Yanchao Chen

Chinese Academy of Medical Sciences & Peking Union Medical College

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Jifeng Zhang

University of Michigan–Ann Arbor

Qiming Wang

Hunan Agricultural University

Chunyan Lei

First Affiliated Hospital of Kunming Medical University

Liqun Rao

Hunan Agricultural University

X. Peter

University of Michigan–Ann Arbor

Zhenchao Gao

Shanghai Public Health Clinical Center

Guangling Yang

Shanghai Public Health Clinical Center

Tianyao Zhou

The First Affiliated Hospital, Sun Yat-sen University

Bo Wu

Sichuan University

Yutong Gu

Zhongshan Hospital

Cooperative Institutions

Sichuan University

Central South University

Fudan University

Chinese Academy of Sciences

Sun Yat-sen University

Chinese Academy of Medical Sciences & Peking Union Medical College

University of Michigan–Ann Arbor

West China Hospital of Sichuan University

Shanghai Jiao Tong University

Zhejiang University

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Coexistence and Competition of the Short-Range Incommensurate Antiferromagnetic Order with the Superconducting State ofBaFe2−xNixAs2

Physical Review Letters (2012)

Huiqian Luo Rui Zhang M. Laver Z. Yamani Meng Wang

Superconductivity in the iron pnictides develops near antiferromagnetism, and the antiferromagnetic (AF) phase appears to overlap with the superconducting phase in some materials such as ${\mathrm{BaFe}}_{2\ensuremath{-}x}{T}_{x}{\mathrm{As}}_{2}$ (where $T=\mathrm{Co}$ or Ni). Here we use neutron scattering to demonstrate that genuine long-range AF order and superconductivity do not coexist in ${\mathrm{BaFe}}_{2\ensuremath{-}x}{\mathrm{Ni}}_{x}{\mathrm{As}}_{2}$ near optimal superconductivity. In addition, we find a first-order-like AF-to-superconductivity phase transition with no evidence for a magnetic quantum critical point. Instead, the data reveal that incommensurate short-range AF order coexists and competes with superconductivity, where the AF spin correlation length is comparable to the superconducting coherence length.

10.1103/physrevlett.108.247002

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Citations (96)

A Comparison of Murine Smooth Muscle Cells Generated from Embryonic versus Induced Pluripotent Stem Cells

Stem Cells and Development (2008)

Chang‐Qing Xie Huarong Huang Wei Sheng Long‐Sheng Song Jifeng Zhang

Smooth muscle cell (SMC) differentiation and dedifferentiation play a critical role in the pathogenesis of cardiovascular diseases. The lack of a good and simple in vitro SMC differentiation system has hampered the progress of SMC field for years. The generation of such an in vitro system would be invaluable for exploring molecular mechanisms of SMC differentiation and dedifferentiation. Recently, the establishment of induced pluripotent stem (iPS) cells has offered a novel therapeutic strategy to generate patient-specific stem cell lines. Here we have investigated whether iPS cells are able to differentiate into SMCs in vitro. Mouse iPS cell (O9 and TT025) monolayers were treated with 10(-5) mol/L all-trans retinoid acid (RA). After 8 days of RA treatment, we found that >40% of the O9 iPS cells expressed the SMC-markers including SMalpha-actin and SM myosin heavy chain. Also, we documented that iPS-derived SMCs acquired SMC functional characteristics including contraction and calcium influx in response to stimuli. Moreover, our results indicated that there were differences in SMC-specific gene expression patterns between SMCs derived from O9 and TT025 iPS as well as normal embryonic stem cells. These differences might be due to disparity in the current iPS technology. Taken together, our data have established a simple iPS-SMC system to generate SMCs in vitro, which has tremendous potential to generate individualized SMCs for vascular tissue engineering and personalized drug screening.

