Bin Gao

National Institute on Alcohol Abuse and Alcoholism

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Dechun Feng

National Institute on Alcohol Abuse and Alcoholism

Ogyi Park

National Institute on Alcohol Abuse and Alcoholism

George Kunos

National Institute on Alcohol Abuse and Alcoholism

Hua Wang

The University of Texas MD Anderson Cancer Center

Adrien Guillot

Charité - Universitätsmedizin Berlin

Yukun Guan

National Institutes of Health

Huamin Han

Chinese Academy of Sciences

Bryan Mackowiak

National Institute on Alcohol Abuse and Alcoholism

Pál Pacher

National Institutes of Health

Won‐Il Jeong

Korea Advanced Institute of Science and Technology

Cooperative Institutions

National Institutes of Health

Chinese Academy of Sciences

National Institute on Alcohol Abuse and Alcoholism

Sun Yat-sen University

Peking University

University of Chinese Academy of Sciences

Chinese Academy of Medical Sciences & Peking Union Medical College

Shanghai Jiao Tong University

Wuhan University

Indiana University – Purdue University Indianapolis

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Neutrophil–Hepatic Stellate Cell Interactions Promote Fibrosis in Experimental Steatohepatitis

Cellular and Molecular Gastroenterology and Hepatology (2018)

Zhou Zhou Mingjiang Xu Yan Cai Wei Wang Joy Jiang

Hepatic infiltration of neutrophils is a hallmark of steatohepatitis; however, the role of neutrophils in the progression of steatohepatitis remains unknown.

Hepatic stellate cell

Steatohepatitis

Hepatic fibrosis

10.1016/j.jcmgh.2018.01.003

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Citations (132)

Sa1510 – Increased Serotonin (5HT) Biliary Synthesis Due to Enhanced Expression of Tryptophan Hydroxylase1 (TPH1) and Reduced Monoamine-Oxidase-A (MAO-A) Expression is Couple with Alcohol-Induced Liver Injury (ALI)

Gastroenterology (2019)

Konstantina Kyritsi Lixian Chen Julie Venter Tianhao Zhou Ludovica Ceci

Alcoholic Hepatitis

10.1016/s0016-5085(19)40060-7

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Citations (0)

Paracrine Effects of Adipose-Derived Stem Cells on Matrix Stiffness-Induced Cardiac Myofibroblast Differentiation via Angiotensin II Type 1 Receptor and Smad7

Scientific Reports (2016)

Kar Wey Yong Yuhui Li Fusheng Liu Bin Gao Tian Jian Lu

Abstract Human mesenchymal stem cells (hMSCs) hold great promise in cardiac fibrosis therapy, due to their potential ability of inhibiting cardiac myofibroblast differentiation (a hallmark of cardiac fibrosis). However, the mechanism involved in their effects remains elusive. To explore this, it is necessary to develop an in vitro cardiac fibrosis model that incorporates pore size and native tissue-mimicking matrix stiffness, which may regulate cardiac myofibroblast differentiation. In the present study, collagen coated polyacrylamide hydrogel substrates were fabricated, in which the pore size was adjusted without altering the matrix stiffness. Stiffness is shown to regulate cardiac myofibroblast differentiation independently of pore size. Substrate at a stiffness of 30 kPa, which mimics the stiffness of native fibrotic cardiac tissue, was found to induce cardiac myofibroblast differentiation to create in vitro cardiac fibrosis model. Conditioned medium of hMSCs was applied to the model to determine its role and inhibitory mechanism on cardiac myofibroblast differentiation. It was found that hMSCs secrete hepatocyte growth factor (HGF) to inhibit cardiac myofibroblast differentiation via downregulation of angiotensin II type 1 receptor (AT 1 R) and upregulation of Smad7. These findings would aid in establishment of the therapeutic use of hMSCs in cardiac fibrosis therapy in future.

