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Featured researches published by Qi Cheng.


Transplantation | 2015

Early Application of Auxiliary Partial Orthotopic Liver Transplantation in Murine Model of Wilson Disease.

Qi Cheng; Songqing He; Dan Gao; Biao Lei; Xin Long; Hui-fang Liang; Peng Zhu; Junfei Jin; Bo Tang; Stephen Tomlinson; Zhi-Ying Wu; Xiaoping Chen

Background Liver transplantation (LT) is the only option of treatment for Wilson disease (WD) when chelation therapy fails, but it is limited due to the shortage of donor. Auxiliary partial orthotopic LT (APOLT) has been performed successfully in end-stage WD patients, which expands the donor pool. Methods Atp7b−/−mice were used as experimental model of WD. Eight- and 20-week-old mice were used as different timepoints to perform APOLT. Serum copper, tissue copper, serum ceruloplasmin (CP), and liver histological examination were observed after operation. Results Hepatic and serum copper levels in Atp7b−/− mice decreased after APOLT, and copper metabolism disorder of WD mice was relieved at both early and late stages. The progression of pathology in the native liver was delayed only when transplantation was performed at an early stage. Conclusions Auxiliary partial orthotopic LT can significantly improve copper metabolism disorder in the Atp7b−/− mice, and early transplantation may prevent the disease progression.


Journal of Molecular and Cellular Cardiology | 2018

HDAC inhibition helps post-MI healing by modulating macrophage polarization

Denise M Kimbrough; Sabina H. Wang; Lillianne H. Wright; Santhosh K. Mani; Harinath Kasiganesan; Amanda C. LaRue; Qi Cheng; Satish N. Nadig; Carl Atkinson; Donald R. Menick

AIMS Following an acute myocardial infarction (MI) the extracellular matrix (ECM) undergoes remodeling in order to prevent dilation of the infarct area and maintain cardiac output. Excessive and prolonged inflammation following an MI exacerbates adverse ventricular remodeling. Macrophages are an integral part of the inflammatory response that contribute to this remodeling. Treatment with histone deacetylase (HDAC) inhibitors preserves LV function and myocardial remodeling in the post-MI heart. This study tested whether inhibition of HDAC activity resulted in preserving post-MI LV function through the regulation of macrophage phenotype and early resolution of inflammation. METHODS AND RESULTS HDAC inhibition does not affect the recruitment of CD45+ leukocytes, CD45+/CD11b+ inflammatory monocytes or CD45+/CD11b+CD86+ inflammatory macrophages for the first 3 days following infarct. Further, HDAC inhibition does not change the high expression level of the inflammatory cytokines in the first days following MI. However, by day 7, there was a significant reduction in the levels of CD45+/Cd11b+ and CD45+/CD11b+/CD86+ cells with HDAC inhibition. Remarkably, HDAC inhibition resulted in the dramatic increase in the recruitment of CD45+/CD11b+/CD206+ alternatively activated macrophages as early as 1 day which remained significantly elevated until 5 days post-MI. qRT-PCR revealed that HDAC inhibitor treatment shifts the cytokine and chemokine environment towards an M2 phenotype with upregulation of M2 markers at 1 and 5 days post-MI. Importantly, HDAC inhibition correlates with significant preservation of both LV ejection fraction and end-diastolic volume and is associated with a significant increase in micro-vessel density in the border zone at 14 days post-MI. CONCLUSION Inhibition of HDAC activity result in the early recruitment of reparative CD45+/CD11b+/CD206+ macrophages in the post-MI heart and correlates with improved ventricular function and remodeling. This work identifies a very promising therapeutic opportunity to manage macrophage phenotype and enhance resolution of inflammation in the post-MI heart.


