are reprogrammed into cancer-associated adipocytes and secrete adipokines to affect tumor cells. Moreover, the liver is the central metabolic hub. Adipose tissue and the liver cooperatively regulate whole-body energy homeostasis via adipokines. Obesity, the excessive accumulation of adipose tissue due to hyperplasia and hypertrophy, is currently considered a global epidemic and is related to low-grade systemic inflammation characterized by altered adipokine regulation. Obesity-related digestive diseases, including gastroesophageal reflux disease, Barrett's esophagus, esophageal cancer, colon polyps and cancer, non-alcoholic fatty liver disease, viral hepatitis-related diseases, cholelithiasis, gallbladder cancer, cholangiocarcinoma, pancreatic cancer, and diabetes, might cause specific alterations in adipokine profiles. These patterns and associated bases potentially contribute to the identification of prognostic biomarkers and therapeutic approaches for the associated digestive diseases. This review highlights important findings about altered adipokine profiles relevant to digestive diseases, including hepatic, pancreatic, gastrointestinal, and biliary tract diseases, with a perspective on clinical implications and mechanistic explorations.
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Affiliation(s)
- Ming-Ling Chang
- Department of Medicine, College of Medicine, Chang Gung University, Taoyuan 33305, Taiwan
- Division of Hepatology, Department of Gastroenterology and Hepatology, Chang Gung Memorial Hospital, Taoyuan 33305, Taiwan
| | - Zinger Yang
- Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01655, USA;
| | - Sien-Sing Yang
- Liver Center, Cathay General Hospital Medical Center, Taipei 10630, Taiwan;
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8
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Evaluation of serum resistin levels in patients with hepatocellular carcinoma before and after treatment. EGYPTIAN LIVER JOURNAL 2018. [DOI: 10.1097/01.elx.0000546516.15821.c2] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/26/2022] Open
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9
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Tang R, Liu H, Yuan Y, Xie K, Xu P, Liu X, Wen J. Genetic factors associated with risk of metabolic syndrome and hepatocellular carcinoma. Oncotarget 2018; 8:35403-35411. [PMID: 28515345 PMCID: PMC5471064 DOI: 10.18632/oncotarget.15893] [Citation(s) in RCA: 15] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/04/2016] [Accepted: 02/15/2017] [Indexed: 01/01/2023] Open
Abstract
Although the metabolic syndrome is a commonplace topic, its potential threats to public health is a problem that cannot be neglected. As the living conditions improved significantly over the past few years, the morbidity of metabolic syndrome has also steadily risen, and the onset age is becoming younger. The hepatocellular carcinoma (HCC), is one of the most prevalent life-threatening human cancers worldwide, incidence of which is also on the rise, gradually occupied the top of the list associated with metabolic syndrome related complication. Despite the advanced improvement of HCC management, the lifestyle, environmental factors, obesity, hepatitis B virus (HBV) infection have been recognized as risk factors for the development of liver cancer. In recent years, genetic studies, especially the genome-wide association studies (GWASs) were widely performed, a new era of the human genome research was created, which has significantly promoted the study of complex disease genetics. These progresses have contributed to the discovery of abundant number of genomic loci convincingly linked with complex metabolic feature and HCC. In this review, we briefly summarize the association between metabolic syndrome and HCC, focusing on the genetic factors contributed to metabolic syndrome and HCC.
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Affiliation(s)
- Ranran Tang
- Nanjing Maternity and Child Health Care Institute, Nanjing Maternity and Child Health Care Hospital, Obstetrics and Gynecology Hospital Affiliated to Nanjing Medical University, Nanjing, China.,State Key Laboratory of Reproductive Medicine, Nanjing Maternity and Child Health Care Hospital, Obstetrics and Gynecology Hospital Affiliated to Nanjing Medical University, Nanjing, China
| | - Heng Liu
- Department of Pediatrics, Nanjing Maternity and Child Health Care Hospital, Obstetrics and Gynecology Hospital Affiliated to Nanjing Medical University, Nanjing, China
| | - Yingdi Yuan
- Nanjing Maternity and Child Health Care Institute, Nanjing Maternity and Child Health Care Hospital, Obstetrics and Gynecology Hospital Affiliated to Nanjing Medical University, Nanjing, China
| | - Kaipeng Xie
- Nanjing Maternity and Child Health Care Institute, Nanjing Maternity and Child Health Care Hospital, Obstetrics and Gynecology Hospital Affiliated to Nanjing Medical University, Nanjing, China.,State Key Laboratory of Reproductive Medicine, Nanjing Maternity and Child Health Care Hospital, Obstetrics and Gynecology Hospital Affiliated to Nanjing Medical University, Nanjing, China
| | - Pengfei Xu
- Nanjing Maternity and Child Health Care Institute, Nanjing Maternity and Child Health Care Hospital, Obstetrics and Gynecology Hospital Affiliated to Nanjing Medical University, Nanjing, China.,State Key Laboratory of Reproductive Medicine, Nanjing Maternity and Child Health Care Hospital, Obstetrics and Gynecology Hospital Affiliated to Nanjing Medical University, Nanjing, China
| | - Xiaoyun Liu
- Department of Endocrinology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China
| | - Juan Wen