Directed differentiation

10.1089/scd.2008.0179

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Citations (74)

Vascular PPARδ Protects Against Stroke-Induced Brain Injury

Arteriosclerosis Thrombosis and Vascular Biology (2011)

Ke‐Jie Yin Zhen Deng Michael R. Hamblin Jifeng Zhang Yanchao Chen

To investigate the effects of peroxisome proliferator-activated receptor (PPAR)δ in the cerebral vasculature following stroke-induced brain injury.Here, we report a novel finding that selective PPARδ genetic deletion in vascular smooth muscle cells (VSMCs) resulted in increased cerebrovascular permeability and brain infarction in mice after middle cerebral artery occlusion (MCAO). Mechanistically, we revealed for the first time that PPARδ expression is reduced, but matrix metalloproteinase (MMP)-9 activity is increased in cultured VSMCs after oxygen-glucose deprivation and also in the cerebral cortex of mice following MCAO. Moreover, gain- and loss of PPARδ function in VSMCs significantly reduces and increases oxygen-glucose deprivation-induced MMP-9 activity, respectively. We have further identified that MMP-9 is a direct target of PPARδ-mediated transrepression by chromatin immunoprecipitation and PPARδ transcriptional activity assays. Furthermore, inhibition of MMP-9 activity by lentiviral MMP-9 short hairpin RNA effectively improves cerebrovascular permeability and reduces brain infarction in VSMC-selective PPARδ conditional knockout mice after MCAO.Our data demonstrate that PPARδ in VSMCs can prevent ischemic brain injury by inhibition of MMP-9 activation and attenuation of postischemic inflammation. The pharmacological activation of PPARδ may provide a new therapeutic strategy to treat stroke-induced vascular and neuronal damage.

Chromatin immunoprecipitation

Stroke

10.1161/atvbaha.110.221267

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Citations (48)

Direct Reprogramming of Fibroblasts Into Smooth Muscle-Like Cells With Defined Transcription Factors—Brief Report

Arteriosclerosis Thrombosis and Vascular Biology (2018)

Hiroyuki Hirai Bo Yang Minerva T. Garcia-Barrio Oren Rom X. Peter

Objective- To identify the transcription factors that could contribute to direct reprogramming of fibroblasts toward smooth muscle cell fate. Approach and Results- We screened various combinations of transcription factors, including Myocd (myocardin), Mef2C (myocyte enhancer factor 2C), Mef2B (myocyte enhancer factor 2B), Mkl1 (MKL [megakaryoblastic leukemia]/Myocd-like 1), Gata4 (GATA-binding protein 4), Gata5 (GATA-binding protein 5), Gata6 (GATA-binding protein 6), Ets1 (E26 avian leukemia oncogene 1, 5' domain), and their corresponding carboxyterminal fusions to the transactivation domain of MyoD (myogenic differentiation 1)-indicated by *-for their effects on reprogramming mouse embryonic fibroblasts and human adult dermal fibroblasts to the smooth muscle cell fate as determined by the expression of specific markers. The combination of 3 transcription factors, Myocd (or Myocd*) with Mef2C (or Mef2C*) and Gata6, was the most efficient in enhancing the expression of smooth muscle marker genes and decreasing fibroblast gene expression. Additionally, the derived induced smooth muscle-like cells showed a contractile phenotype in response to carbachol. Conclusions- Combination of Myocd and Gata6 with Mef2C* (MG2*) could sufficiently and efficiently direct differentiation of mouse embryonic and human dermal fibroblasts into induced smooth muscle-like cells, thus opening new opportunities for disease modeling, tissue engineering, and personalized medicine.