American Journal of Transplantation | 2018

Donor pretreatment with nebulized complement C3a receptor antagonist mitigates brain-death induced immunological injury post-lung transplant

Qi Cheng; Kunal Patel; Biao Lei; Lindsay Rucker; D. Patterson Allen; Peng Zhu; Chentha Vasu; Paulo N. Martins; Martin Goddard; Satish N. Nadig; Carl Atkinson

Donor brain death (BD) is an inherent part of lung transplantation (LTx) and a key contributor to ischemia‐reperfusion injury (IRI). Complement activation occurs as a consequence of BD in other solid organ Tx and exacerbates IRI, but the role of complement in LTx has not been investigated. Here, we investigate the utility of delivering nebulized C3a receptor antagonist (C3aRA) pretransplant to BD donor lungs in order to reduce post‐LTx IRI. BD was induced in Balb/c donors, and lungs nebulized with C3aRA or vehicle 30 minutes prior to lung procurement. Lungs were then cold stored for 18 hours before transplantation into C57Bl/6 recipients. Donor lungs from living donors (LD) were removed and similarly stored. At 6 hours and 5 days post‐LTx, recipients of BD donor lungs had exacerbated IRI and acute rejection (AR), respectively, compared to recipients receiving LD lungs, as determined by increased histopathological injury, immune cells, and cytokine levels. A single pretransplant nebulized dose of C3aRA to the donor significantly reduced IRI as compared to vehicle‐treated BD donors, and returned IRI and AR grades to that seen following LD LTx. These data demonstrate a role for complement inhibition in the amelioration of IRI post‐LTx in the context of donor BD.


American Journal of Translational Research | 2017

Memory CD4+ T cells are suppressed by CD8+ regulatory T cells in vitro and in vivo

Xin Long; Qi Cheng; Hui-fang Liang; Jianping Zhao; Jian Wang; Wei Wang; Stephen Tomlinson; Lin Chen; Carl Atkinson; Bixiang Zhang; Xiaoping Chen; Peng Zhu


RSC Advances | 2018

Organ preservation with targeted rapamycin nanoparticles: a pre-treatment strategy preventing chronic rejection in vivo

Peng Zhu; Carl Atkinson; Suraj Dixit; Qi Cheng; Danh Tran; Kunal Patel; Yu-Lin Jiang; Scott Esckilsen; Kayla Miller; Grace Bazzle; Patterson Allen; Alfred Moore; Ann-Marie Broome; Satish N. Nadig


Molecular Immunology | 2018

Perfusion of vascularized composite allografts with a complement inhibitor protects against brain death induced injury and IRI

Mahdi Sleiman; Biao Lei; Qi Cheng; Stephen Tomlinson; Carl Atkinson


Journal of Heart and Lung Transplantation | 2018

Modification of Complement Activity in Donor Lungs with Cigarette Smoke Exposure History Improves Post-Lung Transplantation Outcomes

Kunal Patel; Qi Cheng; D.P. Allen; S. Esckilsen; Martin Goddard; Satish N. Nadig; Carl Atkinson


Journal of Heart and Lung Transplantation | 2018

Emphysema Induces Lung-Specific Autoantibodies that Exacerbate Ischemia Reperfusion Injury Post-Lung Transplantation

Kunal Patel; Qi Cheng; D.P. Allen; S. Stephenson; Martin Goddard; Satish N. Nadig; Carl Atkinson


Journal of Heart and Lung Transplantation | 2018

Recipient Emphysema Differentially Affects Immunologic Responses During Acute Lung Allograft Rejection in a Pre-Clinical Model

Kunal Patel; Qi Cheng; D.P. Allen; A. Aliweah; H. Knochelmann; C. Paulos; Martin Goddard; Satish N. Nadig; Carl Atkinson


Journal of Heart and Lung Transplantation | 2017

(159) - Donor Organ Pretreatment with a Gap and Tight Junction Stabilizing Peptide Prevents IRI in a Mouse Lung Transplant Model

Qi Cheng; Kunal Patel; Peng Zhu; L. Rucker; P. Allen; C. Vasu; Satish N. Nadig; Carl Atkinson

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Carl Atkinson

Medical University of South Carolina

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Satish N. Nadig

Medical University of South Carolina

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Kunal Patel

Medical University of South Carolina

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Peng Zhu

Medical University of South Carolina

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Biao Lei

Guilin Medical University

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L. Rucker

Medical University of South Carolina

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Stephen Tomlinson

Medical University of South Carolina

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Hui-fang Liang

Huazhong University of Science and Technology

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Xiaoping Chen

Huazhong University of Science and Technology

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