Myofibroblast

Cardiac Fibrosis

10.1038/srep33067

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Citations (53)

Pharmacological Mobilization of Endogenous Bone Marrow Stem Cells Promotes Liver Regeneration after Extensive Liver Resection in Rats

Scientific Reports (2018)

Rujun Zhai Yongchun Wang Le Qi G. Melville Williams Bin Gao

Abstract Rapid regeneration of the remnant liver is critical for preventing liver failure and promoting recovery after extensive liver resection. Numerous studies have demonstrated the involvement of bone marrow-derived stem cells in liver regeneration and the potential benefits of bone marrow stem cell therapy. To avoid the preparation of stem cells, we proposed in this study to mobilize endogenous bone marrow stem cells pharmacologically with a combination of AMD3100 (A), an antagonist of CXCR4 and low-dose FK506 (F). Here we show that AF combination therapy significantly increased lineage negative (Lin-) CD34+ and Lin-CD133+ stem cells in peripheral blood and enhanced recruitment of CD133+ cells into the remnant liver in a rat model of 85% partial hepatectomy. Recruiting CD133+ stem cells in the remnant liver was associated with increased proliferation of hepatic oval cells and paralleled the increased SDF-1, CXCR4 and HGF expression. Importantly, AF combination therapy increased the number of Ki67 positive hepatocytes and BrdU incorporation in the remnant liver and improved serum levels of albumin. Our results demonstrate that pharmacological mobilization of endogenous bone marrow stem cells with AF combination therapy can enhance endogenous stem cell mobilization to promote liver regeneration and improve liver function after extensive hepatectomy.

Liver Regeneration

10.1038/s41598-018-21961-2

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Citations (18)

Hippo signaling is intrinsically regulated during cell cycle progression by APC/C ^Cdh1

Proceedings of the National Academy of Sciences (2019)

Wantae Kim Yong Suk Cho Xiaohui Wang Ogyi Park Xueyan Ma

The Hippo-YAP/TAZ signaling pathway plays a pivotal role in growth control during development and regeneration and its dysregulation is widely implicated in various cancers. To further understand the cellular and molecular mechanisms underlying Hippo signaling regulation, we have found that activities of core Hippo signaling components, large tumor suppressor (LATS) kinases and YAP/TAZ transcription factors, oscillate during mitotic cell cycle. We further identified that the anaphase-promoting complex/cyclosome (APC/C) Cdh1 E3 ubiquitin ligase complex, which plays a key role governing eukaryotic cell cycle progression, intrinsically regulates Hippo signaling activities. CDH1 recognizes LATS kinases to promote their degradation and, hence, YAP/TAZ regulation by LATS phosphorylation is under cell cycle control. As a result, YAP/TAZ activities peak in G1 phase. Furthermore, we show in Drosophila eye and wing development that Cdh1 is required in vivo to regulate the LATS homolog Warts with a conserved mechanism. Cdh1 reduction increased Warts levels, which resulted in reduction of the eye and wing sizes in a Yorkie dependent manner. Therefore, LATS degradation by APC/C Cdh1 represents a previously unappreciated and evolutionarily conserved layer of Hippo signaling regulation.

Hippo signaling pathway

CDH1

E2F

Anaphase-promoting complex

10.1073/pnas.1821370116

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Citations (55)

Gaps in Knowledge and Research Priorities for Alcoholic Hepatitis

Gastroenterology (2015)

Arun J. Sanyal Bin Gao Gyöngyi Szabó

Alcoholic Hepatitis

Steatohepatitis

Hepatitis C

Etiology

Viral Hepatitis

10.1053/j.gastro.2015.05.015

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Citations (21)

Distinct fate, dynamics and niches of renal macrophages of bone marrow or embryonic origins

Nature Communications (2020)