MEF2C

Myocardin

Reprogramming

Mef2

GATA4

Microphthalmia-associated transcription factor

Myogenic regulatory factors

10.1161/atvbaha.118.310870

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Citations (24)

The protective effects of apelin-13 in HIV-1 tat- induced macrophage infiltration and BBB impairment

Tissue Barriers (2024)

Qi Cao Zeng Wei Jingmin Nie Yongjun Ye Yanchao Chen

Impairment of the blood - brain barrier (BBB) and subsequent inflammatory responses contribute to the development of human immunodeficiency virus (HIV)-1-associated neurocognitive disorders (HAND). Apelin-13, the most abundant member of the apelin family, acts as the ligand of the angiotensin receptor-like 1 (APJ). However, its pharmacological function in HAND and its underlying mechanism are unknown. In the current study, we report that the presence of HIV-1 Tat reduced the levels of Apelin-13 and APJ in the cortex tissue of mice. Importantly, Apelin-13 preserved BBB integrity against HIV-1 Tat in mice by increasing the expression of the tight junction protein zonula occludens-1 (ZO-1) and occludin. Interestingly, increased macrophage infiltration, indicated by elevated CD68-positive staining was observed in the cortex after stimulation with HIV-1, which was mitigated by the administration of Apelin-13. Correspondingly, Apelin-13 reduced the expression of monocyte chemoattractant protein-1; (MCP-1). An

Infiltration (HVAC)

10.1080/21688370.2024.2392361

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Citations (0)

Current challenges and therapeutic advances of CAR-T cell therapy for solid tumors

Cancer Cell International (2024)

T. R. Chen Mingzhao Wang Yanchao Chen Yutao Liu

Abstract The application of chimeric antigen receptor (CAR) T cells in the management of hematological malignancies has emerged as a noteworthy therapeutic breakthrough. Nevertheless, the utilization and effectiveness of CAR-T cell therapy in solid tumors are still limited primarily because of the absence of tumor-specific target antigen, the existence of immunosuppressive tumor microenvironment, restricted T cell invasion and proliferation, and the occurrence of severe toxicity. This review explored the history of CAR-T and its latest advancements in the management of solid tumors. According to recent studies, optimizing the design of CAR-T cells, implementing logic-gated CAR-T cells and refining the delivery methods of therapeutic agents can all enhance the efficacy of CAR-T cell therapy. Furthermore, combination therapy shows promise as a way to improve the effectiveness of CAR-T cell therapy. At present, numerous clinical trials involving CAR-T cells for solid tumors are actively in progress. In conclusion, CAR-T cell therapy has both potential and challenges when it comes to treating solid tumors. As CAR-T cell therapy continues to evolve, further innovations will be devised to surmount the challenges associated with this treatment modality, ultimately leading to enhanced therapeutic response for patients suffered solid tumors.

Cell therapy

Solid tumor

CAR T-cell therapy

10.1186/s12935-024-03315-3

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Citations (17)

Analysis of the influencing factors of the clinical effect of respiratory humidifier in treating AIDS complicated with severe Pneumocystis jiroveci pneumonia.

PubMed (2021)

Qi Cao Wei Zeng Jingmin Nie Yongjun Ye Yanchao Chen

To analyze the factors influencing the clinical effect of using respiratory humidifier in patients with AIDS complicated with severe Pneumocystis jiroveci pneumonia (PCP).According to the treatment results, AIDS patients with severe PCP were divided into two groups, successful group (n=68) and failure group (n=94), to compare the early ventilation changes between the two groups.The ICU ratio of the successful group was lower than that of the failure group (P<0.05). The respiratory frequency, heart rate, PaO2, C-reactive protein and SOFA score of the successful group were lower than those in the failure group (P<0.05), while SpO2, FiO2, PaO2/FiO2, SpO2/FiO2, Rox index and IL-10 levels were increased in the successful group (P<0.05). The successful group had higher IL-6 and IL-1β level than that of the failure group. The levels of IL-8 were decreased (P<0.05). The success of respiratory humidifier was negatively correlated with the score of SOFA (P<0.05).The clinical effect of respiratory humidifier in the treatment of AIDS patients with severe PCP was related to PaO2/FiO2, PaO2, ROX index, SOFA score, and IL-6 and IL-8 levels.