- Nanjing Maternity and Child Health Care Institute, Nanjing Maternity and Child Health Care Hospital, Obstetrics and Gynecology Hospital Affiliated to Nanjing Medical University, Nanjing, China.,State Key Laboratory of Reproductive Medicine, Nanjing Maternity and Child Health Care Hospital, Obstetrics and Gynecology Hospital Affiliated to Nanjing Medical University, Nanjing, China
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10
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Deshmukh SK, Srivastava SK, Zubair H, Bhardwaj A, Tyagi N, Al-Ghadhban A, Singh AP, Dyess DL, Carter JE, Singh S. Resistin potentiates chemoresistance and stemness of breast cancer cells: Implications for racially disparate therapeutic outcomes. Cancer Lett 2017; 396:21-29. [PMID: 28302531 PMCID: PMC5437742 DOI: 10.1016/j.canlet.2017.03.010] [Citation(s) in RCA: 31] [Impact Index Per Article: 3.9] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/14/2017] [Revised: 03/04/2017] [Accepted: 03/07/2017] [Indexed: 12/27/2022]
Abstract
Breast cancer (BC) continues to be the most frequently diagnosed cancer in American women, which disproportionately affects women of African-American (AA) descent. Previously, we reported greater serum levels of resistin in AA BC patients relative to Caucasian-American (CA) patients, and established its role in growth and aggressiveness of breast tumor cells. Here we have investigated the role of resistin in BC-chemoresistance. MDA-MB-231 and MDA-MB-468 BC cells of CA and AA origin, respectively, were incubated with resistin prior to doxorubicin treatment. Our data suggest that resistin conferred chemoresistance to both BC cell lines; however, the effect on AA cells was more profound. Furthermore, the resistin-induced doxorubicin-resistance was shown to occur due to suppression of apoptosis. Resistin treatment also affected the stemness of BC cells, as suggested by reduced cell surface expression of CD24, induced expression of CD44 and ALDH1, and increased capability of cells to form mammospheres. Mechanistic studies revealed that resistin-induced chemoresistance, apoptosis and stemness of BC cells were mediated through STAT3 activation. Taken together, our findings provide novel insight into the role of resistin in BC biology, and strengthen its role in racially disparate clinical outcomes.
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Affiliation(s)
- Sachin K Deshmukh
- Department of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, AL, USA
| | - Sanjeev K Srivastava
- Department of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, AL, USA
| | - Haseeb Zubair
- Department of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, AL, USA
| | - Arun Bhardwaj
- Department of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, AL, USA
| | - Nikhil Tyagi
- Department of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, AL, USA
| | - Ahmed Al-Ghadhban
- Department of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, AL, USA
| | - Ajay P Singh
- Department of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, AL, USA; Department of Biochemistry and Molecular Biology, College of Medicine, University of South Alabama, Mobile, AL, USA
| | - Donna L Dyess
- Department of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, AL, USA
| | - James E Carter
- Department of Pathology, College of Medicine, University of South Alabama, Mobile, AL, USA
| | - Seema Singh
- Department of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, AL, USA; Department of Biochemistry and Molecular Biology, College of Medicine, University of South Alabama, Mobile, AL, USA.
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11
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Jiang CY, Wang W. Resistin aggravates the expression of proinflammatory cytokines in cerulein-stimulated AR42J pancreatic acinar cells. Mol Med Rep 2016; 15:502-506. [DOI: 10.3892/mmr.2016.6027] [Citation(s) in RCA: 11] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/17/2015] [Accepted: 11/14/2016] [Indexed: 11/06/2022] Open
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12
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Diagnostic Potential of Evaluation of SDF-1α and sRAGE Levels in Threatened Premature Labor. BIOMED RESEARCH INTERNATIONAL 2016; 2016:2719460. [PMID: 27556030 PMCID: PMC4983339 DOI: 10.1155/2016/2719460] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 04/27/2016] [Revised: 06/28/2016] [Accepted: 07/03/2016] [Indexed: 12/28/2022]
Abstract
Preterm birth remains the most prevalent cause of neonatal morbidity. This study aimed to evaluate the diagnostic value of SDF-1α, resistin, secretory RAGE (sRAGE), and endogenous secretory RAGE (esRAGE) in preterm labor. A total of 211 pregnant women participated in the study. Group A contained 72 women between 22 and 36 weeks of gestation, with premature labor, who finally had preterm birth. Group B contained 66 women in labor between 37 and 41 weeks of gestation. Women in group A had lower SDF-1α and sRAGE levels than those in group B. Moreover, in group A, SDF-1α and sRAGE levels were correlated with the latency period from the occurrence of premature labor symptoms until delivery. Sensitivity and specificity of studied parameters for prediction of preterm birth were 95% and 40% for SDF-1α and 51.3% and 93.5% for sRAGE, respectively. The prognostic value of plasma SDF-1α and sRAGE levels was comparable with that of cervical length ultrasound measurement and serum C-reactive protein levels. We conclude that SDF-1α and sRAGE appear to play a major role in the diagnosis of preterm birth and its evaluation could be convenient and useful for predicting preterm birth.
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