Fengming Liu Shen Dai Dechun Feng Zhongnan Qin Xiao Peng

Abstract Renal macrophages (RMs) participate in tissue homeostasis, inflammation and repair. RMs consist of embryo-derived (EMRMs) and bone marrow-derived RMs (BMRMs), but the fate, dynamics, replenishment, functions and metabolic states of these two RM populations remain unclear. Here we investigate and characterize RMs at different ages by conditionally labeling and ablating RMs populations in several transgenic lines. We find that RMs expand and mature in parallel with renal growth after birth, and are mainly derived from fetal liver monocytes before birth, but self-maintain through adulthood with contribution from peripheral monocytes. Moreover, after the RMs niche is emptied, peripheral monocytes rapidly differentiate into BMRMs, with the CX3CR1/CX3CL1 signaling axis being essential for the maintenance and regeneration of both EMRMs and BMRMs. Lastly, we show that EMRMs have a higher capacity for scavenging immune complex, and are more sensitive to immune challenge than BMRMs, with this difference associated with their distinct glycolytic capacities.

Monocyte

Homeostasis

10.1038/s41467-020-16158-z

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Citations (85)

Tumor suppressor p53 cooperates with SIRT6 to regulate gluconeogenesis by promoting FoxO1 nuclear exclusion

Proceedings of the National Academy of Sciences (2014)

Ping Zhang Bo Tu Hua Wang Ziyang Cao Ming Tang

Significance Beyond its canonical functions in processes such as cell-cycle arrest, apoptosis, and senescence, the tumor suppressor p53 has been increasingly implicated in metabolism. Here, in vitro and in vivo studies establish a role for p53 in gluconeogenesis through a previously unidentified mechanism involving ( i ) direct activation of the gene encoding the NAD-dependent deacetylase sirtuin 6 (SIRT6), ( ii ) SIRT6-dependent deacetylation and nuclear exclusion of forkhead box protein O1 (FoxO1), and ( iii ) down-regulation of FoxO1-activated genes (G6PC and PCK1) that are rate-limiting for gluconeogenesis. These results have implications for proposed tumor-suppressor functions of p53 through regulation of metabolic pathways.

FOXO1

Gluconeogenesis

SIRT6

Sirtuin 1

10.1073/pnas.1411026111

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Citations (207)

Mo1534 AQUAPROINE-9 AFFECTS HEPATIC ACETALDEHYDE ABSORPTION AND DRINKING BEHAVIOR

Gastroenterology (2024)

Cheng Chen Yaojie Fu Yuhong Lin Bryan Mackowiak Bin Gao

10.1016/s0016-5085(24)04328-2

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Citations (0)

HER2 as a Promising Target for Cytotoxicity T Cells in Human Melanoma Therapy

PLoS ONE (2013)

Juan Ma Huamin Han Deruo Liu Wei Li Hongxiang Feng

Anti-HER2/neu antibody therapy has been reported to mediate tumor regression of HER2/ neu+ tumors. Here we demonstrated the expression of HER2 in a wide range of human melanoma cells including a primary culture and seven cell lines, and we further investigated whether HER2 could be served as a target for T cell mediated immunotherapy of human melanoma. Specific cytolytic activity of activated T cells (ATC) armed with anti-CD3 x anti-HER2 bispecific antibody (HER2Bi-Ab) against Malme-3M-luc cells was evaluated by bioluminescent signal generated by luciferase reporter which did not alter HER2 expression or proliferation ability of Malme-3M cells. Contrast with unarmed ATC, increased cytotoxic activity of HER2Bi-armed ATC against Malme-3M-luc cells was observed at effector/target (E/T) ratios of 1:1, 5:1, and 20:1. Moreover, HER2Bi-armed ATC expressed higher level of activation marker CD69 and secreted significantly higher level of IFN-γ than unarmed ATC counterpart at the E/T ratio of 20:1. In addition, compared with anti-HER2 mAb (Herceptin®) or unarmed ATC, HER2Bi-armed ATC showed remarkable suppression effect on Malme-3M-luc tumor cells. Furthermore, in melanoma tumor cell xenograft mice, infusion of HER2Bi-armed ATC successfully inhibited the growth of melanoma tumors. The anti-tumor effect of HER2Bi-armed ATC may provide a promising immunotherapy for melanoma in the future.

Cancer Immunotherapy

10.1371/journal.pone.0073261

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Citations (32)