SOFA score

Acute respiratory failure

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Engineering vascular tissue with functional smooth muscle cells derived from human iPS cells and nanofibrous scaffolds

Biomaterials (2014)

Yongyu Wang Jiang Hu Jiao Jiao Zhongning Liu Zhou Zhou

Regenerative Medicine

Germ layer

Matrix (chemical analysis)

10.1016/j.biomaterials.2014.07.011

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Citations (121)

Strong-coupling superconductivity in NaFe1−xCoxAs: Validity of Eliashberg theory

Physical Review B (2013)

Guotai Tan P. Zheng Xiancheng Wang Yanchao Chen Xiaotian Zhang

We study the normal-state and superconducting properties of the NaFe${}_{1\ensuremath{-}x}$Co${}_{x}$As system by specific heat measurements. Both the normal-state Sommerfeld coefficient and superconducting condensation energy are strongly suppressed in the underdoped and heavily overdoped samples. The low-temperature electronic specific heat can be well fitted by either a one-gap or a two-gap BCS-type function for all the superconducting samples. The ratio ${\ensuremath{\gamma}}_{N}{T}_{c}^{2}/{H}_{c}^{2}(0)$ can nicely associate the neutron spin resonance as the bosons in the standard Eliashberg model. However, the value of $\ensuremath{\Delta}C/{T}_{c}{\ensuremath{\gamma}}_{N}$ near optimal doping is larger than the maximum value the model can obtain. Our results suggest that the high-${T}_{c}$ superconductivity in the Fe-based superconductors may be understood within the framework of boson-exchange mechanism but significant modification may be needed to account for the finite-temperature properties.

Specific heat

BCS theory

10.1103/physrevb.87.144512

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Citations (30)

KLF11 mediates PPARγ cerebrovascular protection in ischaemic stroke

Brain (2013)

Ke‐Jie Yin Yanbo Fan Michael R. Hamblin Jifeng Zhang Tainqing Zhu

Peroxisome proliferator-activated receptor gamma (PPARγ) is emerging as a major regulator in neurological diseases. However, the role of (PPARγ) and its co-regulators in cerebrovascular endothelial dysfunction after stroke is unclear. Here, we have demonstrated that (PPARγ) activation by pioglitazone significantly inhibited both oxygen–glucose deprivation-induced cerebral vascular endothelial cell death and middle cerebral artery occlusion-triggered cerebrovascular damage. Consistent with this finding, selective (PPARγ) genetic deletion in vascular endothelial cells resulted in increased cerebrovascular permeability and brain infarction in mice after focal ischaemia. Moreover, we screened for (PPARγ) co-regulators using a genome-wide and high-throughput co-activation system and revealed KLF11 as a novel (PPARγ) co-regulator, which interacted with (PPARγ) and regulated its function in mouse cerebral vascular endothelial cell cultures. Interestingly, KLF11 was also found as a direct transcriptional target of (PPARγ). Furthermore, KLF11 genetic deficiency effectively abolished pioglitazone cytoprotection in mouse cerebral vascular endothelial cell cultures after oxygen–glucose deprivation, as well as pioglitazone-mediated cerebrovascular protection in a mouse middle cerebral artery occlusion model. Mechanistically, we demonstrated that KLF11 enhanced (PPARγ) transcriptional suppression of the pro-apoptotic microRNA-15a (miR-15a) gene, resulting in endothelial protection in cerebral vascular endothelial cell cultures and cerebral microvasculature after ischaemic stimuli. Taken together, our data demonstrate that recruitment of KLF11 as a novel (PPARγ) co-regulator plays a critical role in the cerebrovascular protection after ischaemic insults. It is anticipated that elucidating the coordinated actions of KLF11 and (PPARγ) will provide new insights into understanding the molecular mechanisms underlying (PPARγ) function in the cerebral vasculature and help to develop a novel therapeutic strategy for the treatment of stroke.

Pioglitazone

10.1093/brain/awt002

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Citations (85)